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Journal articles on the topic 'Neuronal concentration'

Author: Grafiati

Published: 2 June 2025

Last updated: 31 July 2025

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1

Violet, J. M., D. L. Downie, R. C. Nakisa, W. R. Lieb, and N. P. Franks. "Differential Sensitivities of Mammalian Neuronal and Muscle Nicotinic Acetylcholine Receptors to General Anesthetics." Anesthesiology 86, no. 4 (1997): 866–74. http://dx.doi.org/10.1097/00000542-199704000-00017.

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Background Nicotinic acetylcholine receptors (nAChRs) are members of a superfamily of fast neurotransmitter-gated receptor channels that includes the gamma-aminobutyric acidA (GABAA), glycine and serotonin type 3 (5-HT3) receptors. Most previous work on the interactions of general anesthetics with nAChRs has involved the muscle-type receptor. The authors investigate the effects of general anesthetics on defined mammalian neuronal and muscle nAChRs expressed in Xenopus oocytes. Methods Complementary deoxyribonucleic acid (cDNA) or messenger ribonucleic acid (mRNA) encoding for various neuronal

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Sætra, Marte J., and Yoichiro Mori. "An electrodiffusive network model with multicompartmental neurons and synaptic connections." PLOS Computational Biology 20, no. 11 (2024): e1012114. http://dx.doi.org/10.1371/journal.pcbi.1012114.

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Most computational models of neurons assume constant ion concentrations, disregarding the effects of changing ion concentrations on neuronal activity. Among the models that do incorporate ion concentration dynamics, simplifications are often made that sacrifice biophysical consistency, such as neglecting the effects of ionic diffusion on electrical potentials or the effects of electric drift on ion concentrations. A subset of models with ion concentration dynamics, often referred to as electrodiffusive models, account for ion concentration dynamics in a way that ensures a biophysical consisten

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3

Delpire, Eric, and Kevin J. Staley. "Novel determinants of the neuronal Cl − concentration." Journal of Physiology 592, no. 19 (2014): 4099–114. http://dx.doi.org/10.1113/jphysiol.2014.275529.

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López-León, Clara F., Ramon Planet, and Jordi Soriano. "Preparation and Mechano-Functional Characterization of PEGylated Fibrin Hydrogels: Impact of Thrombin Concentration." Gels 10, no. 2 (2024): 116. http://dx.doi.org/10.3390/gels10020116.

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Three-dimensional (3D) neuronal cultures grown in hydrogels are promising platforms to design brain-like neuronal networks in vitro. However, the optimal properties of such cultures must be tuned to ensure a hydrogel matrix sufficiently porous to promote healthy development but also sufficiently rigid for structural support. Such an optimization is difficult since it implies the exploration of different hydrogel compositions and, at the same time, a functional analysis to validate neuronal culture viability. To advance in this quest, here we present a combination of a rheological protocol and

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Tas, A., S. Arat, and H. Dalcik. "206 COMPARATIVE EVALUATION OF VARIOUS PROTOCOLS FOR NEURAL DIFFERENTIATION OF MOUSE EMBRYONIC STEM CELLS." Reproduction, Fertility and Development 18, no. 2 (2006): 211. http://dx.doi.org/10.1071/rdv18n2ab206.

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Mouse embryonic stem (ES) cells derived from the inner cell mass of blastocysts can differentiate into neuronal cells by treatment with retinoic acid (RA). ES cells cultured as aggregates and as single cell suspensions were then exposed to RA which induced multiple phenotypes of neuronal cells. Differentiation was dependent on the concentration of RA and the time of exposure. In this study, we cultured ES cells as a suspension in which they formed embryoid bodies (EBs). The EBs were treated with varying concentrations of RA for differing times. We used increasing concentrations of RA (50 nM, 1

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Shindo, Yutaka, Ryu Yamanaka, Kohji Hotta, and Kotaro Oka. "Inhibition of Mg2+ Extrusion Attenuates Glutamate Excitotoxicity in Cultured Rat Hippocampal Neurons." Nutrients 12, no. 9 (2020): 2768. http://dx.doi.org/10.3390/nu12092768.

