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1

Engel, T. A., L. Schimansky-Geier, A. V. M. Herz, S. Schreiber, and I. Erchova. "Subthreshold Membrane-Potential Resonances Shape Spike-Train Patterns in the Entorhinal Cortex." Journal of Neurophysiology 100, no. 3 (September 2008): 1576–89. http://dx.doi.org/10.1152/jn.01282.2007.

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Many neurons exhibit subthreshold membrane-potential resonances, such that the largest voltage responses occur at preferred stimulation frequencies. Because subthreshold resonances are known to influence the rhythmic activity at the network level, it is vital to understand how they affect spike generation on the single-cell level. We therefore investigated both resonant and nonresonant neurons of rat entorhinal cortex. A minimal resonate-and-fire type model based on measured physiological parameters captures fundamental properties of neuronal firing statistics surprisingly well and helps to shed light on the mechanisms that shape spike patterns: 1) subthreshold resonance together with a spike-induced reset of subthreshold oscillations leads to spike clustering and 2) spike-induced dynamics influence the fine structure of interspike interval (ISI) distributions and are responsible for ISI correlations appearing at higher firing rates (≥3 Hz). Both mechanisms are likely to account for the specific discharge characteristics of various cell types.
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2

Khundakar, Ahmad, Christopher Morris, Arthur Oakley, William McMeekin, and Alan J. Thomas. "Morphometric analysis of neuronal and glial cell pathology in the dorsolateral prefrontal cortex in late-life depression." British Journal of Psychiatry 195, no. 2 (August 2009): 163–69. http://dx.doi.org/10.1192/bjp.bp.108.052688.

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BackgroundLate-life depression has been associated with cerebrovascular disease and especially with ischaemic white matter hyperintensities on magnetic resonance imaging. Neuroimaging and morphometric studies have identified abnormalities in the dorsolateral prefrontal cortex.AimsTo examine glial and neuronal density and neuronal volume in the dorsolateral prefrontal cortex in late-life major depression.MethodWe used the disector and nucleator methods to estimate neuronal density and volume and glial density of cells in the dorsolateral prefrontal cortex in a post-mortem study of 17 individuals with late-life major depression and 10 age-matched controls.ResultsWe found a reduction in the volume of pyramidal neurones in the whole cortex, which was also present in layer 3 and more markedly in layer 5. There were no comparable changes in non-pyramidal neurones and no glial differences.ConclusionsOverall, we found a decrease in pyramidal neuronal size in the dorsolateral prefrontal cortex in late-life depression.
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3

Yang, Xiao Li, and Xiao Qiang Liu. "How electromagnetic induction and coupled delay affect stochastic resonance in a modified neuronal network subject to phase noise." International Journal of Modern Physics B 33, no. 26 (October 20, 2019): 1950302. http://dx.doi.org/10.1142/s0217979219503028.

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Through introducing the ingredients of electromagnetic induction and coupled time delay into the original Fitzhugh–Nagumo (FHN) neuronal network, the dynamics of stochastic resonance in a model of modified FHN neuronal network in the environment of phase noise is explored by numerical simulations in this study. On one hand, we demonstrate that the phenomenon of stochastic resonance can appear when the intensity of phase noise is appropriately adjusted, which is further verified to be robust to the edge-added probability of small-world network. Moreover, under the influence of electromagnetic induction, the phase noise-induced resonance response is suppressed, meanwhile, a large noise intensity is required to induce stochastic resonance as the feedback gain of induced current increases. On the other hand, when the coupled time delay is incorporated into this model, the results indicate that the properly tuned time delay can induce multiple stochastic resonances in this neuronal network. However, the phenomenon of multiple stochastic resonances is found to be restrained upon increasing feedback gain of induced current. Surprisingly, by changing the period of phase noise, multiple stochastic resonances can still emerge when the coupled time delay is appropriately tuned to be integer multiples of the period of phase noise.
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4

Liu, Xiaoqiang, and Xiaoli Yang. "Coherence resonance in a modified FHN neuron with autapse and phase noise." International Journal of Modern Physics B 32, no. 30 (December 10, 2018): 1850332. http://dx.doi.org/10.1142/s0217979218503320.

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The influences of phase noise together with autapse on the resonance dynamics in a modified FitzHugh–Nagumo (FHN) neuron are investigated by numerical simulation, where the neuronal model is in the environment of electromagnetic induction. First, it is found that phase noise can induce double coherence resonances, which is further confirmed to be robust to the feedback gain of induction current. Surprisingly, by individually changing the period of phase noise and the feedback gain, a resonance-like behavior also appears. Subsequently, the significant phenomenon of autapse-induced multiple coherence resonances is discovered. Moreover, the phenomenon of multiple coherence resonances can emerge at a broad parameter range of autaptic strength and autaptic delay.
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5

STOCKS, N. G., D. ALLINGHAM, and R. P. MORSE. "THE APPLICATION OF SUPRATHRESHOLD STOCHASTIC RESONANCE TO COCHLEAR IMPLANT CODING." Fluctuation and Noise Letters 02, no. 03 (September 2002): L169—L181. http://dx.doi.org/10.1142/s0219477502000774.

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In this paper we explore the possibility of using a recently discovered form of stochastic resonance - termed suprathreshold stochastic resonance - to improve speech comprehension in patients fitted with cochlear implants. A leaky-integrate-and-fire (LIF) neurone is used to model cochlear nerve activity when subject to electrical stimulation. This model, in principle, captures key aspects of temporal coding in analogue cochlear implants. Estimates for the information transmitted by a population of nerve fibres is obtained as a function of internal (neuronal) noise level. We conclude that SSR does indeed provide a possible mechanism by which information transmission along the cochlear nerve can be improved - and thus may well lead to improved speech comprehension.
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6

Thompson, Richard B., and Peter S. Allen. "The role of the N-acetylaspartate multiplet in the quantification of brain metabolites." Biochemistry and Cell Biology 76, no. 2-3 (May 1, 1998): 497–502. http://dx.doi.org/10.1139/o98-065.

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N-Acetylaspartate, whose methyl singlet is the primary magnetic resonance marker of neuronal dysfunction, also gives rise to a sequence-dependent, strongly coupled multiplet that overlaps the resonances of several other metabolites. Results are presented in this paper of a full numerical calculation of the response of the strongly coupled aspartate multiplet of N-acetylaspartate to a PRESS pulse sequence employing practical slice-selective pulses. These calculations, confirmed by experiments on phantoms, demonstrate the ability to predict the dependence of the response of strongly coupled spins on pulse design, as well as on interpulse evolutions, thereby facilitating a more rigorous comparison of the use of spectral fitting routines employed to extract metabolite concentrations on different instruments.Key words: magnetic resonance spectroscopy, N-acetylaspartate, NAA, brain, quantification, PRESS.
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7

Beatty, Joseph A., Soomin C. Song, and Charles J. Wilson. "Cell-type-specific resonances shape the responses of striatal neurons to synaptic input." Journal of Neurophysiology 113, no. 3 (February 1, 2015): 688–700. http://dx.doi.org/10.1152/jn.00827.2014.

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Neurons respond to synaptic inputs in cell-type-specific ways. Each neuron type may thus respond uniquely to shared patterns of synaptic input. We applied statistically identical barrages of artificial synaptic inputs to four striatal cell types to assess differences in their responses to a realistic input pattern. Each interneuron type fired in phase with a specific input-frequency component. The fast-spiking interneuron fired in relation to the gamma-band (and higher) frequencies, the low-threshold spike interneuron to the beta-band frequencies, and the cholinergic neurons to the delta-band frequencies. Low-threshold spiking and cholinergic interneurons showed input impedance resonances at frequencies matching their spiking resonances. Fast-spiking interneurons showed resonance of input impedance but at lower than gamma frequencies. The spiny projection neuron's frequency preference did not have a fixed frequency but instead tracked its own firing rate. Spiny cells showed no input impedance resonance. Striatal interneurons are each tuned to a specific frequency band corresponding to the major frequency components of local field potentials. Their influence in the circuit may fluctuate along with the contribution of that frequency band to the input. In contrast, spiny neurons may tune to any of the frequency bands by a change in firing rate.
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8

Puil, E., B. Gimbarzevsky, and I. Spigelman. "Primary involvement of K+ conductance in membrane resonance of trigeminal root ganglion neurons." Journal of Neurophysiology 59, no. 1 (January 1, 1988): 77–89. http://dx.doi.org/10.1152/jn.1988.59.1.77.

