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Nelson, Matthew J., Silvana Valtcheva, and Laurent Venance. "Magnitude and behavior of cross-talk effects in multichannel electrophysiology experiments." Journal of Neurophysiology 118, no. 1 (July 1, 2017): 574–94. http://dx.doi.org/10.1152/jn.00877.2016.
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Modern neurophysiological experiments frequently involve multiple channels separated by very small distances. A unique methodological concern for multiple-electrode experiments is that of capacitive coupling (cross-talk) between channels. Yet the nature of the cross-talk recording circuit is not well known in the field, and the extent to which it practically affects neurophysiology experiments has never been fully investigated. Here we describe a simple electrical circuit model of simultaneous recording and stimulation with two or more channels and experimentally verify the model using ex vivo brain slice and in vivo whole-brain preparations. In agreement with the model, we find that cross-talk amplitudes increase nearly linearly with the impedance of a recording electrode and are larger for higher frequencies. We demonstrate cross-talk contamination of action potential waveforms from intracellular to extracellular channels, which is observable in part because of the different orders of magnitude between the channels. This contamination is electrode impedance-dependent and matches predictions from the model. We use recently published parameters to simulate cross-talk in high-density multichannel extracellular recordings. Cross-talk effectively spatially smooths current source density (CSD) estimates in these recordings and induces artefactual phase shifts where underlying voltage gradients occur; however, these effects are modest. We show that the effects of cross-talk are unlikely to affect most conclusions inferred from neurophysiology experiments when both originating and receiving electrode record signals of similar magnitudes. We discuss other types of experiments and analyses that may be susceptible to cross-talk, techniques for detecting and experimentally reducing cross-talk, and implications for high-density probe design. NEW & NOTEWORTHY We develop and experimentally verify an electrical circuit model describing cross-talk that necessarily occurs between two channels. Recorded cross-talk increased with electrode impedance and signal frequency. We recorded cross-talk contamination of spike waveforms from intracellular to extracellular channels. We simulated high-density multichannel extracellular recordings and demonstrate spatial smoothing and phase shifts that cross-talk enacts on CSD measurements. However, when channels record similar-magnitude signals, effects are modest and unlikely to affect most conclusions.
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Morizio, James, and Vinson Go. "Proceedings #30: Implantable Neural Recording and Stimulation Technologies for in vivo Electrophysiology." Brain Stimulation 12, no. 2 (March 2019): e96-e97. http://dx.doi.org/10.1016/j.brs.2018.12.199.
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Noguchi, Asako, Yuji Ikegaya, and Nobuyoshi Matsumoto. "In Vivo Whole-Cell Patch-Clamp Methods: Recent Technical Progress and Future Perspectives." Sensors 21, no. 4 (February 19, 2021): 1448. http://dx.doi.org/10.3390/s21041448.
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Brain functions are fundamental for the survival of organisms, and they are supported by neural circuits consisting of a variety of neurons. To investigate the function of neurons at the single-cell level, researchers often use whole-cell patch-clamp recording techniques. These techniques enable us to record membrane potentials (including action potentials) of individual neurons of not only anesthetized but also actively behaving animals. This whole-cell recording method enables us to reveal how neuronal activities support brain function at the single-cell level. In this review, we introduce previous studies using in vivo patch-clamp recording techniques and recent findings primarily regarding neuronal activities in the hippocampus for behavioral function. We further discuss how we can bridge the gap between electrophysiology and biochemistry.
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Hong, Guosong, Tian-Ming Fu, Mu Qiao, Robert D. Viveros, Xiao Yang, Tao Zhou, Jung Min Lee, Hong-Gyu Park, Joshua R. Sanes, and Charles M. Lieber. "A method for single-neuron chronic recording from the retina in awake mice." Science 360, no. 6396 (June 28, 2018): 1447–51. http://dx.doi.org/10.1126/science.aas9160.
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The retina, which processes visual information and sends it to the brain, is an excellent model for studying neural circuitry. It has been probed extensively ex vivo but has been refractory to chronic in vivo electrophysiology. We report a nonsurgical method to achieve chronically stable in vivo recordings from single retinal ganglion cells (RGCs) in awake mice. We developed a noncoaxial intravitreal injection scheme in which injected mesh electronics unrolls inside the eye and conformally coats the highly curved retina without compromising normal eye functions. The method allows 16-channel recordings from multiple types of RGCs with stable responses to visual stimuli for at least 2 weeks, and reveals circadian rhythms in RGC responses over multiple day/night cycles.
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Fiáth, Richárd, Patrícia Beregszászi, Domonkos Horváth, Lucia Wittner, Arno A. A. Aarts, Patrick Ruther, Hercules P. Neves, Hajnalka Bokor, László Acsády, and István Ulbert. "Large-scale recording of thalamocortical circuits: in vivo electrophysiology with the two-dimensional electronic depth control silicon probe." Journal of Neurophysiology 116, no. 5 (November 1, 2016): 2312–30. http://dx.doi.org/10.1152/jn.00318.2016.
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Recording simultaneous activity of a large number of neurons in distributed neuronal networks is crucial to understand higher order brain functions. We demonstrate the in vivo performance of a recently developed electrophysiological recording system comprising a two-dimensional, multi-shank, high-density silicon probe with integrated complementary metal-oxide semiconductor electronics. The system implements the concept of electronic depth control (EDC), which enables the electronic selection of a limited number of recording sites on each of the probe shafts. This innovative feature of the system permits simultaneous recording of local field potentials (LFP) and single- and multiple-unit activity (SUA and MUA, respectively) from multiple brain sites with high quality and without the actual physical movement of the probe. To evaluate the in vivo recording capabilities of the EDC probe, we recorded LFP, MUA, and SUA in acute experiments from cortical and thalamic brain areas of anesthetized rats and mice. The advantages of large-scale recording with the EDC probe are illustrated by investigating the spatiotemporal dynamics of pharmacologically induced thalamocortical slow-wave activity in rats and by the two-dimensional tonotopic mapping of the auditory thalamus. In mice, spatial distribution of thalamic responses to optogenetic stimulation of the neocortex was examined. Utilizing the benefits of the EDC system may result in a higher yield of useful data from a single experiment compared with traditional passive multielectrode arrays, and thus in the reduction of animals needed for a research study.
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Holst, Gregory L., William Stoy, Bo Yang, Ilya Kolb, Suhasa B. Kodandaramaiah, Lu Li, Ulf Knoblich, et al. "Autonomous patch-clamp robot for functional characterization of neurons in vivo: development and application to mouse visual cortex." Journal of Neurophysiology 121, no. 6 (June 1, 2019): 2341–57. http://dx.doi.org/10.1152/jn.00738.2018.
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Patch clamping is the gold standard measurement technique for cell-type characterization in vivo, but it has low throughput, is difficult to scale, and requires highly skilled operation. We developed an autonomous robot that can acquire multiple consecutive patch-clamp recordings in vivo. In practice, 40 pipettes loaded into a carousel are sequentially filled and inserted into the brain, localized to a cell, used for patch clamping, and disposed. Automated visual stimulation and electrophysiology software enables functional cell-type classification of whole cell-patched cells, as we show for 37 cells in the anesthetized mouse in visual cortex (V1) layer 5. We achieved 9% yield, with 5.3 min per attempt over hundreds of trials. The highly variable and low-yield nature of in vivo patch-clamp recordings will benefit from such a standardized, automated, quantitative approach, allowing development of optimal algorithms and enabling scaling required for large-scale studies and integration with complementary techniques. NEW & NOTEWORTHY In vivo patch-clamp is the gold standard for intracellular recordings, but it is a very manual and highly skilled technique. The robot in this work demonstrates the most automated in vivo patch-clamp experiment to date, by enabling production of multiple, serial intracellular recordings without human intervention. The robot automates pipette filling, wire threading, pipette positioning, neuron hunting, break-in, delivering sensory stimulus, and recording quality control, enabling in vivo cell-type characterization.
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Wei, Wen Jing, Yi Lin Song, Wen Tao Shi, Chun Xiu Liu, Ting Jun Jiang, and Xin Xia Cai. "A Novel Microelectrode Array Probe Integrated with Electrophysiology Reference Electrode for Neural Recording." Key Engineering Materials 562-565 (July 2013): 67–73. http://dx.doi.org/10.4028/www.scientific.net/kem.562-565.67.
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Nowadays, the study of brain function is advanced by implantable microelectrode arrays for they can simultaneously record signals from different groups of neurons regarding complex neural processes. This article presents the fabrication, characterization and use in vivo neural recording of an implantable microelectrode array probe which integrated with electrophysiology reference electrode. The probe was implemented on Silicon-On-Insulator (SOI) wafer using Micro-Electro-Mechanical-Systems (MEMS) methods, so the recording-site configurations and high-density electrode placement could be precisely defined. The 16 recording sites and the reference electrode were made of platinum. Double layers of platinum electrodes were used so that the width of the reference electrode was as small as 6 μm. The average impedance of the microelectrodes was 0.13 MΩ at 1 kHz. The probe has been employed to record the neural signals of rat, and the results showed that the signal-to-noise ratio (SNR) of the novel probe was as high as 10 and the ordinary probe was 3. Among the 16 recording sites, there are 9 effective sites having recorded useful signals for the probe with reference electrode and 6 for the ordinary probe.
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Lee, Peter, Jorge G. Quintanilla, José M. Alfonso-Almazán, Carlos Galán-Arriola, Ping Yan, Javier Sánchez-González, Nicasio Pérez-Castellano, et al. "In vivo ratiometric optical mapping enables high-resolution cardiac electrophysiology in pig models." Cardiovascular Research 115, no. 11 (February 7, 2019): 1659–71. http://dx.doi.org/10.1093/cvr/cvz039.