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1. The complex impedances and impedance magnitude functions were obtained from neurons in in vitro slices of trigeminal root ganglia using frequency-domain analyses of intracellularly recorded voltage responses to specified oscillatory input currents. A neuronal model derived from linearized Hodgkin-Huxley-like equations was used to fit the complex impedance data. This procedure yielded estimates for membrane electrical properties. 2. Membrane resonance was observed in the impedance magnitude functions of all investigated neurons at their initial resting membrane potentials and was similar to that reported previously for trigeminal root ganglion neurons in vivo. Tetrodotoxin (10(-6) M), a Na+-channel blocker, applied in the bathing medium for 20 min produced only minor changes, if any, in the resonance, although gross impairment of Na+-spike electrogenesis was apparent in most of the neurons. Brief applications (1-5 min) of a K+-channel blocker, tetraethylammonium (TEA; 10(-2) M), increased the impedance magnitude and abolished, in a reversible manner, the resonant behavior. In all cases, the resonant frequency was decreased by TEA administration prior to total blockade of resonance. 3. The TEA-induced blockade of resonance was associated with decreases in the estimates of the membrane conductances, without significant alterations of input capacitance. A particularly large decrease was observed in Gr, the time-invariant resting conductance that includes a lumped leak conductance component. The voltage- and time-dependent conductance, GL, and associated relaxation time constant, tau u, also declined progressively during administration of TEA. 4. Systematic variations in the membrane potentials of trigeminal root ganglion neurons were produced by intracellular injections of long-lasting step currents with superposition of the oscillatory current stimuli, in order to assess the effects of TEA on the relationship of the electrical properties to the membrane potential. Applications of TEA led to a depolarizing shift in the dependence of the membrane property estimates, suggesting voltage-dependence of the effects of TEA on presumed K+ channels in the membrane. 5. These data suggest a primary involvement of K+ conductance in the genesis of membrane resonance. This electrical behavior or its ionic mechanism is a major modulator of the subthreshold electrical responsiveness of trigeminal root ganglion neurons.
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9

Ebisu, Toshihiko, William D. Rooney, Steven H. Graham, Michael W. Weiner, and Andrew A. Maudsley. "N-Acetylaspartate as an in vivo Marker of Neuronal Viability in Kainate-Induced Status Epilepticus: 1H Magnetic Resonance Spectroscopic Imaging." Journal of Cerebral Blood Flow & Metabolism 14, no. 3 (May 1994): 373–82. http://dx.doi.org/10.1038/jcbfm.1994.48.

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N-acetylaspartate (NAA) has been proposed as a marker of neuronal density. Therefore, regional measurement of NAA by magnetic resonance spectroscopic imaging (MRSI) may provide a sensitive method for detection of selective neuronal loss, in contrast to conventional imaging techniques such as magnetic resonance imaging (MRI). To test this hypothesis, we produced selective neuronal injury by kainate-induced status epilepticus. Three days later three-dimensional 1H-MRSI was obtained and compared with conventional T2-weighted MRI and histological findings in normal and kainatetreated rats. Reduction of NAA determined by MRSI in piriform cortex, amygdala, and hippocampus correlated well with neuronal injury determined from histology. Changes of NAA, without any MRI changes in hippocampus, indicated greater sensitivity of MRSI for detection of neuronal injury. These results are consistent with the hypothesis that reduction of NAA measured by MRSI may be a sensitive marker of neuronal injury in vivo in a variety of disease states.
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10

Hunter, John D., John G. Milton, Peter J. Thomas, and Jack D. Cowan. "Resonance Effect for Neural Spike Time Reliability." Journal of Neurophysiology 80, no. 3 (September 1, 1998): 1427–38. http://dx.doi.org/10.1152/jn.1998.80.3.1427.

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Hunter, John D., John G. Milton, Peter J. Thomas, and Jack D. Cowan. Resonance effect for neural spike time reliability. J. Neurophysiol. 80: 1427–1438, 1998. The spike timing reliability of Aplysia motoneurons stimulated by repeated presentation of periodic or aperiodic input currents is investigated. Two properties of the input are varied, the frequency content and the relative amplitude of the fluctuations to the mean (expressed as the coefficient of variation; CV). It is shown that, for small relative amplitude fluctuations (CV ≈ 0.05–0.15), the reliability of spike timing is enhanced if the input contains a resonant frequency equal to the firing rate of the neuron in response to the DC component of the input. This resonance-related enhancement in reliability decreases as the relative amplitude of the fluctuations increases (CV → 1). Similar results were obtained for a leaky integrate-and-fire neuronal model, suggesting that these effects are a general property of encoders that combine a threshold with a leaky integrator. These observations suggest that, when the magnitude of input fluctuations is small, changes in the power spectrum of the current fluctuations or in the spike discharge rate can have a pronounced effect on the ability of the neuron to encode a time-varying input with reliably timed spikes.
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11

Yarmish, Gail, and Michael L. Lipton. "Functional Magnetic Resonance Imaging: From Acquisition to Application." Einstein Journal of Biology and Medicine 20, no. 1 (March 2, 2016): 2. http://dx.doi.org/10.23861/ejbm200320103.

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Functional magnetic resonance imaging (fMRI) is a technique that exploits magnetic resonance imaging (MRI) to detect regional brain activity through measurement of the hemodynamic response that is coupled to electrical neuronal activity. The most common fMRI method detects blood oxygen level dependent (BOLD) contrast. The BOLD effect represents alteration in the ratio of deoxygenated to oxygenated hemoglobin within brain tissue following neuronal activity. Alterations in this hemoglobin ratio result from changes in cerebral oxygen extraction, cerebral blood flow, and cerebral blood volume that occur in response to neuronal activity. The small, but detectable, change in magnetics resonance signal intensity is due to the sensitivity of magnetic resonance (MR) images to the paramagnetic deoxygenated state of hemoglobin that is the basis of contrast in fMRI applications. This review describes the physical and physiological bases of the MR signal, the principle of the BOLD effect, technical issues related to fMRI implementation, and fMRI experimental design. Research and clinical applications of fMRI are presented, including the use of fMRI in neurosurgical planning. Since it provides an individualized map of brain function, fMRI enables accurate localization of eloquent brain regions prior to surgery, allowing assessment of surgical risk and prognosis, as well as planning surgical approach.
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12

Jones, Andrew P., Windsor J. Gunawardena, Christopher M. A. Coutinho, John A. Gatt, Ian C. Shaw, and J. Douglas Mitchell. "Preliminary results of proton magnetic resonance spectroscopy in motor neurone disease (amytrophic lateral sclerosis)." Journal of the Neurological Sciences 129 (May 1995): 85–89. http://dx.doi.org/10.1016/0022-510x(95)00072-a.

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13

Dautry, Caroline, Françoise Vaufrey, Emmanuel Brouillet, Nicolas Bizat, Pierre-Gilles Henry, Françoise Condé, Gilles Bloch, and Philippe Hantraye. "Early N-Acetylaspartate Depletion Is a Marker of Neuronal Dysfunction in Rats and Primates Chronically Treated with the Mitochondrial Toxin 3-Nitropropionic Acid." Journal of Cerebral Blood Flow & Metabolism 20, no. 5 (May 2000): 789–99. http://dx.doi.org/10.1097/00004647-200005000-00005.

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N-acetylaspartate (NAA) quantification by 1H-magnetic resonance spectroscopy has been commonly used to assess in vivo neuronal loss in neurodegenerative disorders. Here, the authors used ex vivo and in vivo1H-magnetic resonance spectroscopy in rat and primate models of progressive striatal degeneration induced by the mitochondrial toxin 3-nitropropionate (3NP) to determine whether early NAA depletions could also be associated with neuronal dysfunction. In rats that were treated for 3 days with 3NP and had motor symptoms, the authors found a significant decrease in NAA concentrations, specifically restricted to the striatum. No cell loss or dying cells were found at this stage in these animals. After 5 days of 3NP treatment, a further decrease in striatal NAA concentrations was observed in association with the occurrence of dying neurons in the dorsolateral striatum. In 3NP-treated primates, a similar striatal-selective and early decrease in NAA concentrations was observed after only a few weeks of neurotoxic treatment, without any sign of ongoing cell death. This early decrease in striatal NAA was partially reversed after 4 weeks of 3NP withdrawal. These results demonstrate that early NAA depletions reflect a reversible state of neuronal dysfunction preceding cell degeneration and suggest that in vivo quantification of NAA 1H-magnetic resonance spectroscopy may become a valuable tool for assessing early neuronal dysfunction and the effects of potential neuroprotective therapies in neurodegenerative disorders.
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14

Cecil, K. M. "Effects of early low-level lead exposure on human brain structure, organization and functions." Journal of Developmental Origins of Health and Disease 2, no. 1 (September 28, 2010): 17–24. http://dx.doi.org/10.1017/s2040174410000486.