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Abstract Aims Cardiac optical mapping is the gold standard for measuring complex electrophysiology in ex vivo heart preparations. However, new methods for optical mapping in vivo have been elusive. We aimed at developing and validating an experimental method for performing in vivo cardiac optical mapping in pig models. Methods and results First, we characterized ex vivo the excitation-ratiometric properties during pacing and ventricular fibrillation (VF) of two near-infrared voltage-sensitive dyes (di-4-ANBDQBS/di-4-ANEQ(F)PTEA) optimized for imaging blood-perfused tissue (n = 7). Then, optical-fibre recordings in Langendorff-perfused hearts demonstrated that ratiometry permits the recording of optical action potentials (APs) with minimal motion artefacts during contraction (n = 7). Ratiometric optical mapping ex vivo also showed that optical AP duration (APD) and conduction velocity (CV) measurements can be accurately obtained to test drug effects. Secondly, we developed a percutaneous dye-loading protocol in vivo to perform high-resolution ratiometric optical mapping of VF dynamics (motion minimal) using a high-speed camera system positioned above the epicardial surface of the exposed heart (n = 11). During pacing (motion substantial) we recorded ratiometric optical signals and activation via a 2D fibre array in contact with the epicardial surface (n = 7). Optical APs in vivo under general anaesthesia showed significantly faster CV [120 (63–138) cm/s vs. 51 (41–64) cm/s; P = 0.032] and a statistical trend to longer APD90 [242 (217–254) ms vs. 192 (182–233) ms; P = 0.095] compared with ex vivo measurements in the contracting heart. The average rate of signal-to-noise ratio (SNR) decay of di-4-ANEQ(F)PTEA in vivo was 0.0671 ± 0.0090 min−1. However, reloading with di-4-ANEQ(F)PTEA fully recovered the initial SNR. Finally, toxicity studies (n = 12) showed that coronary dye injection did not generate systemic nor cardiac damage, although di-4-ANBDQBS injection induced transient hypotension, which was not observed with di-4-ANEQ(F)PTEA. Conclusions In vivo optical mapping using voltage ratiometry of near-infrared dyes enables high-resolution cardiac electrophysiology in translational pig models.
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Eckardt, Lars, Andreas Meißner, Paulus Kirchhof, Thomas Weber, Martin Borggrefe, Günter Breithardt, Hugo Van Aken, and Wilhelm Haverkamp. "In vivo recording of monophasic action potentials in awake dogs - new applications for experimental electrophysiology." Basic Research in Cardiology 96, no. 2 (March 1, 2001): 169–74. http://dx.doi.org/10.1007/s003950170067.
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Jeon, Saeyeong, Youjin Lee, Daeho Ryu, Yoon Kyung Cho, Yena Lee, Sang Beom Jun, and Chang-Hyeon Ji. "Implantable Optrode Array for Optogenetic Modulation and Electrical Neural Recording." Micromachines 12, no. 6 (June 19, 2021): 725. http://dx.doi.org/10.3390/mi12060725.
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During the last decade, optogenetics has become an essential tool for neuroscience research due to its unrivaled feature of cell-type-specific neuromodulation. There have been several technological advances in light delivery devices. Among them, the combination of optogenetics and electrophysiology provides an opportunity for facilitating optogenetic approaches. In this study, a novel design of an optrode array was proposed for realizing optical modulation and electrophysiological recording. A 4 × 4 optrode array and five-channel recording electrodes were assembled as a disposable part, while a reusable part comprised an LED (light-emitting diode) source and a power line. After the characterization of the intensity of the light delivered at the fiber tips, in vivo animal experiment was performed with transgenic mice expressing channelrhodopsin, showing the effectiveness of optical activation and neural recording.
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Cox, David D., Alexander M. Papanastassiou, Daniel Oreper, Benjamin B. Andken, and James J. DiCarlo. "High-Resolution Three-Dimensional Microelectrode Brain Mapping Using Stereo Microfocal X-ray Imaging." Journal of Neurophysiology 100, no. 5 (November 2008): 2966–76. http://dx.doi.org/10.1152/jn.90672.2008.
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Much of our knowledge of brain function has been gleaned from studies using microelectrodes to characterize the response properties of individual neurons in vivo. However, because it is difficult to accurately determine the location of a microelectrode tip within the brain, it is impossible to systematically map the fine three-dimensional spatial organization of many brain areas, especially in deep structures. Here, we present a practical method based on digital stereo microfocal X-ray imaging that makes it possible to estimate the three-dimensional position of each and every microelectrode recording site in “real time” during experimental sessions. We determined the system's ex vivo localization accuracy to be better than 50 μm, and we show how we have used this method to coregister hundreds of deep-brain microelectrode recordings in monkeys to a common frame of reference with median error of <150 μm. We further show how we can coregister those sites with magnetic resonance images (MRIs), allowing for comparison with anatomy, and laying the groundwork for more detailed electrophysiology/functional MRI comparison. Minimally, this method allows one to marry the single-cell specificity of microelectrode recording with the spatial mapping abilities of imaging techniques; furthermore, it has the potential of yielding fundamentally new kinds of high-resolution maps of brain function.
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Hamodi, Ali S., and Kara G. Pratt. "The horizontal brain slice preparation: a novel approach for visualizing and recording from all layers of the tadpole tectum." Journal of Neurophysiology 113, no. 1 (January 1, 2015): 400–407. http://dx.doi.org/10.1152/jn.00672.2014.
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The Xenopus tadpole optic tectum is a multisensory processing center that receives direct visual input as well as nonvisual mechanosensory input. The tectal neurons that comprise the optic tectum are organized into layers. These neurons project their dendrites laterally into the neuropil where visual inputs target the distal region of the dendrite and nonvisual inputs target the proximal region of the same dendrite. The Xenopus tadpole tectum is a popular model to study the development of sensory circuits. However, whole cell patch-clamp electrophysiological studies of the tadpole tectum (using the whole brain or in vivo preparations) have focused solely on the deep-layer tectal neurons because only neurons of the deep layer are visible and accessible for whole cell electrophysiological recordings. As a result, whereas the development and plasticity of these deep-layer neurons has been well-studied, essentially nothing has been reported about the electrophysiology of neurons residing beyond this layer. Hence, there exists a large gap in our understanding about the functional development of the amphibian tectum as a whole. To remedy this, we developed a novel isolated brain preparation that allows visualizing and recording from all layers of the tectum. We refer to this preparation as the “horizontal brain slice preparation.” Here, we describe the preparation method and illustrate how it can be used to characterize the electrophysiology of neurons across all of the layers of the tectum as well as the spatial pattern of synaptic input from the different sensory modalities.
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Harrison, Reid R., Ilya Kolb, Suhasa B. Kodandaramaiah, Alexander A. Chubykin, Aimei Yang, Mark F. Bear, Edward S. Boyden, and Craig R. Forest. "Microchip amplifier for in vitro, in vivo, and automated whole cell patch-clamp recording." Journal of Neurophysiology 113, no. 4 (February 15, 2015): 1275–82. http://dx.doi.org/10.1152/jn.00629.2014.
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Patch clamping is a gold-standard electrophysiology technique that has the temporal resolution and signal-to-noise ratio capable of reporting single ion channel currents, as well as electrical activity of excitable single cells. Despite its usefulness and decades of development, the amplifiers required for patch clamping are expensive and bulky. This has limited the scalability and throughput of patch clamping for single-ion channel and single-cell analyses. In this work, we have developed a custom patch-clamp amplifier microchip that can be fabricated using standard commercial silicon processes capable of performing both voltage- and current-clamp measurements. A key innovation is the use of nonlinear feedback elements in the voltage-clamp amplifier circuit to convert measured currents into logarithmically encoded voltages, thereby eliminating the need for large high-valued resistors, a factor that has limited previous attempts at integration. Benchtop characterization of the chip shows low levels of current noise [1.1 pA root mean square (rms) over 5 kHz] during voltage-clamp measurements and low levels of voltage noise (8.2 μV rms over 10 kHz) during current-clamp measurements. We demonstrate the ability of the chip to perform both current- and voltage-clamp measurement in vitro in HEK293FT cells and cultured neurons. We also demonstrate its ability to perform in vivo recordings as part of a robotic patch-clamping system. The performance of the patch-clamp amplifier microchip compares favorably with much larger commercial instrumentation, enabling benchtop commoditization, miniaturization, and scalable patch-clamp instrumentation.
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Annecchino, Luca A., and Simon R. Schultz. "Progress in automating patch clamp cellular physiology." Brain and Neuroscience Advances 2 (January 1, 2018): 239821281877656. http://dx.doi.org/10.1177/2398212818776561.
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Patch clamp electrophysiology has transformed research in the life sciences over the last few decades. Since their inception, automatic patch clamp platforms have evolved considerably, demonstrating the capability to address both voltage- and ligand-gated channels, and showing the potential to play a pivotal role in drug discovery and biomedical research. Unfortunately, the cell suspension assays to which early systems were limited cannot recreate biologically relevant cellular environments, or capture higher order aspects of synaptic physiology and network dynamics. In vivo patch clamp electrophysiology has the potential to yield more biologically complex information and be especially useful in reverse engineering the molecular and cellular mechanisms of single-cell and network neuronal computation, while capturing important aspects of human disease mechanisms and possible therapeutic strategies. Unfortunately, it is a difficult procedure with a steep learning curve, which has restricted dissemination of the technique. Luckily, in vivo patch clamp electrophysiology seems particularly amenable to robotic automation. In this review, we document the development of automated patch clamp technology, from early systems based on multi-well plates through to automated planar-array platforms, and modern robotic platforms capable of performing two-photon targeted whole-cell electrophysiological recordings in vivo.
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Wicks, Robert T., Mark R. Witcher, Daniel E. Couture, Adrian W. Laxton, Gautam Popli, Christopher T. Whitlow, Dustin Fetterhoff, et al. "Hippocampal CA1 and CA3 neural recording in the human brain: validation of depth electrode placement through high-resolution imaging and electrophysiology." Neurosurgical Focus 49, no. 1 (July 2020): E5. http://dx.doi.org/10.3171/2020.4.focus20164.
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OBJECTIVEIntracranial human brain recordings typically utilize recording systems that do not distinguish individual neuron action potentials. In such cases, individual neurons are not identified by location within functional circuits. In this paper, verified localization of singly recorded hippocampal neurons within the CA3 and CA1 cell fields is demonstrated.METHODSMacro-micro depth electrodes were implanted in 23 human patients undergoing invasive monitoring for identification of epileptic seizure foci. Individual neurons were isolated and identified via extracellular action potential waveforms recorded via macro-micro depth electrodes localized within the hippocampus. A morphometric survey was performed using 3T MRI scans of hippocampi from the 23 implanted patients, as well as 46 normal (i.e., nonepileptic) patients and 26 patients with a history of epilepsy but no history of depth electrode placement, which provided average dimensions of the hippocampus along typical implantation tracks. Localization within CA3 and CA1 cell fields was tentatively assigned on the basis of recording electrode site, stereotactic positioning of the depth electrode in comparison with the morphometric survey, and postsurgical MRI. Cells were selected as candidate CA3 and CA1 principal neurons on the basis of waveform and firing rate characteristics and confirmed within the CA3-to-CA1 neural projection pathways via measures of functional connectivity.RESULTSCross-correlation analysis confirmed that nearly 80% of putative CA3-to-CA1 cell pairs exhibited positive correlations compatible with feed-forward connection between the cells, while only 2.6% exhibited feedback (inverse) connectivity. Even though synchronous and long-latency correlations were excluded, feed-forward correlation between CA3-CA1 pairs was identified in 1071 (26%) of 4070 total pairs, which favorably compares to reports of 20%–25% feed-forward CA3-CA1 correlation noted in published animal studies.CONCLUSIONSThis study demonstrates the ability to record neurons in vivo from specified regions and subfields of the human brain. As brain-machine interface and neural prosthetic research continues to expand, it is necessary to be able to identify recording and stimulation sites within neural circuits of interest.
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Vaillant, Fanny, Julie Magat, Pierre Bour, Jérôme Naulin, David Benoist, Virginie Loyer, Delphine Vieillot, et al. "Magnetic resonance-compatible model of isolated working heart from large animal for multimodal assessment of cardiac function, electrophysiology, and metabolism." American Journal of Physiology-Heart and Circulatory Physiology 310, no. 10 (May 15, 2016): H1371—H1380. http://dx.doi.org/10.1152/ajpheart.00825.2015.
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To provide a model close to the human heart, and to study intrinsic cardiac function at the same time as electromechanical coupling, we developed a magnetic resonance (MR)-compatible setup of isolated working perfused pig hearts. Hearts from pigs (40 kg, n = 20) and sheep ( n = 1) were blood perfused ex vivo in the working mode with and without loaded right ventricle (RV), for 80 min. Cardiac function was assessed by measuring left intraventricular pressure and left ventricular (LV) ejection fraction (LVEF), aortic and mitral valve dynamics, and native T1 mapping with MR imaging (1.5 Tesla). Potential myocardial alterations were assessed at the end of ex vivo perfusion from late-Gadolinium enhancement T1 mapping. The ex vivo cardiac function was stable across the 80 min of perfusion. Aortic flow and LV-dP/d tmin were significantly higher ( P < 0.05) in hearts perfused with loaded RV, without differences for heart rate, maximal and minimal LV pressure, LV-dP/d tmax, LVEF, and kinetics of aortic and mitral valves. T1 mapping analysis showed a spatially homogeneous distribution over the LV. Simultaneous recording of hemodynamics, LVEF, and local cardiac electrophysiological signals were then successfully performed at baseline and during electrical pacing protocols without inducing alteration of MR images. Finally, 31P nuclear MR spectroscopy (9.4 T) was also performed in two pig hearts, showing phosphocreatine-to-ATP ratio in accordance with data previously reported in vivo. We demonstrate the feasibility to perfuse isolated pig hearts in the working mode, inside an MR environment, allowing simultaneous assessment of cardiac structure, mechanics, and electrophysiology, illustrating examples of potential applications.
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Gambrill, Abigail C., Regina L. Faulkner, and Hollis T. Cline. "Experience-dependent plasticity of excitatory and inhibitory intertectal inputs in Xenopus tadpoles." Journal of Neurophysiology 116, no. 5 (November 1, 2016): 2281–97. http://dx.doi.org/10.1152/jn.00611.2016.
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Communication between optic tecta/superior colliculi is thought to be required for sensorimotor behaviors by comparing inputs across the midline; however, the development of and the role of visual experience in the function and plasticity of intertectal connections are unclear. We combined neuronal labeling, in vivo time-lapse imaging, and electrophysiology to characterize the structural and functional development of intertectal axons and synapses in Xenopus tadpole optic tectum. We find that intertectal connections are established early during optic tectal circuit development. We determined the neurotransmitter identity of intertectal neurons using both rabies virus-mediated tracing combined with post hoc immunohistochemistry and electrophysiology. Excitatory and inhibitory intertectal neuronal somata are similarly distributed throughout the tectum. Excitatory and inhibitory intertectal axons are structurally similar and elaborate broadly in the contralateral tectum. We demonstrate that intertectal and retinotectal axons converge onto tectal neurons by recording postsynaptic currents after stimulating intertectal and retinotectal inputs. Cutting the intertectal commissure removes synaptic responses to contralateral tectal stimulation. In vivo time-lapse imaging demonstrated that visual experience drives plasticity in intertectal bouton size and dynamics. Finally, visual experience drives the maturation of excitatory intertectal inputs by increasing AMPA-to- N-methyl-d-aspartate (NMDA) ratios, comparable to experience-dependent maturation of retinotectal inputs, and coordinately increases intertectal GABA receptor-mediated currents. These data indicate that visual experience regulates plasticity of excitatory and inhibitory intertectal inputs, maintaining the balance of excitatory to inhibitory intertectal input. These studies place intertectal inputs as key players in tectal circuit development and suggest that they may play a role in sensory information processing critical to sensorimotor behaviors.
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Kita, H., and S. T. Kitai. "Electrophysiology of rat thalamo-cortical relay neurons: an in vivo intracellular recordingf and labeling study." Brain Research 371, no. 1 (April 1986): 80–89. http://dx.doi.org/10.1016/0006-8993(86)90812-7.
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Rosolen, Serge Georges, Bogdan Kolomiets, Oscar Varela, and Serge Picaud. "Retinal electrophysiology for toxicology studies: Applications and limits of ERG in animals and ex vivo recordings." Experimental and Toxicologic Pathology 60, no. 1 (June 2008): 17–32. http://dx.doi.org/10.1016/j.etp.2007.11.012.
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Rohatgi, Pratik, Nicholas B. Langhals, Daryl R. Kipke, and Parag G. Patil. "In vivo performance of a microelectrode neural probe with integrated drug delivery." Neurosurgical Focus 27, no. 1 (July 2009): E8. http://dx.doi.org/10.3171/2009.4.focus0983.
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Object The availability of sophisticated neural probes is a key prerequisite in the development of future brain-machine interfaces (BMIs). In this study, the authors developed and validated a neural probe design capable of simultaneous drug delivery and electrophysiology recordings in vivo. Focal drug delivery promises to extend dramatically the recording lives of neural probes, a limiting factor to clinical adoption of BMI technology. Methods To form the multifunctional neural probe, the authors affixed a 16-channel microfabricated silicon electrode array to a fused silica catheter. Three experiments were conducted in rats to characterize the performance of the device. Experiment 1 examined cellular damage from probe insertion and the drug distribution in tissue. Experiment 2 measured the effects of saline infusions delivered through the probe on concurrent electrophysiological measurements. Experiment 3 demonstrated that a physiologically relevant amount of drug can be delivered in a controlled fashion. For these experiments, Hoechst and propidium iodide stains were used to assess insertion trauma and the tissue distribution of the infusate. Artificial CSF (aCSF) and tetrodotoxin (TTX) were injected to determine the efficacy of drug delivery. Results The newly developed multifunctional neural probes were successfully inserted into rat cortex and were able to deliver fluids and drugs that resulted in the expected electrophysiological and histological responses. The damage from insertion of the device into brain tissue was substantially less than the volume of drug dispersion in tissue. Electrophysiological activity, including both individual spikes as well as local field potentials, was successfully recorded with this device during real-time drug delivery. No significant changes were seen in response to delivery of aCSF as a control experiment, whereas delivery of TTX produced the expected result of suppressing all spiking activity in the vicinity of the catheter outlet. Conclusions Multifunctional neural probes such as the ones developed and validated within this study have great potential to help further understand the design space and criteria for the next generation of neural probe technology. By incorporating integrated drug delivery functionality into the probes, new treatment options for neurological disorders and regenerative neural interfaces using localized and feedback-controlled delivery of drugs can be realized in the near future.
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Uta, Daisuke, Takumi Oti, Tatsuya Sakamoto, and Hirotaka Sakamoto. "In Vivo Electrophysiology of Peptidergic Neurons in Deep Layers of the Lumbar Spinal Cord after Optogenetic Stimulation of Hypothalamic Paraventricular Oxytocin Neurons in Rats." International Journal of Molecular Sciences 22, no. 7 (March 26, 2021): 3400. http://dx.doi.org/10.3390/ijms22073400.
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The spinal ejaculation generator (SEG) is located in the central gray (lamina X) of the rat lumbar spinal cord and plays a pivotal role in the ejaculatory reflex. We recently reported that SEG neurons express the oxytocin receptor and are activated by oxytocin projections from the paraventricular nucleus of hypothalamus (PVH). However, it is unknown whether the SEG responds to oxytocin in vivo. In this study, we analyzed the characteristics of the brain–spinal cord neural circuit that controls male sexual function using a newly developed in vivo electrophysiological technique. Optogenetic stimulation of the PVH of rats expressing channel rhodopsin under the oxytocin receptor promoter increased the spontaneous firing of most lamina X SEG neurons. This is the first demonstration of the in vivo electrical response from the deeper (lamina X) neurons in the spinal cord. Furthermore, we succeeded in the in vivo whole-cell recordings of lamina X neurons. In vivo whole-cell recordings may reveal the features of lamina X SEG neurons, including differences in neurotransmitters and response to stimulation. Taken together, these results suggest that in vivo electrophysiological stimulation can elucidate the neurophysiological response of a variety of spinal neurons during male sexual behavior.
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Nunez, A., F. Amzica, and M. Steriade. "Electrophysiology of cat association cortical cells in vivo: intrinsic properties and synaptic responses." Journal of Neurophysiology 70, no. 1 (July 1, 1993): 418–30. http://dx.doi.org/10.1152/jn.1993.70.1.418.