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Advanced neuroimaging techniques offer unique insights into how childhood lead exposure impacts the brain. Volumetric magnetic resonance imaging affords anatomical information about the size of global, regional and subcomponent structures within the brain. Diffusion tensor imaging provides information about white matter architecture by quantitatively describing how water molecules diffuse within it. Proton magnetic resonance spectroscopy generates quantitative measures of neuronal, axonal and glial elements via concentration levels of select metabolites. Functional magnetic resonance imaging infers neuronal activity associated with a given task performed. Employing these techniques in the study of the Cincinnati Lead Study, a relatively homogeneous birth cohort longitudinally monitored for over 30 years, one can non-invasively and quantitatively explore how childhood lead exposure is associated with adult brain structure, organization and function. These studies yield important findings how environmental lead exposure impacts human health.
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15

Hu, Xiaoping, Tuong Le, Seong-Gi Kim, and Kamil Ugurbil. "An overview of functional magnetic-resonance imaging." Proceedings, annual meeting, Electron Microscopy Society of America 54 (August 11, 1996): 886–87. http://dx.doi.org/10.1017/s0424820100166890.

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In the past few years, one of the most significant developments in magnetic resonance imaging (MRI) is the use of MR imaging to non-invasively map human cortical function without the use of exogenous contrast agents . Since its introduction in 1992, functional magnetic resonance imaging (fMRI) has emerged as a powerful tool for studying neuronal function and generated an enormous amount of interest among neuroscientists, NMR scientists, and clinicians. The purpose of this paper is to outline the principle of fMRI and the associated technical issues and illustrate the utility of fMRI with representative applications.The basis of fMRI is the blood oxygenation level dependent (BOLD) contrast which is derived from the fact that deoxyhemoglobin is paramagnetic and changes in the local concentration of deoxyhemoglobin within the brain lead to alterations in the magnetic resonance signal. Neuronal activation within the cerebral cortex causes an increase in blood flow without a commensurate increase in oxygen extraction.
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16

Shulman, Robert G., Fahmeed Hyder, and Douglas L. Rothman. "Insights from Neuroenergetics into the Interpretation of Functional Neuroimaging: An Alternative Empirical Model for Studying the Brain's Support of Behavior." Journal of Cerebral Blood Flow & Metabolism 34, no. 11 (August 27, 2014): 1721–35. http://dx.doi.org/10.1038/jcbfm.2014.145.

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Functional neuroimaging measures quantitative changes in neurophysiological parameters coupled to neuronal activity during observable behavior. These results have usually been interpreted by assuming that mental causation of behavior arises from the simultaneous actions of distinct psychological mechanisms or modules. However, reproducible localization of these modules in the brain using functional magnetic resonance imaging (MRI) and positron emission tomography (PET) imaging has been elusive other than for sensory systems. In this paper, we show that neuroenergetic studies using PET, calibrated functional magnetic resonance imaging (fMRI), 13C magnetic resonance spectroscopy, and electrical recordings do not support the standard approach, which identifies the location of mental modules from changes in brain activity. Of importance in reaching this conclusion is that changes in neuronal activities underlying the fMRI signal are many times smaller than the high ubiquitous, baseline neuronal activity, or energy in resting, awake humans. Furthermore, the incremental signal depends on the baseline activity contradicting theoretical assumptions about linearity and insertion of mental modules. To avoid these problems, while making use of these valuable results, we propose that neuroimaging should be used to identify observable brain activities that are necessary for a person's observable behavior rather than being used to seek hypothesized mental processes.
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17

Schroeter, Aileen, Joanes Grandjean, Felix Schlegel, Bechara J. Saab, and Markus Rudin. "Contributions of structural connectivity and cerebrovascular parameters to functional magnetic resonance imaging signals in mice at rest and during sensory paw stimulation." Journal of Cerebral Blood Flow & Metabolism 37, no. 7 (October 1, 2016): 2368–82. http://dx.doi.org/10.1177/0271678x16666292.

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Previously, we reported widespread bilateral increases in stimulus-evoked functional magnetic resonance imaging signals in mouse brain to unilateral sensory paw stimulation. We attributed the pattern to arousal-related cardiovascular changes overruling cerebral autoregulation thereby masking specific signal changes elicited by local neuronal activity. To rule out the possibility that interhemispheric neuronal communication might contribute to bilateral functional magnetic resonance imaging responses, we compared stimulus-evoked functional magnetic resonance imaging responses to unilateral hindpaw stimulation in acallosal I/LnJ, C57BL/6, and BALB/c mice. We found bilateral blood-oxygenation-level dependent signal changes in all three strains, ruling out a dominant contribution of transcallosal communication as reason for bilaterality. Analysis of functional connectivity derived from resting-state functional magnetic resonance imaging, revealed that bilateral cortical functional connectivity is largely abolished in I/LnJ animals. Cortical functional connectivity in all strains correlated with structural connectivity in corpus callosum as revealed by diffusion tensor imaging. Given the profound influence of systemic hemodynamics on stimulus-evoked functional magnetic resonance imaging outcomes, we evaluated whether functional connectivity data might be affected by cerebrovascular parameters, i.e. baseline cerebral blood volume, vascular reactivity, and reserve. We found that effects of cerebral hemodynamics on functional connectivity are largely outweighed by dominating contributions of structural connectivity. In contrast, contributions of transcallosal interhemispheric communication to the occurrence of ipsilateral functional magnetic resonance imaging response of equal amplitude to unilateral stimuli seem negligible.
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18

Cirstea, Carmen M., In-Young Choi, Phil Lee, Huiling Peng, Christina L. Kaufman, and Scott H. Frey. "Magnetic resonance spectroscopy of current hand amputees reveals evidence for neuronal-level changes in former sensorimotor cortex." Journal of Neurophysiology 117, no. 4 (April 1, 2017): 1821–30. http://dx.doi.org/10.1152/jn.00329.2016.

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Deafferentation is accompanied by large-scale functional reorganization of maps in the primary sensory and motor areas of the hemisphere contralateral to injury. Animal models of deafferentation suggest a variety of cellular-level changes including depression of neuronal metabolism and even neuronal death. Whether similar neuronal changes contribute to patterns of reorganization within the contralateral sensorimotor cortex of chronic human amputees is uncertain. We used functional MRI-guided proton magnetic resonance spectroscopy to test the hypothesis that unilateral deafferentation is associated with lower levels of N-acetylaspartate (NAA, a putative marker of neuronal integrity) in the sensorimotor hand territory located contralateral to the missing hand in chronic amputees ( n = 19) compared with the analogous hand territory of age- and sex-matched healthy controls ( n = 28). We also tested whether former amputees [i.e., recipients of replanted ( n = 3) or transplanted ( n = 2) hands] exhibit NAA levels that are indistinguishable from controls, possible evidence for reversal of the effects of deafferentation. As predicted, relative to controls, current amputees exhibited lower levels of NAA that were negatively and significantly correlated with the time after amputation. Contrary to our prediction, NAA levels in both replanted and transplanted patients fell within the range of the current amputees. We suggest that lower levels of NAA in current amputees reflects altered neuronal integrity consequent to chronic deafferentation. Thus local changes in NAA levels may provide a means of assessing neuroplastic changes in deafferented cortex. Results from former amputees suggest that these changes may not be readily reversible through reafferentation. NEW & NOTEWORTHY This study is the first to use functional magnetic resonance-guided magnetic resonance spectroscopy to examine neurochemical mechanisms underlying functional reorganization in the primary somatosensory and motor cortices consequent to upper extremity amputation and its potential reversal through hand replantation or transplantation. We provide evidence for selective alteration of cortical neuronal integrity associated with amputation-related deafferentation that may not be reversible.
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19

Hasselmo, Michael E. "Neuronal rebound spiking, resonance frequency and theta cycle skipping may contribute to grid cell firing in medial entorhinal cortex." Philosophical Transactions of the Royal Society B: Biological Sciences 369, no. 1635 (February 5, 2014): 20120523. http://dx.doi.org/10.1098/rstb.2012.0523.

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Data show a relationship of cellular resonance and network oscillations in the entorhinal cortex to the spatial periodicity of grid cells. This paper presents a model that simulates the resonance and rebound spiking properties of entorhinal neurons to generate spatial periodicity dependent upon phasic input from medial septum. The model shows that a difference in spatial periodicity can result from a difference in neuronal resonance frequency that replicates data from several experiments. The model also demonstrates a functional role for the phenomenon of theta cycle skipping in the medial entorhinal cortex.
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Cohen-Gadol, Aaron A., Jullie W. Pan, Jung H. Kim, Dennis D. Spencer, and Hoby H. Hetherington. "Mesial temporal lobe epilepsy: a proton magnetic resonance spectroscopy study and a histopathological analysis." Journal of Neurosurgery 101, no. 4 (October 2004): 613–20. http://dx.doi.org/10.3171/jns.2004.101.4.0613.