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1. The intrinsic properties and synaptic responses of association cortical neurons (n = 179) recorded from cat's areas 5 and 7 were studied in vivo. Intracellular recordings were performed under urethane anesthesia. Resting membrane potential (Vm) was -71.7 +/- 1.2 (SE) mV, amplitude of action potential was 83.7 +/- 2.3 mV, and input resistance was 18.4 +/- 1.8 M omega. Cells were identified ortho- and antidromically from lateroposterior and centrolateral thalamic nuclei and from homotopic foci in the contralateral cortex. Physiologically identified neurons were intracellularly stained with Lucifer yellow (LY) and found to be pyramidal-shaped elements (n = 21). 2. We classified the neurons as regular-spiking and intrinsically bursting cells. Regular-spiking cells were further classified as slow- and fast-adapting according to the adaptation of spike frequency during long-lasting depolarizing current pulses. 3. Regular-spiking, slow-adapting neurons had a monophasic afterhyperpolarization (AHP) or a biphasic AHP with fast and medium components (FAHP, mAHP). Slow-adapting behavior was observed in 84% (n = 119) of the regular-spiking cells. 4. Regular-spiking, fast-adapting cells only fired a train of spikes at the beginning of the pulse. Thereafter, the Vm remained as a depolarizing plateau, occasionally triggering some spikes. These neurons had a monophasic AHP and represented 16% (n = 23) of the regular-spiking neurons. 5. Intrinsically bursting neurons (n = 37) were observed in 20% of neocortical cells at depolarized Vm. Their action potential was followed by a marked depolarizing afterpotential (DAP). Rhythmic (4-10 Hz) bursts occurred during long-lasting depolarizing current pulses. 6. Small (3-10 mV), fast (1.5-4 ms), all-or-none depolarizing potentials were triggered by depolarizing current pulses. They are tentatively regarded as dendritic spikes recorded from the soma because their rate of occurrence changed as a function of the Vm and they were eventually blocked by hyperpolarization. 7. Synaptic stimulation of either thalamic or homotopic contralateral cortical areas elicited a sequence of excitatory postsynaptic potentials (EPSPs) and inhibitory postsynaptic potentials (IPSPs). Two components of the EPSP were revealed. At a hyperpolarized Vm, the initial component of the EPSP increased in amplitude, whereas the secondary component was blocked. Repetitive (10 Hz) stimulation of the thalamus or contralateral cortex elicited incremental responses. The augmentation phenomenon was due to an increase in the secondary component of the EPSP. The cortically elicited augmenting responses survived extensive thalamic lesions. A short IPSP and a long-lasting IPSP were evoked by thalamic or cortical stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)
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Wallace, Michael L., Geeske M. van Woerden, Ype Elgersma, Spencer L. Smith, and Benjamin D. Philpot. "Ube3a loss increases excitability and blunts orientation tuning in the visual cortex of Angelman syndrome model mice." Journal of Neurophysiology 118, no. 1 (July 1, 2017): 634–46. http://dx.doi.org/10.1152/jn.00618.2016.
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Angelman syndrome (AS) is a neurodevelopmental disorder caused by loss of the maternally inherited allele of UBE3A. Ube3aSTOP/p+ mice recapitulate major features of AS in humans and allow conditional reinstatement of maternal Ube3a with the expression of Cre recombinase. We have recently shown that AS model mice exhibit reduced inhibitory drive onto layer (L)2/3 pyramidal neurons of visual cortex, which contributes to a synaptic excitatory/inhibitory imbalance. However, it remains unclear how this loss of inhibitory drive affects neural circuits in vivo. Here we examined visual cortical response properties in individual neurons to explore the consequences of Ube3a loss on intact cortical circuits and processing. Using in vivo patch-clamp electrophysiology, we measured the visually evoked responses to square-wave drifting gratings in L2/3 regular-spiking (RS) neurons in control mice, Ube3a-deficient mice, and mice in which Ube3a was conditionally reinstated in GABAergic neurons. We found that Ube3a-deficient mice exhibited enhanced pyramidal neuron excitability in vivo as well as weaker orientation tuning. These observations are the first to show alterations in cortical computation in an AS model, and they suggest a basis for cortical dysfunction in AS. NEW & NOTEWORTHY Angelman syndrome (AS) is a severe neurodevelopmental disorder caused by the loss of the gene UBE3A. Using electrophysiological recording in vivo, we describe visual cortical dysfunctions in a mouse model of AS. Aberrant cellular properties in AS model mice could be improved by reinstating Ube3a in inhibitory neurons. These findings suggest that inhibitory neurons play a substantial role in the pathogenesis of AS.
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Jia, Xiaoxuan, Joshua H. Siegle, Corbett Bennett, Samuel D. Gale, Daniel J. Denman, Christof Koch, and Shawn R. Olsen. "High-density extracellular probes reveal dendritic backpropagation and facilitate neuron classification." Journal of Neurophysiology 121, no. 5 (May 1, 2019): 1831–47. http://dx.doi.org/10.1152/jn.00680.2018.
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Different neuron types serve distinct roles in neural processing. Extracellular electrical recordings are extensively used to study brain function but are typically blind to cell identity. Morphoelectrical properties of neurons measured on spatially dense electrode arrays have the potential to distinguish neuron types. We used high-density silicon probes to record from cortical and subcortical regions of the mouse brain. Extracellular waveforms of each neuron were detected across many channels and showed distinct spatiotemporal profiles among brain regions. Classification of neurons by brain region was improved with multichannel compared with single-channel waveforms. In visual cortex, unsupervised clustering identified the canonical regular-spiking (RS) and fast-spiking (FS) classes but also indicated a subclass of RS units with unidirectional backpropagating action potentials (BAPs). Moreover, BAPs were observed in many hippocampal RS cells. Overall, waveform analysis of spikes from high-density probes aids neuron identification and can reveal dendritic backpropagation. NEW & NOTEWORTHY It is challenging to identify neuron types with extracellular electrophysiology in vivo. We show that spatiotemporal action potentials measured on high-density electrode arrays can capture cell type-specific morphoelectrical properties, allowing classification of neurons across brain structures and within the cortex. Moreover, backpropagating action potentials are reliably detected in vivo from subpopulations of cortical and hippocampal neurons. Together, these results enhance the utility of dense extracellular electrophysiology for cell-type interrogation of brain network function.
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Bear, Christine E., and Eldon A. Shaffer. "Hepatocellular water and electrolyte secretion." Canadian Journal of Physiology and Pharmacology 66, no. 10 (October 1, 1988): 1253–60. http://dx.doi.org/10.1139/y88-206.
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The study of hepatocellular water and electrolyte secretion has been hampered because of the inaccessibility of the hepatobiliary secretory lumen, the canaliculus. The advent of novel experimental models has allowed the application of electrophysiological techniques to investigate the ionic basis of hepatocellular secretion. The "hepatocyte couplet" isolated from the liver in primary monolayer cultures consists of two hepatocytes which enclose a single canalicular unit. The canaliculus of the couplet appears to behave as it would in vivo, exhibiting both secretory and contractile activity. Intracellular microelectrode recordings from this functional unit have permitted direct electrophysiological assessment of cellular and canalicular potentials and measurement of individual ion conductances across the basolateral membrane surface. Further, the application of patch-clamp electrophysiology to study hepatocellular ion transport pathways has characterized individual channel proteins. Intracellular and (or) patch-clamp electrophysiology has elucidated the ion conductance changes activated by bile salts like taurocholate, neurotransmitters like adrenaline, and hormones such as glucagon. These innovative approaches hold much promise in the future study of the ionic basis of hepatocellular secretion.
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Gristwood, R. W., and A. L. Rothaul. "The ex-vivo effects of thyroid status and extracellular calcium concentration on rat atrial and ventricular electrophysiology." Canadian Journal of Physiology and Pharmacology 66, no. 1 (January 1, 1988): 90–94. http://dx.doi.org/10.1139/y88-017.
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The purpose of this study was to explore the relationship between the thyroid status and both ventricular and atrial electrophysiology in the rat. The study was extended to consider the effects of altering the extracellular calcium concentration. The work was performed in two sections. First, hypothyroid animals were compared with euthyroid (untreated animals); second, hypothyroid animals were compared with hyperthyroid animals. Rats were rendered hypothyroid by pretreatment with the goitrogen methimazole and hyperthyroid by additional treatment with triiodothyronine. Action potential recordings were obtained using standard microelectrode techniques. Action potential measurements were made initially in a Krebs solution to which had been added 2.55 mM calcium (higher Ca Krebs solution) and at the end of each experiment after stabilization with Krebs solution to which had been added 1.28 mM calcium (lower Ca Krebs solution). Assessment of the change in action potential duration on transition from higher to lower Ca Krebs solution revealed that the euthyroid preparations demonstrated less prolongation of action potential duration than the hypothyroid group, and the hyperthyroid group showed hardly any response to reduction in calcium concentration.
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Petric, Stella, Sofia Klein, Lisa Dannenberg, Tillman Lahres, Lukas Clasen, Klaus G. Schmidt, Zhaoping Ding, and Birgit C. Donner. "Pannexin-1 Deficient Mice Have an Increased Susceptibility for Atrial Fibrillation and Show a QT-Prolongation Phenotype." Cellular Physiology and Biochemistry 38, no. 2 (2016): 487–501. http://dx.doi.org/10.1159/000438645.
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Background/Aims: Pannexin-1 (Panx1) is an ATP release channel that is ubiquitously expressed and coupled to several ligand-gated receptors. In isolated cardiac myocytes, Panx1 forms large conductance channels that can be activated by Ca2+ release from the sarcoplasmic reticulum. Here we characterized the electrophysiological function of these channels in the heart in vivo, taking recourse to mice with Panx1 ablation. Methods: Cardiac phenotyping of Panx1 knock-out mice (Panx1-/-) was performed by employing a molecular, cellular and functional approach, including echocardiography, surface and telemetric ECG recordings with QT analysis, physical stress testing and quantification of heart rate variability. In addition, an in vivo electrophysiological study entailed programmed electrical stimulation using an intracardiac octapolar catheter. Results: Panx1 deficiency results in a higher incidence of AV-block, delayed ventricular depolarisation, significant prolongation of QT- and rate corrected QT-interval and a higher incidence of atrial fibrillation after intraatrial burst stimulation. Conclusion: Panx1 seems to play an important role in murine cardiac electrophysiology and warrants further consideration in the context of hereditary forms of atrial fibrillation.
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Porter, James T., and Dalila Nieves. "Presynaptic GABAB Receptors Modulate Thalamic Excitation of Inhibitory and Excitatory Neurons in the Mouse Barrel Cortex." Journal of Neurophysiology 92, no. 5 (November 2004): 2762–70. http://dx.doi.org/10.1152/jn.00196.2004.