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Object. Proton magnetic resonance (MR) spectroscopy imaging of the ratio of N-acetylaspartate (NAA) to creatine (Cr) has proved efficacious as a localizing tool in demonstrating the metabolic changes associated with temporal lobe epilepsy. To analyze the significance of these MR spectroscopy findings further, the authors explored the relationship between regional alterations in the NAA/Cr ratio in hippocampi measured preoperatively and histopathological findings in hippocampi resected in patients with intractable mesial temporal lobe epilepsy (MTLE). Methods. Twelve patients in whom the diagnosis of MTLE had been made and 12 healthy volunteers with no known history of neurological disease underwent high-resolution 1H MR spectroscopy imaging of NAA and Cr (0.64 cm3 nominal voxel resolution) in five voxels spanning the anteroposterior length of the hippocampus. The authors correlated the NAA/Cr ratio with neuropathological findings in resected hippocampi, specifically glial fibrillary acidic protein (GFAP) immunoreactivity and pyramidal neuronal loss. A linear regression analysis of the ipsilateral NAA/Cr ratio revealed a statistically significant relation to the extent of hippocampal neuronal loss in only the CA2 sector (correlation coefficient [r] = −0.66, p < 0.03). The ipsilateral NAA/Cr ratio displayed significant regressions with GFAP immunoreactivity from all the CA sectors (r values ranged from −0.69 and p < 0.01 for the CA4 sector to −0.88 and p < 0.001 for the CA2 sector) except for the CA1. The extent of neuronal cell loss in every hippocampal subfield (r = 0.71−0.74, p < 0.007), except the CA2 (p = 0.08), correlated to the extent of neuronal cell loss in the dentate gyrus. There was no significant relationship between the duration or frequency of seizures and the mean ipsilateral NAA/Cr ratio; however, the mean density of GFAP-immunopositive cells correlated with seizure frequency (p < 0.03). Conclusions. The NAA/Cr ratio may not measure the full extent of hippocampal neuronal cell loss. The significant association of the NAA/Cr ratio with the GFAP immunoreactivity of most CA sectors indicates that the NAA/Cr ratio may provide a more accurate measurement of recent neuronal injury caused by epileptic activity. The coupling between neuronal impairment and astroglial GFAP expression may indicate the close association between neuronal and glial dysfunction in patients with epilepsy.
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Delgado, Teresa C., Inês R. Violante, Laura Nieto-Charques, and Sebastián Cerdán. "Neuroglial Metabolic Compartmentation Underlying Leptin Deficiency in the Obese ob/ob Mice as Detected by Magnetic Resonance Imaging and Spectroscopy Methods." Journal of Cerebral Blood Flow & Metabolism 31, no. 12 (October 5, 2011): 2257–66. http://dx.doi.org/10.1038/jcbfm.2011.134.

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Manganese-Enhanced Magnetic Resonance Imaging (MEMRI), 1H and 13C High-Resolution-Magic Angle Spinning (HR-MAS) Spectroscopy, and genomic approaches were used to compare cerebral activation and neuronal and glial oxidative metabolism in ad libitum fed C57BL6/J leptin-deficient, genetically obese ob/ob mice. T1-weighted Magnetic Resonance Images across the hypothalamic Arcuate and the Ventromedial nuclei were acquired kinetically after manganese infusion. Neuroglial compartmentation was investigated in hypothalamic biopsies after intraperitoneal injections of [1-13C]glucose or [2-13C]acetate. Total RNA was extracted to determine the effects of leptin deficiency in the expression of representative genes coding for regulatory enzymes of hypothalamic energy pathways and glutamatergic neurotransmission. Manganese-Enhanced Magnetic Resonance Imaging revealed enhanced cerebral activation in the hypothalamic Arcuate and Ventromedial nuclei of the ob/ob mice. 13C HR-MAS analysis showed increased 13C accumulation in the hypothalamic glutamate and glutamine carbons of ob/ob mice after the administration of [1-13C]glucose, a primarily neuronal substrate. Hypothalamic expression of the genes coding for glucokinase, phosphofructokinase, pyruvate dehydrogenase, and glutamine synthase was not significantly altered while pyruvate kinase expression was slightly upregulated. In conclusion, leptin deficiency associated with obesity led to increased cerebral activation in the hypothalamic Arcuate and Ventromedial nuclei, concomitant with significant increases in neuronal oxidative metabolism and glutamatergic neurotransmission.
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Kim, Sanga, Bup Kyung Choi, Ji Ae Park, Hyung Joong Kim, Tong In Oh, Won Sub Kang, Jong Woo Kim, and Hae Jeong Park. "Identification of Brain Damage after Seizures Using an MR-Based Electrical Conductivity Imaging Method." Diagnostics 11, no. 3 (March 22, 2021): 569. http://dx.doi.org/10.3390/diagnostics11030569.

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Previous imaging studies have shown the morphological malformation and the alterations of ionic mobility, water contents, electrical properties, or metabolites in seizure brains. Magnetic resonance electrical properties tomography (MREPT) is a recently developed technique for the measurement of electrical tissue properties with a high frequency that provides cellular information regardless of the cell membrane. In this study, we examined the possibility of MREPT as an applicable technique to detect seizure-induced functional changes in the brain of rats. Ultra-high field (9.4 T) magnetic resonance imaging (MRI) was performed, 2 h, 2 days, and 1 week after the injection of N-methyl-D-aspartate (NMDA; 75 mg/kg). The conductivity images were reconstructed from B1 phase images using a magnetic resonance conductivity imaging (MRCI) toolbox. The high-frequency conductivity was significantly decreased in the hippocampus among various brain regions of NMDA-treated rats. Nissl staining showed shrunken cell bodies and condensed cytoplasm potently at 2 h after NMDA treatment, and neuronal cell loss at all time points in the hippocampus. These results suggest that the reduced electrical conductivity may be associated with seizure-induced neuronal loss in the hippocampus. Magnetic resonance (MR)-based electrical conductivity imaging may be an applicable technique to non-invasively identify brain damage after a seizure.
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Kanelis, Voula, Neil A. Farrow, Lewis E. Kay, Daniela Rotin, and Julie D. Forman-Kay. "NMR studies of tandem WW domains of Nedd4 in complex with a PY motif-containing region of the epithelial sodium channel." Biochemistry and Cell Biology 76, no. 2-3 (May 1, 1998): 341–50. http://dx.doi.org/10.1139/o98-042.

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Nedd4 (neuronal precursor cell-expressed developmentally down-regulated 4) is a ubiquitin-protein ligase containing multiple WW domains. We have previously demonstrated the association between the WW domains of Nedd4 and PPxY (PY) motifs of the epithelial sodium channel (ENaC). In this paper, we report the assignment of backbone 1Hα, 1HN, 15N, 13C', 13Cα, and aliphatic 13C resonances of a fragment of rat Nedd4 (rNedd4) containing the two C-terminal WW domains, WW(II+III), complexed to a PY motif-containing peptide derived from the β subunit of rat ENaC, the βP2 peptide. The secondary structures of these two WW domains, determined from chemical shifts of 13Cα and 13Cβ resonances, are virtually identical to those of the WW domains of the Yes-associated protein YAP65 and the peptidyl-prolyl isomerase Pin1. Triple resonance experiments that detect the 1Hα chemical shift were necessary to complete the chemical shift assignment, owing to the large number of proline residues in this fragment of rNedd4. A new experiment, which correlates sequential residues via their 15N nuclei and also detects 1Hα chemical shifts, is introduced and its utility for the chemical shift assignment of sequential proline residues is discussed. Data collected on the WW(II+III)-βP2 complex indicate that these WW domains have different affinities for the βP2 peptide.Key words: WW domain, PY motif, Nedd4, ENaC, NMR.
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24

Lin, Ai-Ling, Daniel Coman, Lihong Jiang, Douglas L. Rothman, and Fahmeed Hyder. "Caloric Restriction Impedes Age-Related Decline of Mitochondrial Function and Neuronal Activity." Journal of Cerebral Blood Flow & Metabolism 34, no. 9 (July 2, 2014): 1440–43. http://dx.doi.org/10.1038/jcbfm.2014.114.