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Cortical inhibition plays an important role in the processing of sensory information, and the enlargement of receptive fields by the in vivo application of GABAB receptor antagonists indicates that GABAB receptors mediate some of this cortical inhibition. Although there is evidence of postsynaptic GABAB receptors on cortical neurons, there is no evidence of GABAB receptors on thalamocortical terminals. Therefore to determine if presynaptic GABAB receptors modulate the thalamic excitation of layer IV inhibitory neurons and excitatory neurons in layers II–III and IV of the somatosensory “barrel” cortex of mice, we used a thalamocortical slice preparation and patch-clamp electrophysiology. Stimulation of the ventrobasal thalamus elicited excitatory postsynaptic currents (EPSCs) in cortical neurons. Bath application of baclofen, a selective GABAB receptor agonist, reversibly decreased AMPA receptor-mediated and N-methyl-d-aspartate (NMDA) receptor-mediated EPSCs in inhibitory and excitatory neurons. The GABAB receptor antagonist, CGP 35348, reversed the inhibition produced by baclofen. Blocking the postsynaptic GABAB receptor-mediated effects with a Cs+-based recording solution did not affect the inhibition, suggesting a presynaptic effect of baclofen. Baclofen reversibly increased the paired-pulse ratio and the coefficient of variation, consistent with the presynaptic inhibition of glutamate release. Our results indicate that the presynaptic activation of GABAB receptors modulates thalamocortical excitation of inhibitory and excitatory neurons and provide another mechanism by which cortical inhibition can modulate the processing of sensory information.
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Ghose, Geoffrey M., and Daniel Y. Ts'O. "Form Processing Modules in Primate Area V4." Journal of Neurophysiology 77, no. 4 (April 1, 1997): 2191–96. http://dx.doi.org/10.1152/jn.1997.77.4.2191.
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Ghose, Geoffrey M. and Daniel Y. Ts'o. Form processing modules in primate area V4. J. Neurophysiol. 77: 2191–2196, 1997. Area V4 occupies a central position among the areas of the primate cerebral cortex involved with object recognition and analysis. Consistent with this role, neurons in V4 are selective for many visual attributes including color, orientation, and binocular disparity. However, it is uncertain whether cells within V4 are organized with respect to these properties. In this study we used in vivo optical imaging and electrophysiology in macaque visual cortex to show that cells that share certain physiological properties are indeed grouped together in V4. Our results revealed regions containing cells with common orientation selectivity. These regions were similar in size to those seen in V2 and much larger than those seen in V1 and were confirmed by appropriately targeted single-unit recording. Surprisingly, orientation organization visible through imaging was limited to the portion of V4 representing the central visual fields. Optical imaging also revealed a functional organization related to stimulus size. Size-sensitive regions (S regions) contained cells that were strongly suppressed by large stimuli. In contrast to V2, S regions in V4 contain orientation domains. These results suggest that V4 contains modular assemblies of cells related to particular aspects of form analysis. Such organization may contribute to the construction of object-based representations.
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Etzion, Yoram, Michal Mor, Aryeh Shalev, Shani Dror, Ohad Etzion, Amir Dagan, Ofer Beharier, Arie Moran, and Amos Katz. "New insights into the atrial electrophysiology of rodents using a novel modality: the miniature-bipolar hook electrode." American Journal of Physiology-Heart and Circulatory Physiology 295, no. 4 (October 2008): H1460—H1469. http://dx.doi.org/10.1152/ajpheart.00414.2008.
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Studies of atrial electrophysiology (EP) in rodents are challenging, and available data are sparse. Herein, we utilized a novel type of bipolar electrode to evaluate the atrial EP of rodents through small lateral thoracotomy. In anesthetized rats and mice, we attached two bipolar electrodes to the right atrium and a third to the right ventricle. This standard setup enabled high-resolution EP studies. Moreover, a permanent implantation procedure enabled EP studies in conscious freely moving rats. Atrial EP was evaluated in anesthetized rats, anesthetized mice (ICR and C57BL6 strains), and conscious rats. Signal resolution enabled atrial effective refractory period (AERP) measurements and first time evaluation of the failed 1:1 atrial capture, which was unexpectedly longer than the AERP recorded at near normal cycle length by 27.2 ± 2.3% in rats ( P < 0.0001; n = 35), 31.7 ± 8.3% in ICR mice ( P = 0.0001; n = 13), and 57.7 ± 13.7% in C57BL6 mice ( P = 0.015; n = 4). While AERP rate adaptation was noted when 10 S1s at near normal basic cycle lengths were followed by S2 at varying basic cycle length and S3 for AERP evaluation, such rate adaptation was absent using conventional S1S2 protocols. Atrial tachypacing in rats shortened the AERP values on a timescale of hours, but a reverse remodeling phase was noted thereafter. Comparison of left vs. right atrial pacing in rats was also feasible with the current technique, resulting in similar AERP values recorded in the low right atrium. In conclusion, our findings indicate that in vivo rate adaptation of the rodent atria is different than expected based on previous ex vivo recordings. In addition, atrial electrical remodeling of rats shows unique remodeling-reverse remodeling characteristics that are described here for the first time. Further understanding of these properties should help to determine the clinical relevance as well as limitations of atrial arrhythmia models in rodents.
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Masino, Susan A. "Quantitative Comparison Between Functional Imaging and Single-Unit Spiking in Rat Somatosensory Cortex." Journal of Neurophysiology 89, no. 3 (March 1, 2003): 1702–12. http://dx.doi.org/10.1152/jn.00860.2002.
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The profile of activity across rat somatosensory cortex on stimulation of a single whisker was examined using both intrinsic signal imaging and electrophysiological recording. In the same animals, under sodium pentobarbital anesthesia, the intrinsic signal response to a 5-Hz stimulation of whisker C2 was recorded through a thinned skull. Subsequently, the thinned skull was removed, and individual cortical neurons were recorded at multiple locations and in all cortical layers in response to the same whisker stimulation paradigm. The amplitude of the evoked response obtained with both techniques was quantified across the cortical surface with respect to distance (≤1.6 mm) from the peak intrinsic signal activity. Cortical neurons were rated as having a significant or nonsignificant whisker-evoked response as compared with a baseline period of spontaneous firing; a minority of neurons exhibited a small but significant increase in neuronal spiking even at long distances (>1.6 mm) from the optically determined peak of activity. Overall, this analysis shows a significant correlation between the two techniques in terms of the profile of evoked activity across the cortical surface. Furthermore, this data set affords a detailed and quantitative comparison between the two activity-dependent techniques—one measuring an intrinsic decrease in light reflectance based largely on metabolic changes and one measuring neuronal firing patterns. Studies such as this, comparing directly between imaging and detailed electrophysiology, may influence the interpretation of the extent of the activated area as assessed with in vivo functional imaging techniques.
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Kalmykov, Anna, Changjin Huang, Jacqueline Bliley, Daniel Shiwarski, Joshua Tashman, Arif Abdullah, Sahil K. Rastogi, et al. "Organ-on-e-chip: Three-dimensional self-rolled biosensor array for electrical interrogations of human electrogenic spheroids." Science Advances 5, no. 8 (August 2019): eaax0729. http://dx.doi.org/10.1126/sciadv.aax0729.
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Cell-cell communication plays a pivotal role in coordination and function of biological systems. Three-dimensional (3D) spheroids provide venues to explore cellular communication for tissue development and drug discovery, as their 3D architecture mimics native in vivo microenvironments. Cellular electrophysiology is a prevalent signaling paradigm for studying electroactive cells. Currently, electrophysiological studies do not provide direct, multisite, simultaneous investigation of tissues in 3D. In this study, 3D self-rolled biosensor arrays (3D-SR-BAs) of either active field-effect transistors or passive microelectrodes were implemented to interface human cardiac spheroids in 3D. The arrays provided continuous and stable multiplexed recordings of field potentials with high sensitivity and spatiotemporal resolution, supported with simultaneous calcium imaging. Our approach enables electrophysiological investigation and monitoring of the complex signal transduction in 3D cellular assemblies toward an organ-on-an-electronic-chip (organ-on-e-chip) platform for tissue maturation investigations and development of drugs for disease treatment, such as arrhythmias.
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Martinez, Diana, Richard C. Rogers, Gerlinda E. Hermann, Eileen M. Hasser, and David D. Kline. "Astrocytic glutamate transporters reduce the neuronal and physiological influence of metabotropic glutamate receptors in nucleus tractus solitarii." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 318, no. 3 (March 1, 2020): R545—R564. http://dx.doi.org/10.1152/ajpregu.00319.2019.
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Astrocytic excitatory amino acid transporters (EAATs) are critical to restraining synaptic and neuronal activity in the nucleus tractus solitarii (nTS). Relief of nTS EAAT restraint generates two opposing effects, an increase in neuronal excitability that reduces blood pressure and breathing and an attenuation in afferent [tractus solitarius (TS)]-driven excitatory postsynaptic current (EPSC) amplitude. Although the former is due, in part, to activation of ionotropic glutamate receptors, there remains a substantial contribution from another unidentified glutamate receptor. In addition, the mechanism(s) by which EAAT inhibition reduced TS-EPSC amplitude is unknown. Metabotropic glutamate receptors (mGluRs) differentially modulate nTS excitability. Activation of group I mGluRs on nTS neuron somas leads to depolarization, whereas group II/III mGluRs on sensory afferents decrease TS-EPSC amplitude. Thus we hypothesize that EAATs control postsynaptic excitability and TS-EPSC amplitude via restraint of mGluR activation. To test this hypothesis, we used in vivo recording, brain slice electrophysiology, and imaging of glutamate release and TS-afferent Ca2+. Results show that EAAT blockade in the nTS with (3 S)-3-[[3-[[4-(trifluoromethyl)benzoyl]amino]phenyl]methoxy]-l-aspartic acid (TFB-TBOA) induced group I mGluR-mediated depressor, bradycardic, and apneic responses that were accompanied by neuronal depolarization, elevated discharge, and increased spontaneous synaptic activity. Conversely, upon TS stimulation TFB-TBOA elevated extracellular glutamate to decrease presynaptic Ca2+ and TS-EPSC amplitude via activation of group II/III mGluRs. Together, these data suggest an important role of EAATs in restraining mGluR activation and overall cardiorespiratory function.