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Caloric restriction (CR) prolongs lifespan and retards many detrimental effects of aging, but its effect on brain mitochondrial function and neuronal activity—especially in healthy aging—remains unexplored. Here we measured rates of neuronal glucose oxidation and glutamate–glutamine neurotransmitter cycling in young control, old control (i.e., healthy aging), and old CR rats using in vivo nuclear magnetic resonance spectroscopy. We found that, compared with the young control, neuronal energy production and neurotransmission rates were significantly reduced in healthy aging, but were preserved in old CR rats. The results suggest that CR mitigated the age-related deceleration of brain physiology.
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Sutherland, Garnette R., Howard Lesiuk, Paul Hazendonk, James Peeling, Richard Buist, Piotr Kozlowski, Andrzej Jazinski, and John K. Saunders. "Magnetic Resonance Imaging and 31P Magnetic Resonance Spectroscopy Study of the Effect of Temperature on Ischemic Brain Injury." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 19, no. 3 (August 1992): 317–25. http://dx.doi.org/10.1017/s0317167100041937.

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ABSTRACT:Transient forebrain ischemia was induced in rats whose brain temperature was 31, 33, 35, 38, or 40°C. The development of regional injury was followed using magnetic resonance (MR) imaging, with the ultimate extent of neuronal injury quantified histopathologically. Animals in the hypothermic groups showed minimal changes in MR images over 4 days; normothermic animals snowed intensity enhancement attributed to progressive edema developing in the striatum and, later, in the hippocampus. Ischemia at 40°C resulted in widespread edema formation by I day post-ischemia; animals in this group did not survive beyond 30 hours. Histopathological analysis at 4 days (1 day for the hyperthermic group) post-ischemia showed that neuronal damage in the normothermic group was confined to the hippocampus and striatum. Minimal damage was found in the hypothermic groups; damage in the hyperthermic group was severe throughout the forebrain. There were no differences in the pre-ischemia 31P MR spectra for the different groups. During ischemia, the increase in intensity of the Pi peak and the fall in tissue pH increased with temperature in the order hypothermic < normothermic < hyperthermic group of animals. Post-ischemia energy recovery was similar in all groups, while pH recovered more rapidly in hypothermic animals.
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Maier, M., M. A. Ron, G. J. Barker, and P. S. Tofts. "Proton magnetic resonance spectroscopy: an in vivo method of estimating hippocampal neuronal depletion in schizophrenia." Psychological Medicine 25, no. 6 (November 1995): 1201–9. http://dx.doi.org/10.1017/s0033291700033171.

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SynopsisDiffuse loss of cortical volume and ventricular enlargement have been demonstrated in schizophrenia using imaging. In addition, histological studies have provided evidence that the number of neurons in the medial temporal lobe structures is reduced and that the cytoarchitecture is abnormal. In an attempt to correlate these histological findings with in vivo estimates of neuronal integrity we have studied the concentration of the neuronal marker N-acetyl aspartate (NAA) in the hippocampi of schizophrenics using in vivo Magnetic Resonance Spectroscopy (MRS). Compared with a group of healthy volunteers schizophrenics showed a 22% loss of NAA in the left hippocampus. Two other metabolites, choline and creatine showed bilateral reduction in schizophrenics and these achieved significance in the left hippocampus. These results indicate a significant depletion of NAA in schizophrenia and are in close agreement with the reported neuronal loss in the hippocampus detected histologically. We propose that in vivo MRS is a valid measure of integrity of neuronal populations in schizophrenia.
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Roach, James P., Aleksandra Pidde, Eitan Katz, Jiaxing Wu, Nicolette Ognjanovski, Sara J. Aton, and Michal R. Zochowski. "Resonance with subthreshold oscillatory drive organizes activity and optimizes learning in neural networks." Proceedings of the National Academy of Sciences 115, no. 13 (March 15, 2018): E3017—E3025. http://dx.doi.org/10.1073/pnas.1716933115.

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Network oscillations across and within brain areas are critical for learning and performance of memory tasks. While a large amount of work has focused on the generation of neural oscillations, their effect on neuronal populations’ spiking activity and information encoding is less known. Here, we use computational modeling to demonstrate that a shift in resonance responses can interact with oscillating input to ensure that networks of neurons properly encode new information represented in external inputs to the weights of recurrent synaptic connections. Using a neuronal network model, we find that due to an input current-dependent shift in their resonance response, individual neurons in a network will arrange their phases of firing to represent varying strengths of their respective inputs. As networks encode information, neurons fire more synchronously, and this effect limits the extent to which further “learning” (in the form of changes in synaptic strength) can occur. We also demonstrate that sequential patterns of neuronal firing can be accurately stored in the network; these sequences are later reproduced without external input (in the context of subthreshold oscillations) in both the forward and reverse directions (as has been observed following learning in vivo). To test whether a similar mechanism could act in vivo, we show that periodic stimulation of hippocampal neurons coordinates network activity and functional connectivity in a frequency-dependent manner. We conclude that resonance with subthreshold oscillations provides a plausible network-level mechanism to accurately encode and retrieve information without overstrengthening connections between neurons.
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Cakirer, S., B. Yagmurlu, and M. R. Savas. "Sturge‐weber syndrome: diffusion magnetic resonance imaging and proton magnetic resonance spectroscopy findings." Acta Radiologica 46, no. 4 (July 2005): 407–10. http://dx.doi.org/10.1080/02841850510021274.

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We report on the diffusion magnetic resonance imaging (MRI) and proton MR spectroscopy findings of a 26‐year‐old female patient with Sturge‐Weber syndrome. Echo‐planar trace diffusion MRI revealed mildly high signal intensity changes at parieto‐occipital lobes on b = 1000 s/mm2 images, suggesting restricted diffusion. On corresponding apparent diffusion coefficient maps, those areas had moderately high signal intensity and high apparent diffusion coefficient values (around 0.9×10(−3) mm2/s) compared with the contralateral symmetrical normal side of the brain (0.776×10(−3) mm2/s). This finding was consistent with increased motion of water molecules (disintegration of the neural tissue) in these regions. Proton MR spectroscopy revealed decreased N‐acetyl aspartate and increased choline peaks, indicating disintegration of neural tissue associated with neuronal loss as well.
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Sauvage, Maria-Angeles Carrillo-de, Julien Flament, Yann Bramoulle, Lucile Ben Haim, Martine Guillermier, Aurélie Berniard, Gwennaëlle Aurégan, et al. "The Neuroprotective Agent CNTF Decreases Neuronal Metabolites in the Rat Striatum: An in Vivo Multimodal Magnetic Resonance Imaging Study." Journal of Cerebral Blood Flow & Metabolism 35, no. 6 (April 1, 2015): 917–21. http://dx.doi.org/10.1038/jcbfm.2015.48.

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Ciliary neurotrophic factor (CNTF) is neuroprotective against multiple pathologic conditions including metabolic impairment, but the mechanisms are still unclear. To delineate CNTF effects on brain energy homeostasis, we performed a multimodal imaging study, combining in vivo proton magnetic resonance spectroscopy, high-performance liquid chromatography analysis, and in situ glutamate imaging by chemical exchange saturation transfer. Unexpectedly, we found that CNTF expression through lentiviral gene transfer in the rat striatum significantly decreased the levels of neuronal metabolites ( N-acetyl-aspartate, N-acetyl-aspartyl-glutamate, and glutamate). This preclinical study shows that CNTF remodels brain metabolism, and suggests that decreased levels of neuronal metabolites may occur in the absence of neuronal dysfunction.
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30

Cohen Kadosh, Roi, Kathrin Cohen Kadosh, and Avishai Henik. "The Neuronal Correlate of Bidirectional Synesthesia: A Combined Event-related Potential and Functional Magnetic Resonance Imaging Study." Journal of Cognitive Neuroscience 19, no. 12 (December 2007): 2050–59. http://dx.doi.org/10.1162/jocn.2007.19.12.2050.

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The neuronal correlate of a rare explicit bidirectional synesthesia was investigated with numerical and physical size comparison tasks using both functional magnetic resonance imaging and event-related potentials. Interestingly, although participant I.S. exhibited similar congruity effects for both tasks at the behavioral level, subsequent analyses of the imaging data revealed that different brain areas were recruited for each task, and in different time windows. The results support: (1) the genuineness of bidirectional synesthesia at the neuronal level, (2) the possibility that discrepancy in the neuronal correlates of synesthesia between previous studies might be task-related, and (3) the possibility that synesthesia might not be a unitary phenomenon.
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31

Mangia, Silvia, Federico Giove, Ivan Tkáč, Nikos K. Logothetis, Pierre-Gilles Henry, Cheryl A. Olman, Bruno Maraviglia, Francesco Di Salle, and Kâmil Uğurbil. "Metabolic and Hemodynamic Events after Changes in Neuronal Activity: Current Hypotheses, Theoretical Predictions and in vivo NMR Experimental Findings." Journal of Cerebral Blood Flow & Metabolism 29, no. 3 (November 12, 2008): 441–63. http://dx.doi.org/10.1038/jcbfm.2008.134.

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Unraveling the energy metabolism and the hemodynamic outcomes of excitatory and inhibitory neuronal activity is critical not only for our basic understanding of overall brain function, but also for the understanding of many brain disorders. Methodologies of magnetic resonance spectroscopy (MRS) and magnetic resonance imaging (MRI) are powerful tools for the noninvasive investigation of brain metabolism and physiology. However, the temporal and spatial resolution of in vivo MRS and MRI is not suitable to provide direct evidence for hypotheses that involve metabolic compartmentalization between different cell types, or to untangle the complex neuronal microcircuitry, which results in changes of electrical activity. This review aims at describing how the current models of brain metabolism, mainly built on the basis of in vitro evidence, relate to experimental findings recently obtained in vivo by 1H MRS, 13C MRS, and MRI. The hypotheses related to the role of different metabolic substrates, the metabolic neuron—glia interactions, along with the available theoretical predictions of the energy budget of neurotransmission will be discussed. In addition, the cellular and network mechanisms that characterize different types of increased and suppressed neuronal activity will be considered within the sensitivity-constraints of MRS and MRI.
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32

Hunsberger, Eric, Matthew Scott, and Chris Eliasmith. "The Competing Benefits of Noise and Heterogeneity in Neural Coding." Neural Computation 26, no. 8 (August 2014): 1600–1623. http://dx.doi.org/10.1162/neco_a_00621.

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Noise and heterogeneity are both known to benefit neural coding. Stochastic resonance describes how noise, in the form of random fluctuations in a neuron's membrane voltage, can improve neural representations of an input signal. Neuronal heterogeneity refers to variation in any one of a number of neuron parameters and is also known to increase the information content of a population. We explore the interaction between noise and heterogeneity and find that their benefits to neural coding are not independent. Specifically, a neuronal population better represents an input signal when either noise or heterogeneity is added, but adding both does not always improve representation further. To explain this phenomenon, we propose that noise and heterogeneity operate using two shared mechanisms: (1) temporally desynchronizing the firing of neurons in the population and (2) linearizing the response of a population to a stimulus. We first characterize the effects of noise and heterogeneity on the information content of populations of either leaky integrate-and-fire or FitzHugh-Nagumo neurons. We then examine how the mechanisms of desynchronization and linearization produce these effects, and find that they work to distribute information equally across all neurons in the population in terms of both signal timing (desynchronization) and signal amplitude (linearization). Without noise or heterogeneity, all neurons encode the same aspects of the input signal; adding noise or heterogeneity allows neurons to encode complementary aspects of the input signal, thereby increasing information content. The simulations detailed in this letter highlight the importance of heterogeneity and noise in population coding, demonstrate their complex interactions in terms of the information content of neurons, and explain these effects in terms of underlying mechanisms.
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33

Lake, Evelyn M. R., Paolo Bazzigaluppi, and Bojana Stefanovic. "Functional magnetic resonance imaging in chronic ischaemic stroke." Philosophical Transactions of the Royal Society B: Biological Sciences 371, no. 1705 (October 5, 2016): 20150353. http://dx.doi.org/10.1098/rstb.2015.0353.

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Ischaemic stroke is the leading cause of adult disability worldwide. Effective rehabilitation is hindered by uncertainty surrounding the underlying mechanisms that govern long-term ischaemic injury progression. Despite its potential as a sensitive non-invasive in vivo marker of brain function that may aid in the development of new treatments, blood oxygenation level-dependent (BOLD) functional magnetic resonance imaging (fMRI) has found limited application in the clinical research on chronic stage stroke progression. Stroke affects each of the physiological parameters underlying the BOLD contrast, markedly complicating the interpretation of BOLD fMRI data. This review summarizes current progress on application of BOLD fMRI in the chronic stage of ischaemic injury progression and discusses means by which more information may be gained from such BOLD fMRI measurements. Concomitant measurements of vascular reactivity, neuronal activity and metabolism in preclinical models of stroke are reviewed along with illustrative examples of post-ischaemic evolution in neuronal, glial and vascular function. The realization of the BOLD fMRI potential to propel stroke research is predicated on the carefully designed preclinical research establishing an ischaemia-specific quantitative model of BOLD signal contrast to provide the framework for interpretation of fMRI findings in clinical populations. This article is part of the themed issue ‘Interpreting BOLD: a dialogue between cognitive and cellular neuroscience’.
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34

Haugen, Olav H., Sten Andréasson, Lars Ersland, Alexander R. Craven, and Kenneth Hugdahl. "Cerebral Functional Magnetic Resonance Imaging and Multifocal Visual Evoked Potentials in a Patient with Unexplained Impairment of Visual Function: A Case Report." Case Reports in Ophthalmology 9, no. 2 (May 24, 2018): 269–78. http://dx.doi.org/10.1159/000488930.

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We present a case of a young female with a slowly progressing visual impairment who was examined with multifocal visual evoked potentials and functional magnetic resonance imaging (fMRI) for underlying neuronal abnormality. The fMRI examination consisted of presenting black-and-white checkerboard stimuli, and her activation patterns were compared to the patterns from 4 normal-sighted subjects. The results showed clear differences in neuronal activation between the patient and the controls in the occipital and parietal lobes. Although we have shown neuronal correlates in a case of unexplained visual loss, it is still an open question as to whether this has an organic or functional cause, which should be the subject for future research.
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35

Ho, Ying-Jui, Jun-Cheng Weng, Chih-Li Lin, Mei-Shiuan Shen, Hsin-Hua Li, Wen-Chieh Liao, Nu-Man Tsai, Ching-Sui Hung, Te-Jen Lai, and I.-Yen Lee. "Ceftriaxone Treatment for Neuronal Deficits: A Histological and MEMRI Study in a Rat Model of Dementia with Lewy Bodies." Behavioural Neurology 2018 (August 1, 2018): 1–9. http://dx.doi.org/10.1155/2018/4618716.

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Dementia with Lewy bodies (DLB) is characterized by neuronal deficits and α-synuclein inclusions in the brain. Ceftriaxone (CEF), a β-lactam antibiotic, has been suggested as a therapeutic agent in several neurodegenerative disorders for its abilities to counteract glutamate-mediated toxicity and to block α-synuclein polymerization. By using manganese-enhanced magnetic resonance imaging (MEMRI) and immunohistochemistry, we measured the effects of CEF on neuronal activity and α-synuclein accumulation in the brain in a DLB rat model. The data showed that CEF corrected neuronal density and activity in the hippocampal CA1 area, suppressed hyperactivity in the subthalamic nucleus, and reduced α-synuclein accumulation, indicating that CEF is a potential agent in the treatment of DLB.
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Arslan, Harun, Metin Saylık, and Hüseyin Akdeniz. "MRI Findings of Coexistence of Ectopic Neurohypophysis, Corpus Callosum Dysgenesis, and Periventricular Neuronal Heterotopia." Journal of Clinical Imaging Science 4 (April 29, 2014): 22. http://dx.doi.org/10.4103/2156-7514.131649.

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Ectopic neurohypophysis is a pituitary gland abnormality, which can accompany growth hormone deficiency associated with dwarfism. Here we present magnetic resonance imaging (MRI) findings of a rare case of ectopic neurohypophysis, corpus callosum dysgenesis, and periventricular neuronal heterotopia coexisting, with a review of the literature.
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37

Puil, E., B. Gimbarzevsky, and R. M. Miura. "Voltage dependence of membrane properties of trigeminal root ganglion neurons." Journal of Neurophysiology 58, no. 1 (July 1, 1987): 66–86. http://dx.doi.org/10.1152/jn.1987.58.1.66.