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Liu, Xinhuai, Ion R. Popescu, Janna V. Denisova, Rachael L. Neve, Roderick A. Corriveau, and Andrei B. Belousov. "Regulation of Cholinergic Phenotype in Developing Neurons." Journal of Neurophysiology 99, no. 5 (May 2008): 2443–55. http://dx.doi.org/10.1152/jn.00762.2007.
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Specification of neurotransmitter phenotype is critical for neural circuit development and is influenced by intrinsic and extrinsic factors. Recent findings in rat hypothalamus in vitro suggest the role of neurotransmitter glutamate in the regulation of cholinergic phenotype. Here we extended our previous studies on the mechanisms of glutamate-dependent regulation of cholinergic phenotypic properties in hypothalamic neurons. Using immunocytochemistry, electrophysiology, and calcium imaging, we demonstrate that hypothalamic expression of choline acetyltransferase (the cholinergic marker) and responsiveness of neurons to acetylcholine (ACh) receptor agonists increase during chronic administration of an N-methyl-d-aspartate receptor (NMDAR) blocker, MK-801, in developing rats in vivo and genetic and pharmacological inactivation of NMDARs in mouse and rat developing neuronal cultures. In hypothalamic cultures, an inactivation of NMDA receptors also induces ACh-dependent synaptic activity, as do inactivations of PKA, ERK/MAPK, CREB, and NF-κB, which are known to be regulated by NMDA receptors. Interestingly, the increase in cholinergic properties in developing neurons that is induced by NMDAR blockade is prevented by the blockade of ACh receptors, suggesting that function of ACh receptor is required for the cholinergic up-regulation. Using dual recording of monosynaptic excitatory postsynaptic currents, we further demonstrate that chronic inactivation of ionotropic glutamate receptors induces the cholinergic phenotype in a subset of glutamatergic neurons. The phenotypic switch is partial as ACh and glutamate are coreleased. The results suggest that developing neurons may not only coexpress multiple transmitter phenotypes, but can also change the phenotypes following changes in signaling in neuronal circuits.
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Gompf, Heinrich, Jingqiu Chen, Yi Sun, Masashi Yanagisawa, Gary Aston-Jones, and Max B. Kelz. "Halothane-induced Hypnosis Is Not Accompanied by Inactivation of Orexinergic Output in Rodents." Anesthesiology 111, no. 5 (November 1, 2009): 1001–9. http://dx.doi.org/10.1097/aln.0b013e3181b764b3.
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Background One underexploited property of anesthetics is their ability to probe neuronal regulation of arousal. At appropriate doses, anesthetics reversibly obtund conscious perception. However, individual anesthetic agents may accomplish this by altering the function of distinct neuronal populations. Previously the authors showed that isoflurane and sevoflurane inhibit orexinergic neurons, delaying reintegration of sensory perception as denoted by emergence. Here the authors study the effects of halothane. As a halogenated alkane, halothane differs structurally, has a nonoverlapping series of molecular binding partners, and differentially modulates electrophysiologic properties of several ion channels when compared with its halogenated ether relatives. Methods c-Fos immunohistochemistry and in vivo electrophysiology were used to assess neuronal activity. Anesthetic induction and emergence were determined behaviorally in narcoleptic orexin/ataxin-3 mice and control siblings exposed to halothane. Results Halothane-induced hypnosis occurred despite lack of inhibition of orexinergic neurons in mice. In rats, extracellular single-unit recordings within the locus coeruleus showed significantly greater activity during halothane than during a comparable dose of isoflurane. Microinjection of the orexin-1 receptor antagonist SB-334867-A during the active period slowed firing rates of locus coeruleus neurons in halothane-anesthetized rats, but had no effect on isoflurane-anesthetized rats. Surprisingly, orexin/ataxin-3 transgenic mice, which develop narcolepsy with cataplexy because of loss of orexinergic neurons, did not show delayed emergence from halothane. Conclusion Coordinated inhibition of hypothalamic orexinergic and locus coeruleus noradrenergic neurons is not required for anesthetic induction. Normal emergence from halothane-induced hypnosis in orexin-deficient mice suggests that additional wake-promoting systems likely remain active during general anesthesia produced by halothane.
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Benkwitz, Claudia, Mark Liao, Michael J. Laster, James M. Sonner, Edmond I. Eger, and Robert A. Pearce. "Determination of the EC50Amnesic Concentration of Etomidate and Its Diffusion Profile in Brain Tissue." Anesthesiology 106, no. 1 (January 1, 2007): 114–23. http://dx.doi.org/10.1097/00000542-200701000-00020.
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Background Etomidate is a widely used general anesthetic that has become a useful tool to investigate mechanisms of anesthetic action in vivo and in brain slices. However, the free aqueous concentration of etomidate that corresponds to amnesia in vivo and the diffusion profile of etomidate in brain slices are not known. Methods The authors assessed the effect of intraperitoneally injected etomidate on contextual fear conditioning in mice. Etomidate concentrations in brain tissue were obtained by high-performance liquid chromatography. Uptake studies in 400-microm-thick brain slices were used to calculate the diffusion and partition coefficients of etomidate. A diffusion model was used to calculate the expected concentration profile within a brain slice as a function of time and depth. The predicted rate of drug equilibration was compared with the onset of electrophysiologic effects on inhibitory circuit function in recordings from hippocampal brain slices. Results Etomidate impaired contextual fear conditioning with an ED50 dose of 11.0+/-0.1 mg after intraperitoneal injection, which corresponded to an EC50 brain concentration of 208+/-9 ng/g. The brain:artificial cerebrospinal fluid partition coefficient was 3.35, yielding an EC50,amnesia aqueous concentration of 0.25 microm. The diffusion coefficient was approximately 0.2x10 cm/s. The development of etomidate action in hippocampal brain slices was compatible with the concentration profile predicted by this diffusion coefficient. Conclusions The free aqueous concentration of etomidate corresponding to amnesia, as defined by impaired contextual fear conditioning in mice, is 0.25 microM. Diffusion of etomidate into brain slices requires approximately an hour to reach 80% equilibration at a typical recording depth of 100 microm. This information will be useful in designing and interpreting in vitro studies using etomidate.
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Kokay, I. C., P. M. Bull, R. L. Davis, M. Ludwig, and D. R. Grattan. "Expression of the long form of the prolactin receptor in magnocellular oxytocin neurons is associated with specific prolactin regulation of oxytocin neurons." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 290, no. 5 (May 2006): R1216—R1225. http://dx.doi.org/10.1152/ajpregu.00730.2005.
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Magnocellular neurons of the supraoptic (SON) and paraventricular nuclei (PVN) show considerable plasticity during pregnancy and lactation. Prolactin receptors (PRL-R) have been identified in both these nuclei. The aim of this study was to investigate the cell type(s) expressing mRNA for the long form of prolactin receptor (PRL-RL) and to determine whether patterns of expression change during pregnancy and lactation. In addition, we examined effects of prolactin on excitability of oxytocin and vasopressin neurons. Sections from brains of nonpregnant, pregnant, and lactating rats were hybridized with an 35S-labeled probe to label PRL-RL mRNA together with digoxigenin-labeled probes to detect either oxytocin or vasopressin mRNA. In the SON, PRL-RL mRNA was predominantly colocalized with oxytocin mRNA, with over 80% of oxytocin neurons positive for PRL-RL mRNA. Very few (<10%) vasopressin neurons expressed PRL-RL mRNA. In the PVN, PRL-RL mRNA was also predominantly found in oxytocin neurons, and the proportion of PRL-RL-positive oxytocin neurons increased significantly during pregnancy and lactation. As in the SON, relatively few vasopressin cells contained PRL-RL mRNA. For in vivo electrophysiology, nonpregnant rats were anesthetized, and then extracellular single neuron activity was recorded in identified oxytocin and vasopressin neurons. After a period of baseline recording, the effect of prolactin (1 μg icv) on firing rate was examined. Prolactin treatment of nonpregnant rats induced a significant decrease in firing rates of oxytocin neurons. There was no effect of prolactin on the activity of vasopressin neurons. Together, these data provide strong evidence that prolactin directly and specifically regulates activity of oxytocin neurons.
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Cui, Shuai, Shuqi Yao, Chunxiao Wu, Lulu Yao, Peidong Huang, Yongjun Chen, Chunzhi Tang, and Nenggui Xu. "Electroacupuncture Involved in Motor Cortex and Hypoglossal Neural Control to Improve Voluntary Swallowing of Poststroke Dysphagia Mice." Neural Plasticity 2020 (September 27, 2020): 1–18. http://dx.doi.org/10.1155/2020/8857543.
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The descending motor nerve conduction of voluntary swallowing is mainly launched by primary motor cortex (M1). M1 can activate and regulate peripheral nerves (hypoglossal) to control the swallowing. Acupuncture at “Lianquan” acupoint (CV23) has a positive effect against poststroke dysphagia (PSD). In previous work, we have demonstrated that electroacupuncture (EA) could regulate swallowing-related motor neurons and promote swallowing activity in the essential part of central pattern generator (CPG), containing nucleus ambiguus (NA), nucleus of the solitary tract (NTS), and ventrolateral medulla (VLM) under the physiological condition. In the present work, we have investigated the effects of EA on the PSD mice in vivo and sought evidence for PSD improvement by electrophysiology recording and laser speckle contrast imaging (LSCI). Four main conclusions can be drawn from our study: (i) EA may enhance the local field potential in noninfarction area of M1, activate the swallowing-related neurons (pyramidal cells), and increase the motor conduction of noninfarction area in voluntary swallowing; (ii) EA may improve the blood flow in both M1 on the healthy side and deglutition muscles and relieve PSD symptoms; (iii) EA could increase the motor conduction velocity (MCV) in hypoglossal nerve, enhance the EMG of mylohyoid muscle, alleviate the paralysis of swallowing muscles, release the substance P, and restore the ability to drink water; and (iv) EA can boost the functional compensation of M1 in the noninfarction side, strengthen the excitatory of hypoglossal nerve, and be involved in the voluntary swallowing neural control to improve PSD. This research provides a timely and necessary experimental evidence of the motor neural regulation in dysphagia after stroke by acupuncture in clinic.
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Yue, Zongwei, Isaac G. Freedman, Peter Vincent, John P. Andrews, Christopher Micek, Mark Aksen, Reese Martin, et al. "Up and Down States of Cortical Neurons in Focal Limbic Seizures." Cerebral Cortex 30, no. 5 (November 30, 2019): 3074–86. http://dx.doi.org/10.1093/cercor/bhz295.