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1. Membrane potentials of trigeminal root ganglion neurons were varied systematically by intracellular injections of long-lasting step currents to determine the voltage dependence of their membrane electrical properties. The complex impedance and impedance magnitude functions were first determined using oscillatory input currents superimposed on these step currents. 2. Systematic step variations in the membrane potential led to qualitative changes in the impedance magnitude functions. Depolarization of neurons exhibiting resonance at their initial resting membrane potentials resulted in a reduction in the resonance behavior. Hyperpolarization of these neurons to membrane potentials of about -80 to -90 mV led to a disappearance of the resonant peak but increased the maximum of the impedance magnitude. 3. The complex impedance data were fitted with a neuronal model derived from linearized Hodgkin-Huxley-like equations, yielding estimates for the membrane properties. The four parameters of the model were 1) a time invariant, resting membrane conductance, Gr, 2) a voltage- and time-dependent conductance, GL, 3) a time constant, tau u, for the unknown ionic channels that are activated by the 2- to 5-mV oscillatory perturbation of the stepped membrane potential, and 4) Ci, the input capacitance. 4. The results of the curve-fitting procedures suggested that all parameters depended on membrane voltage. The most voltage-dependent parameters were GL and tau u throughout a 25- to 30-mV range that was subthreshold to the production of action potentials. Both Gr and GL increased with subthreshold depolarization. 5. These impedance data suggest the very important role of the membrane potential of the trigeminal root ganglion neurons on their abilities to synthesize and filter inputted electrical signals.
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38

Fried, Itzhak, Jung H. Kim, and Dennis D. Spencer. "Hippocampal pathology in patients with intractable seizures and temporal lobe masses." Journal of Neurosurgery 76, no. 5 (May 1992): 735–40. http://dx.doi.org/10.3171/jns.1992.76.5.0735.

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✓ The authors examined hippocampal tissue removed during surgical procedures in 17 patients with intractable epilepsy who were found by preoperative magnetic resonance imaging or computerized tomography to have intra-axial masses in the temporal lobe. Neuronal densities in the cornu ammonis (CA) fields of the hippocampus and in the dentate granule cell layer were measured in hematoxylin and eosin-stained sections and were found to be lower compared to a group of 18 autopsy controls. The neuronal densities in all hippocampal fields except CA2 were related to the patient's age at seizure onset. Patients with an earlier onset of seizures had lower neuronal densities. With the exception of CA4, neuronal densities were not significantly related to the duration of the seizure disorder. Cell counts in all fields except CA2 were also related to the location of the lesion in the temporal lobe. Patients with mesial temporal lesions had lower neuronal counts. These results suggest increased vulnerability of hippocampal cytoarchitecture to proximal lesions with early ictal manifestation.
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39

GU, HUAGUANG, HUIMIN ZHANG, CHUNLING WEI, MINGHAO YANG, ZHIQIANG LIU, and WEI REN. "COHERENCE RESONANCE–INDUCED STOCHASTIC NEURAL FIRING AT A SADDLE-NODE BIFURCATION." International Journal of Modern Physics B 25, no. 29 (November 20, 2011): 3977–86. http://dx.doi.org/10.1142/s0217979211101673.

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Coherence resonance at a saddle-node bifurcation point and the corresponding stochastic firing patterns are simulated in a theoretical neuronal model. The characteristics of noise-induced neural firing pattern, such as exponential decay in histogram of interspike interval (ISI) series, independence and stochasticity within ISI series are identified. Firing pattern similar to the simulated results was discovered in biological experiment on a neural pacemaker. The difference between this firing and integer multiple firing generated at a Hopf bifurcation point is also given. The results not only revealed the stochastic dynamics near a saddle-node bifurcation, but also gave practical approaches to identify the saddle-node bifurcation and to distinguish it from the Hopf bifurcation in neuronal system. In addition, many previously observed firing patterns can be attribute to stochastic firing pattern near such a saddle-node bifurcation.
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40

Boillat, Yohan, Lijing Xin, Wietske van der Zwaag, and Rolf Gruetter. "Metabolite concentration changes associated with positive and negative BOLD responses in the human visual cortex: A functional MRS study at 7 Tesla." Journal of Cerebral Blood Flow & Metabolism 40, no. 3 (February 12, 2019): 488–500. http://dx.doi.org/10.1177/0271678x19831022.

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Negative blood oxygenation–level dependent (BOLD) signal observed during task execution in functional magnetic resonance imaging (fMRI) can be caused by different mechanisms, such as a blood-stealing effect or neuronal deactivation. Electrophysiological recordings showed that neuronal deactivation underlies the negative BOLD observed in the occipital lobe during visual stimulation. In this study, the metabolic demand of such a response was studied by measuring local metabolite concentration changes during a visual checkerboard stimulation using functional magnetic resonance spectroscopy (fMRS) at 7 Tesla. The results showed increases of glutamate and lactate concentrations during the positive BOLD response, consistent with previous fMRS studies. In contrast, during the negative BOLD response, decreasing concentrations of glutamate, lactate and gamma-aminobutyric acid (GABA) were found, suggesting a reduction of glycolytic and oxidative metabolic demand below the baseline. Additionally, the respective changes of the BOLD signal, glutamate and lactate concentrations of both groups suggest that a local increase of inhibitory activity might occur during the negative BOLD response.
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41

Koretsky, AP. "Nuclear Magnetic Resonance Detection of the Consequences of Transgene Expression." Physiology 9, no. 5 (October 1, 1994): 197–202. http://dx.doi.org/10.1152/physiologyonline.1994.9.5.197.

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Physiological processes can be altered in a very specific manner using transgenic mouse techniques. Physiological processes can be noninvasively monitored using nuclear magnetic resonance imaging and spectroscopic techniques. Three illustrations of the combination of these two rapidly developing techniques to study neuronal function, energy metabolism, and sickle cell anemia are discussed.
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42

Kringelbach, Morten L., Josephine Cruzat, Joana Cabral, Gitte Moos Knudsen, Robin Carhart-Harris, Peter C. Whybrow, Nikos K. Logothetis, and Gustavo Deco. "Dynamic coupling of whole-brain neuronal and neurotransmitter systems." Proceedings of the National Academy of Sciences 117, no. 17 (April 13, 2020): 9566–76. http://dx.doi.org/10.1073/pnas.1921475117.

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Remarkable progress has come from whole-brain models linking anatomy and function. Paradoxically, it is not clear how a neuronal dynamical system running in the fixed human anatomical connectome can give rise to the rich changes in the functional repertoire associated with human brain function, which is impossible to explain through long-term plasticity. Neuromodulation evolved to allow for such flexibility by dynamically updating the effectivity of the fixed anatomical connectivity. Here, we introduce a theoretical framework modeling the dynamical mutual coupling between the neuronal and neurotransmitter systems. We demonstrate that this framework is crucial to advance our understanding of whole-brain dynamics by bidirectional coupling of the two systems through combining multimodal neuroimaging data (diffusion magnetic resonance imaging [dMRI], functional magnetic resonance imaging [fMRI], and positron electron tomography [PET]) to explain the functional effects of specific serotoninergic receptor (5-HT2AR) stimulation with psilocybin in healthy humans. This advance provides an understanding of why psilocybin is showing considerable promise as a therapeutic intervention for neuropsychiatric disorders including depression, anxiety, and addiction. Overall, these insights demonstrate that the whole-brain mutual coupling between the neuronal and the neurotransmission systems is essential for understanding the remarkable flexibility of human brain function despite having to rely on fixed anatomical connectivity.
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Li, Dongxi, Shuling Song, and Ni Zhang. "Lévy noise-induced inverse stochastic resonance on Newman–Watts networks of Hodgkin–Huxley neurons." International Journal of Modern Physics B 34, no. 19 (July 27, 2020): 2050185. http://dx.doi.org/10.1142/s0217979220501854.

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This paper primarily investigates the inverse stochastic resonance (ISR) of neuron network driven by Lévy noise with electrical autapse and chemical autapse, respectively. Firstly, the discharge of Hodgkin–Huxley (HH) neuron network under different noise parameters, autapse parameters and network coupling strength is shown. Then, the variation of average firing rate with Lévy noise in the case of electrical autapse and chemical autapse is presented. We find that there exists a minimum value of the average firing rate curve caused by stability index and noise intensity of Lévy noise across the whole network, which is the phenomenon of ISR. With the increase of autaptic intensity and coupling strength, the ISR inhibitory effect of neuron discharge is weakened. In addition, with the increase of coupling strength, the neuron discharge of neural network is more intense and regular. As a consequence, our work suggests that autaptic intensity and coupling efficient of neuronal network can regulate the neuronal firing activities and suppress the effect of ISR, and Lévy noise can induce ISR phenomenon in Newman–Watts neuronal network.
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Tatter, Stephen B., Lawrence F. Borges, and David N. Louis. "Central neurocytomas of the cervical spinal cord." Journal of Neurosurgery 81, no. 2 (August 1994): 288–93. http://dx.doi.org/10.3171/jns.1994.81.2.0288.

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✓ Central neurocytoma is a neuronal neoplasm that occurs supratentorially in the lateral or third ventricles. The authors report the clinical, neuroradiological, and neuropathological features of two neurocytomas arising in the spinal cord of two men, aged 65 and 49 years. The patients presented with progressive neurological deficits referable to the cervical spinal cord. Magnetic resonance imaging revealed isodense intramedullary spinal cord tumors at the C3–4 level. Both tumors were initially misdiagnosed as gliomas. In Case 1 the correct diagnosis was made after electron microscopy revealed neuronal features. Immunostaining in Case 2 revealed that tumor cells were positive for synaptophysin and negative for glial fibrillary acidic protein, strongly indicating a neuronal tumor. It is suggested that this spinal cord neoplasm be included under the designation “central neurocytoma.”
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WANG, QING YUN, MATJAŽ PERC, ZHI SHENG DUAN, and GUAN RONG CHEN. "SPATIAL COHERENCE RESONANCE IN DELAYED HODGKIN–HUXLEY NEURONAL NETWORKS." International Journal of Modern Physics B 24, no. 09 (April 10, 2010): 1201–13. http://dx.doi.org/10.1142/s0217979210055317.

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We study the phenomenon of spatial coherence resonance (SCR) on Hodgkin–Huxley (HH) neuronal networks that are characterized with information transmission delay. In particular, we examine the ability of additive Gaussian noise to optimally extract a particular spatial frequency of excitatory waves in diffusive and small-world networks on which information transmission amongst directly connected neurons is not instantaneous. On diffusively coupled HH networks, we find that for short delay lengths, there always exists an intermediate noise level by which the noise-induced spatial dynamics is maximally ordered, hence implying the possibility of SCR in the system. Importantly thereby, the noise level warranting optimally ordered excitatory waves increases linearly with the increasing delay time, suggesting that extremely long delays might nevertheless preclude the observation of SCR on diffusive networks. Moreover, we find that the small-world topology introduces another obstacle for the emergence of ordered spatial dynamics out of noise because the magnitude of SCR fades progressively as the fraction of rewired links increases, hence evidencing decoherence of noise-induced spatial dynamics on delayed small-world HH networks. Presented results thus provide insights that could facilitate the understanding of the joint impact of noise and information transmission delay on realistic neuronal networks.
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46

Howseman, Alistair M., and Richard W. Bowtel. "Functional magnetic resonance imaging: imaging techniques and contrast mechanisms." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 354, no. 1387 (July 29, 1999): 1179–94. http://dx.doi.org/10.1098/rstb.1999.0473.

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Functional magnetic resonance imaging (fMRI) is a widely used technique for generating images or maps of human brain activity. The applications of the technique are widespread in cognitive neuroscience and it is hoped they will eventually extend into clinical practice. The activation signal measured with fMRI is predicated on indirectly measuring changes in the concentration of deoxyhaemoglobin which arise from an increase in blood oxygenation in the vicinity of neuronal firing. The exact mechanisms of this blood oxygenation level dependent (BOLD) contrast are highly complex. The signal measured is dependent on both the underlying physiological events and the imaging physics. BOLD contrast, although sensitive, is not a quantifiable measure of neuronal activity. A number of different imaging techniques and parameters can be used for fMRI, the choice of which depends on the particular requirements of each functional imaging experiment. The high–speed MRI technique, echo–planar imaging provides the basis for most fMRI experiments. The problems inherent to this method and the ways in which these may be overcome are particularly important in the move towards performing functional studies on higher field MRI systems. Future developments in techniques and hardware are also likely to enhance the measurement of brain activity using MRI.
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47

Fabbri, Sara, Alfonso Caramazza, and Angelika Lingnau. "Distributed sensitivity for movement amplitude in directionally tuned neuronal populations." Journal of Neurophysiology 107, no. 7 (April 1, 2012): 1845–56. http://dx.doi.org/10.1152/jn.00435.2011.

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Neurons in macaque primary motor cortex and dorsal premotor cortex are tuned to movement direction. In humans, neuronal populations tuned to movement direction have recently been described using multivoxel pattern analysis and functional magnetic resonance imaging adaptation. It is unclear, however, to what extent directionally tuned neuronal populations are sensitive to movement amplitude. Here we used functional magnetic resonance imaging adaptation to determine whether directionally tuned neuronal populations are modulated by movement amplitude. In different blocks, participants were adapted to small- or large-amplitude hand-reaching movements. On occasional test trials, we parametrically varied the angular difference between adaptation and test direction and the congruency between adapted and tested amplitude (same or different). We predicted that the blood oxygen level-dependent signal in directionally tuned regions should be adapted in proportion to the angular difference between adaptation and test direction. Directionally tuned regions insensitive to movement amplitude should show a transfer of adaptation from the adapted to the nonadapted amplitude. In contrast, regions sensitive to the specific combination of movement direction and amplitude should show directional tuning only for the adapted amplitude. We identified a network of parietal and frontal regions tuned to movement direction. We found that parietal areas contain neuronal populations sensitive to specific combinations of movement direction and amplitude, while frontal areas show transfer from the adapted to the nonadapted amplitude during small-amplitude movements after adaptation to large amplitude, but not vice versa. Our results thus imply different processing of movement amplitude in directionally tuned frontal and parietal areas.
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48

Bozza, Fernando A., Philippe Garteiser, Marcus F. Oliveira, Sabrina Doblas, Rebecca Cranford, Debra Saunders, Inna Jones, Rheal A. Towner, and Hugo C. Castro-Faria-Neto. "Sepsis-Associated Encephalopathy: A Magnetic Resonance Imaging and Spectroscopy Study." Journal of Cerebral Blood Flow & Metabolism 30, no. 2 (October 21, 2009): 440–48. http://dx.doi.org/10.1038/jcbfm.2009.215.

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Brain dysfunction is frequently observed in sepsis as a consequence of changes in cerebral structure and metabolism, resulting in worse outcome and reduced life-quality of surviving patients. However, the mechanisms of sepsis-associated encephalopathy development and a better characterization of this syndrome in vivo are lacking. Here, we used magnetic resonance imaging (MRI) techniques to assess brain morphology and metabolism in a murine sepsis model (cecal ligation and puncture, CLP). Sham-operated and CLP mice were subjected to a complete MRI session at baseline, 6 and 24 h after surgery. Accumulation of vasogenic edematic fluid at the base of the brain was observed in T2-weighted image at 6 and 24 h after CLP. Also, the water apparent diffusion coefficients in both hippocampus and cortex were decreased, suggesting a cytotoxic edema in brains of nonsurvival septic animals. Moreover, the N-acetylaspartate/choline ratio was reduced in brains of septic mice, indicating neuronal damage. In conclusion, noninvasive assessment by MRI allowed the identification of new aspects of brain damage in sepsis, including cytotoxic and vasogenic edema as well as neuronal damage. These findings highlight the potential applications of MRI techniques for the diagnostic and therapeutic studies in sepsis.
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49

Rossi, Silvia, Valeria Studer, Caterina Motta, Valentina De Chiara, Francesca Barbieri, Giorgio Bernardi, and Diego Centonze. "Inflammation inhibits GABA transmission in multiple sclerosis." Multiple Sclerosis Journal 18, no. 11 (March 14, 2012): 1633–35. http://dx.doi.org/10.1177/1352458512440207.

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Abnormal glutamate-dependent synaptic excitation contributes to neuronal damage in multiple sclerosis (MS). Little is known about the involvement of the GABA system in this disorder. Here we found that cerebrospinal fluid (CSF) from MS patients with enhanced brain lesions on magnetic resonance imaging inhibited GABA transmission in mouse brain slices. Enhanced IL-1β neuronal action was responsible for this effect, because IL-1β receptor antagonist blocked, and exogenous IL-1β mimicked the synaptic effect of inflamed CSF. Our results provide evidence that focal inflammation in MS perturbs the cytokine milieu within the circulating CSF, resulting in diffuse GABAergic alteration in neurons.
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Ilves, Norman, Pilvi Ilves, Katrin Õunap, Rael Laugesaar, Dagmar Loorits, Mare Lintrop, Mairi Männamaa, and Tuuli Metsvaht. "Periventricular Venous Infarction in an Extremely Premature Infant as the Cause of Schizencephaly." Journal of Pediatric Neurology 18, no. 05 (September 20, 2019): 267–70. http://dx.doi.org/10.1055/s-0039-1697040.

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AbstractSchizencephaly is a disorder of neuronal migration which has been hypothesized to arise from vascular ischemic lesion during the early phase of neuroembryogenesis. We describe a case of a premature boy born at 23 weeks of gestation with neonatal stroke. On the first day of life cranial ultrasonography detected a grade II intraventricular hemorrhage and on day 12 periventricular venous infarction. At the postconceptional age of 40 weeks, magnetic resonance imaging revealed a gray matter–lined cleft, suggesting schizencephaly. We have evidence of the pathogenesis of schizencephaly following vascular ischemic stroke early in neurodevelopment before neuronal migration is completed.
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