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Abstract Recent work suggests an important role for cortical–subcortical networks in seizure-related loss of consciousness. Temporal lobe seizures disrupt subcortical arousal systems, which may lead to depressed cortical function and loss of consciousness. Extracellular recordings show ictal neocortical slow waves at about 1 Hz, but it is not known whether these simply represent seizure propagation or alternatively deep sleep-like activity, which should include cortical neuronal Up and Down states. In this study, using in vivo whole-cell recordings in a rat model of focal limbic seizures, we directly examine the electrophysiological properties of cortical neurons during seizures and deep anesthesia. We found that during seizures, the membrane potential of frontal cortical secondary motor cortex layer 5 neurons fluctuates between Up and Down states, with decreased input resistance and increased firing rate in Up states when compared to Down states. Importantly, Up and Down states in seizures are not significantly different from those in deep anesthesia, in terms of membrane potential, oscillation frequency, firing rate, and input resistance. By demonstrating these fundamental similarities in cortical electrophysiology between deep anesthesia and seizures, our results support the idea that a state of decreased cortical arousal may contribute to mechanisms of loss of consciousness during seizures.
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Inserra, Antonio, Danilo De Gregorio, Tamim Rezai, Martha Graciela Lopez-Canul, Stefano Comai, and Gabriella Gobbi. "Lysergic acid diethylamide differentially modulates the reticular thalamus, mediodorsal thalamus, and infralimbic prefrontal cortex: An in vivo electrophysiology study in male mice." Journal of Psychopharmacology 35, no. 4 (March 1, 2021): 469–82. http://dx.doi.org/10.1177/0269881121991569.
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Background: The reticular thalamus gates thalamocortical information flow via finely tuned inhibition of thalamocortical cells in the mediodorsal thalamus. Brain imaging studies in humans show that the psychedelic lysergic acid diethylamide (LSD) modulates activity and connectivity within the cortico-striato-thalamo-cortical (CSTC) circuit, altering consciousness. However, the electrophysiological effects of LSD on the neurons in these brain areas remain elusive. Methods: We employed in vivo extracellular single-unit recordings in anesthetized adult male mice to investigate the dose–response effects of cumulative LSD doses (5–160 µg/kg, intraperitoneal) upon reticular thalamus GABAergic neurons, thalamocortical relay neurons of the mediodorsal thalamus, and pyramidal neurons of the infralimbic prefrontal cortex. Results: LSD decreased spontaneous firing and burst-firing activity in 50% of the recorded reticular thalamus neurons in a dose–response fashion starting at 10 µg/kg. Another population of neurons (50%) increased firing and burst-firing activity starting at 40 µg/kg. This modulation was accompanied by an increase in firing and burst-firing activity of thalamocortical neurons in the mediodorsal thalamus. On the contrary, LSD excited infralimbic prefrontal cortex pyramidal neurons only at the highest dose tested (160 µg/kg). The dopamine D2 receptor (D2) antagonist haloperidol administered after LSD increased burst-firing activity in the reticular thalamus neurons inhibited by LSD, decreased firing and burst-firing activity in the mediodorsal thalamus, and showed a trend towards further increasing the firing activity of neurons of the infralimbic prefrontal cortex. Conclusion: LSD modulates firing and burst-firing activity of reticular thalamus neurons and disinhibits mediodorsal thalamus relay neurons at least partially in a D2-mediated fashion. These effects of LSD on thalamocortical gating could explain its consciousness-altering effects in humans.
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Boada, M. Danilo, Silvia Gutierrez, Carol A. Aschenbrenner, Timothy T. Houle, Ken-ichiro Hayashida, Douglas G. Ririe, and James C. Eisenach. "Nerve injury induces a new profile of tactile and mechanical nociceptor input from undamaged peripheral afferents." Journal of Neurophysiology 113, no. 1 (January 1, 2015): 100–109. http://dx.doi.org/10.1152/jn.00506.2014.
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Chronic pain after nerve injury is often accompanied by hypersensitivity to mechanical stimuli, yet whether this reflects altered input, altered processing, or both remains unclear. Spinal nerve ligation or transection results in hypersensitivity to mechanical stimuli in skin innervated by adjacent dorsal root ganglia, but no previous study has quantified the changes in receptive field properties of these neurons in vivo. To address this, we recorded intracellularly from L4 dorsal root ganglion neurons of anesthetized young adult rats, 1 wk after L5 partial spinal nerve ligation (pSNL) or sham surgery. One week after pSNL, hindpaw mechanical withdrawal threshold in awake, freely behaving animals was decreased in the L4 distribution on the nerve-injured side compared with sham controls. Electrophysiology revealed that high-threshold mechanoreceptive cells of A-fiber conduction velocity in L4 were sensitized, with a seven-fold reduction in mechanical threshold, a seven-fold increase in receptive field area, and doubling of maximum instantaneous frequency in response to peripheral stimuli, accompanied by reductions in after-hyperpolarization amplitude and duration. Only a reduction in mechanical threshold (minimum von Frey hair producing neuronal activity) was observed in C-fiber conduction velocity high-threshold mechanoreceptive cells. In contrast, low-threshold mechanoreceptive cells were desensitized, with a 13-fold increase in mechanical threshold, a 60% reduction in receptive field area, and a 40% reduction in instantaneous frequency to stimulation. No spontaneous activity was observed in L4 ganglia, and the likelihood of recording from neurons without a mechanical receptive field was increased after pSNL. These data suggest massively altered input from undamaged sensory afferents innervating areas of hypersensitivity after nerve injury, with reduced tactile and increased nociceptive afferent response. These findings differ importantly from previous preclinical studies, but are consistent with clinical findings in most patients with chronic neuropathic pain.
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Brook, Joseph, Min-young Kim, Simos Koutsoftidis, David Pitcher, Danya Agha-Jaffar, Annam Sufi, Catherine Jenkins, et al. "Development of a pro-arrhythmic ex vivo intact human and porcine model: cardiac electrophysiological changes associated with cellular uncoupling." Pflügers Archiv - European Journal of Physiology 472, no. 10 (September 1, 2020): 1435–46. http://dx.doi.org/10.1007/s00424-020-02446-6.
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Abstract We describe a human and large animal Langendorff experimental apparatus for live electrophysiological studies and measure the electrophysiological changes due to gap junction uncoupling in human and porcine hearts. The resultant ex vivo intact human and porcine model can bridge the translational gap between smaller simple laboratory models and clinical research. In particular, electrophysiological models would benefit from the greater myocardial mass of a large heart due to its effects on far-field signal, electrode contact issues and motion artefacts, consequently more closely mimicking the clinical setting. Porcine (n = 9) and human (n = 4) donor hearts were perfused on a custom-designed Langendorff apparatus. Epicardial electrograms were collected at 16 sites across the left atrium and left ventricle. A total of 1 mM of carbenoxolone was administered at 5 ml/min to induce cellular uncoupling, and then recordings were repeated at the same sites. Changes in electrogram characteristics were analysed. We demonstrate the viability of a controlled ex vivo model of intact porcine and human hearts for electrophysiology with pharmacological modulation. Carbenoxolone reduces cellular coupling and changes contact electrogram features. The time from stimulus artefact to (-dV/dt)max increased between baseline and carbenoxolone (47.9 ± 4.1–67.2 ± 2.7 ms) indicating conduction slowing. The features with the largest percentage change between baseline and carbenoxolone were fractionation + 185.3%, endpoint amplitude − 106.9%, S-endpoint gradient + 54.9%, S point − 39.4%, RS ratio + 38.6% and (-dV/dt)max − 20.9%. The physiological relevance of this methodological tool is that it provides a model to further investigate pharmacologically induced pro-arrhythmic substrates.
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Nesmith, Haley W., Hanyu Zhang, and Jack M. Rogers. "Optical mapping of electromechanics in intact organs." Experimental Biology and Medicine 245, no. 4 (December 16, 2019): 368–73. http://dx.doi.org/10.1177/1535370219894942.
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Optical mapping has become a widely used and important method in cardiac electrophysiology. The method typically uses voltage-sensitive fluorescent dyes and high-speed cameras to image propagation of electrical waves. However, signals are highly susceptible to artifact caused by motion of the target organ. Consequently, cardiac optical mapping is traditionally performed in isolated, perfused organs whose contraction has been pharmacologically arrested. This has prevented optical mapping from being used to study interactions between electrical and mechanical motion. However, recently, a number of groups have developed methods to implement cardiac optical mapping in the presence of motion. These methods employ two basic strategies: (1) compensate for motion by measuring it or (2) ratiometry. In ratiometry, two signals are recorded from each site. The signals have differing sensitivity to membrane potential, but common motion artifact, which can be cancelled by taking the ratio of the two signals. Some methods use both of these strategies. Methods that measure motion have the additional advantage that this information can be used to quantify the organ’s mechanical function. Doing so enables combined “electromechanical mapping,” which allows optical study of electromechanical interactions. By allowing recording in the presence of motion, the new methods open the door to optical recording in in-vivo preparations. In addition, it is possible to implement electromechanical optical mapping techniques in organ systems other than the heart. For example, it was recently shown that optical mapping of slow wave propagation in the swine stomach is feasible. Such studies have the potential to uncover new information on the role of dysrhythmic slow wave propagation in gastric motility disorders. Impact statement Electrical and mechanical functions in the heart are bidirectionally coupled, yet are usually studied separately because of the different instrumentation technologies that are used in the two areas. Optical mapping is a powerful and widespread tool for imaging electrical propagation, but has traditionally required mechanical function to be arrested. Recently new methods have been devised that enable optical mapping to be performed in beating hearts and also to simultaneously quantify mechanical function. These new technologies promise to yield new information about electromechanical interactions in normal and pathological settings. They are also beginning to find application in other organ systems such as the gastrointestinal tract where they may provide new insight into motility disorders.
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Hume, Catherine, Nancy Sabatier, and John Menzies. "High-Sugar, but Not High-Fat, Food Activates Supraoptic Nucleus Neurons in the Male Rat." Endocrinology 158, no. 7 (April 19, 2017): 2200–2211. http://dx.doi.org/10.1210/en.2016-1640.
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Abstract Oxytocin is a potent anorexigen and is believed to have a role in satiety signaling. We developed rat models to study the activity of oxytocin neurons in response to voluntary consumption or oral gavage of foods using c-Fos immunohistochemistry and in vivo electrophysiology. Using c-Fos expression as an indirect marker of neural activation, we showed that the percentage of magnocellular oxytocin neurons expressing c-Fos increased with voluntary consumption of sweetened condensed milk (SCM). To model the effect of food in the stomach, we gavaged anesthetized rats with SCM. The percentage of supraoptic nucleus and paraventricular nucleus magnocellular oxytocin-immunoreactive neurons expressing c-Fos increased with SCM gavage but not with gastric distention. To further examine the activity of the supraoptic nucleus, we made in vivo electrophysiological recordings from SON neurons, where anesthetized rats were gavaged with SCM or single cream. Pharmacologically identified oxytocin neurons responded to SCM gavage with a linear, proportional, and sustained increase in firing rate, but cream gavage resulted in a transient reduction in firing rate. Blood glucose increased after SCM gavage but not cream gavage. Plasma osmolarity and plasma sodium were unchanged throughout. We show that in response to high-sugar, but not high-fat, food in the stomach, there is an increase in the activity of oxytocin neurons. This does not appear to be a consequence of stomach distention or changes in osmotic pressure. Our data suggest that the presence of specific foods with different macronutrient profiles in the stomach differentially regulates the activity of oxytocin neurons.
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Odierna, Gianmaria Lorenzo, and William Donald Phillips. "The Safety Factor for Neuromuscular Transmission: Effects of Dimethylsulphoxide, Cannabinoids and Synaptic Homeostasis." Journal of Neuromuscular Diseases 8, no. 5 (September 14, 2021): 831–44. http://dx.doi.org/10.3233/jnd-210654.
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Background In myasthenia gravis, impaired postsynaptic sensitivity to acetylcholine results in failure of neuromuscular transmission and fatiguing muscle weakness. Objective Develop an ex vivo muscle contraction assay to test cannabinoids and other substances that might act on the myasthenic neuromuscular junction to restore control of the muscle. Methods Tubocurarine was added to an ex vivo, mouse phrenic nerve-hemidiaphragm muscle preparation to reduce acetylcholine sensitivity. This produced a myasthenia-like decrement in twitch force during a train of 10 nerve impulses (3 / sec). Endplate potential (EPP) recordings were used to confirm and extend the findings. Results Surprisingly, addition to the bath of dimethylsulphoxide (DMSO), at concentrations as low as 0.1%(v/v), partially reversed the decrement in nerve-evoked force. Intracellular electrophysiology, conducted in the presence of tubocurarine, showed that DMSO increased the amplitudes of both the spontaneous miniature EPP (MEPP) and the (nerve-evoked) EPP. In the absence of tubocurarine (synaptic potentials at physiological levels), an adaptive fall in quantal content negated the DMSO-induced rise in EPP amplitude. The effects of cannabinoid receptor agonists (solubilized with DMSO) in the contraction assay do not support their further exploration as useful therapeutic agents for myasthenia gravis. CP 55,940 (a dual agonist for cannabinoid receptor types 1 and 2) reversed the beneficial effects of DMSO. Conclusions: We demonstrate a powerful effect of DMSO upon quantal amplitude that might mislead pharmacological studies of synaptic function wherever DMSO is used as a drug vehicle. Our results also show that compounds targeting impaired neuromuscular transmission should be tested under myasthenic-like conditions, so as to avoid confounding effects of synaptic homeostasis.
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Wang, Di, Qingchen Guo, Yu Zhou, Zheng Xu, Su-Wan Hu, Xiang-Xi Kong, Yu-Mei Yu, et al. "GABAergic Neurons in the Dorsal–Intermediate Lateral Septum Regulate Sleep–Wakefulness and Anesthesia in Mice." Anesthesiology 135, no. 3 (July 13, 2021): 463–81. http://dx.doi.org/10.1097/aln.0000000000003868.
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Background The γ-aminobutyric acid–mediated (GABAergic) inhibitory system in the brain is critical for regulation of sleep–wake and general anesthesia. The lateral septum contains mainly GABAergic neurons, being cytoarchitectonically divided into the dorsal, intermediate, and ventral parts. This study hypothesized that GABAergic neurons of the lateral septum participate in the control of wakefulness and promote recovery from anesthesia. Methods By employing fiber photometry, chemogenetic and optogenetic neuronal manipulations, anterograde tracing, in vivo electrophysiology, and electroencephalogram/electromyography recordings in adult male mice, the authors measured the role of lateral septum GABAergic neurons to the control of sleep–wake transition and anesthesia emergence and the corresponding neuron circuits in arousal and emergence control. Results The GABAergic neurons of the lateral septum exhibited high activities during the awake state by in vivo fiber photometry recordings (awake vs. non–rapid eye movement sleep: 3.3 ± 1.4% vs. –1.3 ± 1.2%, P < 0.001, n = 7 mice/group; awake vs. anesthesia: 2.6 ± 1.2% vs. –1.3 ± 0.8%, P < 0.001, n = 7 mice/group). Using chemogenetic stimulation of lateral septum GABAergic neurons resulted in a 100.5% increase in wakefulness and a 51.2% reduction in non–rapid eye movement sleep. Optogenetic activation of these GABAergic neurons promoted wakefulness from sleep (median [25th, 75th percentiles]: 153.0 [115.9, 179.7] s to 4.0 [3.4, 4.6] s, P = 0.009, n = 5 mice/group) and accelerated emergence from isoflurane anesthesia (514.4 ± 122.2 s vs. 226.5 ± 53.3 s, P < 0.001, n = 8 mice/group). Furthermore, the authors demonstrated that the lateral septum GABAergic neurons send 70.7% (228 of 323 cells) of monosynaptic projections to the ventral tegmental area GABAergic neurons, preferentially inhibiting their activities and thus regulating wakefulness and isoflurane anesthesia depth. Conclusions The results uncover a fundamental role of the lateral septum GABAergic neurons and their circuit in maintaining awake state and promoting general anesthesia emergence time. Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New
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Lozano, Andres M. "ELECTROPHYSIOLOGY: UNIT RECORDING IN HUMANS." Journal of Clinical Neurophysiology 15, no. 3 (May 1998): 269–70. http://dx.doi.org/10.1097/00004691-199805000-00014.
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STEVENSON, WILLIAM G., and KYOKO SOEJIMA. "Recording Techniques for Clinical Electrophysiology." Journal of Cardiovascular Electrophysiology 16, no. 9 (September 2005): 1017–22. http://dx.doi.org/10.1111/j.1540-8167.2005.50155.x.
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Mimee, Andrea, Pauline M. Smith, and Alastair V. Ferguson. "Nesfatin-1 influences the excitability of neurons in the nucleus of the solitary tract and regulates cardiovascular function." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 302, no. 11 (June 1, 2012): R1297—R1304. http://dx.doi.org/10.1152/ajpregu.00266.2011.
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Nesfatin-1 has been identified as one of the most potent centrally acting anorexigenic peptides, and it has also been shown to play important roles in the control of cardiovascular function. In situ hybridization and immunohistochemical studies have revealed the expression of nesfatin-1 throughout the brain and, in particular, in the medullary autonomic gateway known as the nucleus of the solitary tract (NTS). The present study was thus undertaken to explore the cellular correlates and functional roles of nesfatin-1 actions in the medial NTS (mNTS). Using current-clamp electrophysiology recordings from mNTS neurons in slice preparation, we show that bath-applied nesfatin-1 directly influences the excitability of the majority of mNTS neurons by eliciting either depolarizing (42%, mean: 7.8 ± 0.8 mV) or hyperpolarizing (21%, mean: −8. 2 ± 1.0 mV) responses. These responses were observed in all electrophysiologically defined cell types in the NTS and were site specific and concentration dependent. Furthermore, post hoc single cell reverse transcriptase polymerase reaction revealed a depolarizing action of nesfatin-1 on NPY and nucleobindin-2-expressing mNTS neurons. We have also correlated these actions of nesfatin-1 on neuronal membrane potential with physiological outcomes, using in vivo microinjection techniques to demonstrate that nesfatin-1 microinjected into the mNTS induces significant increases in both blood pressure (mean AUC = 3354.1 ± 750.7 mmHg·s, n = 6) and heart rate (mean AUC = 164.8 ± 78.5 beats, n = 6) in rats. Our results provide critical insight into the circuitry and physiology involved in the profound effects of nesfatin-1 and highlight the NTS as a key structure mediating these autonomic actions.
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Manta, Stella, Mostafa El Mansari, Guy Debonnel, and Pierre Blier. "Electrophysiological and neurochemical effects of long-term vagus nerve stimulation on the rat monoaminergic systems." International Journal of Neuropsychopharmacology 16, no. 2 (April 17, 2012): 459–70. http://dx.doi.org/10.1017/s1461145712000387.
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Abstract Vagus nerve stimulation (VNS) is an adjunctive treatment for resistant epilepsy and depression. Electrophysiological recordings in the rat brain have already shown that chronic VNS increases norepinephrine (NE) neuronal firing activity and, subsequently, that of serotonin (5-HT) neurons through an activation of their excitatory α1-adrenoceptors. Long-term VNS was shown to increase the tonic activation of post-synaptic 5-HT1A receptors in the hippocampus. This study was aimed at examining the effect of VNS on extracellular 5-HT, NE and dopamine (DA) levels in different brain areas using in vivo microdialysis, on NE transmission in the hippocampus, and DA neuronal firing activity using electrophysiology. Rats were implanted with a VNS device and stimulated for 14 d with standard parameters used in treatment-resistant depression (0.25 mA, 20 Hz, 500 µs, 30 s on–5 min off). The results of the present study revealed that 2-wk VNS significantly increased extracellular NE levels in the prefrontal cortex and the hippocampus and enhanced the tonic activation of post-synaptic α2-adrenoceptors on pyramidal neurons. The electrophysiological experiments revealed a significant decrease in ventral tegmental area DA neuronal firing rate after long-term VNS; extracellular DA levels were nevertheless increased in the prefrontal cortex and nucleus accumbens. Chronic VNS significantly increased extracellular 5-HT levels in the dorsal raphe but not in the hippocampus and prefrontal cortex. In conclusion, the effect of VNS in increasing the transmission of monoaminergic systems targeted in the treatment of resistant depression should be involved, at least in part, in its antidepressant properties observed in patients not responding to many antidepressant strategies.