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Magnesium plays important roles in the nervous system. An increase in the Mg2+ concentration in cerebrospinal fluid enhances neural functions, while Mg2+ deficiency is implicated in neuronal diseases in the central nervous system. We have previously demonstrated that high concentrations of glutamate induce excitotoxicity and elicit a transient increase in the intracellular concentration of Mg2+ due to the release of Mg2+ from mitochondria, followed by a decrease to below steady-state levels. Since Mg2+ deficiency is involved in neuronal diseases, this decrease presumably affects neuronal survi

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Jantas, Danuta, Monika Leśkiewicz, Magdalena Regulska, Magdalena Procner, Piotr Warszyński, and Władysław Lasoń. "Protective Effects of Cannabidiol (CBD) against Qxidative Stress, but Not Excitotoxic-Related Neuronal Cell Damage—An In Vitro Study." Biomolecules 14, no. 5 (2024): 564. http://dx.doi.org/10.3390/biom14050564.

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Cannabidiol (CBD) appears to possess some neuroprotective properties, but experimental data are still inconsistent. Therefore, this in vitro study aimed to compare the effects of CBD in a wide range of concentrations on oxidative stress and excitotoxic-related cell damage. Results showed that low concentrations of CBD ameliorated the H2O2-evoked cell damage of primary cortical neuronal cell culture. However, higher concentrations of CBD alone (5–25 μM) decreased the viability of cortical neurons in a concentration-dependent manner and aggravated the toxic effects of hydrogen peroxide (H2O2). N

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Wilhelm, Stefan, Daqing Ma, Mervyn Maze, and Nicholas P. Franks. "Effects of Xenon on In Vitro and In Vivo Models of Neuronal Injury." Anesthesiology 96, no. 6 (2002): 1485–91. http://dx.doi.org/10.1097/00000542-200206000-00031.

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Background Xenon, the "inert" gaseous anesthetic, is an antagonist at the N-methyl-D-aspartate (NMDA)-type glutamate receptor. Because of the pivotal role that NMDA receptors play in neuronal injury, the authors investigated the efficacy of xenon as a neuroprotectant in both in vitro and in vivo paradigms. Methods In a mouse neuronal-glial cell coculture, injury was provoked either by NMDA, glutamate, or oxygen deprivation and assessed by the release of lactate dehydrogenase into the culture medium. Increasing concentrations of either xenon or nitrogen (10-75% of an atmosphere) were coadminist

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9

Glykys, J., V. Dzhala, K. Egawa, et al. "Local Impermeant Anions Establish the Neuronal Chloride Concentration." Science 343, no. 6171 (2014): 670–75. http://dx.doi.org/10.1126/science.1245423.

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10

Yasuda, R., E. A. Nimchinsky, V. Scheuss, et al. "Imaging Calcium Concentration Dynamics in Small Neuronal Compartments." Science Signaling 2004, no. 219 (2004): pl5. http://dx.doi.org/10.1126/stke.2192004pl5.

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11

Antognini, Joseph F., and Earl Carstens. "Increasing Isoflurane from 0.9 to 1.1 Minimum Alveolar Concentration Minimally Affects Dorsal Horn Cell Responses to Noxious Stimulation." Anesthesiology 90, no. 1 (1999): 208–14. http://dx.doi.org/10.1097/00000542-199901000-00027.

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Background The spinal cord appears to be the site at which isoflurane suppresses movement that occurs in response to a noxious stimulus. In an attempt to localize its site of suppressant action, the authors determined the effect of isoflurane on dorsal horn neuronal responses to supramaximal noxious stimulation at end-tidal concentrations that just permitted and just prevented movement. Methods Rats (n = 14) were anesthetized with isoflurane, and after lumbar laminectomy, the minimum alveolar concentration (MAC) for each rat was determined using a supramaximal mechanical stimulus. In these sam

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Lü, Xiao-Ying, Chen Meng, Shuai An, Yong-Fang Zhao, and Zhi-Gong Wang. "Study on influence of external factors on the electrical excitability of PC12 quasi-neuronal networks through Voltage Threshold Measurement Method." PLOS ONE 17, no. 3 (2022): e0265078. http://dx.doi.org/10.1371/journal.pone.0265078.

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The aim of this paper was to investigate the influence of four different external factors (acetylcholine, ethanol, temperature and lidocaine hydrochloride) on PC12 quasi-neuronal networks by multielectrode-array-based Voltage Threshold Measurement Method (VTMM). At first, VTMM was employed to measure the lowest amplitude of the voltage stimulating pulses that could just trigger the action potential from PC12 quasi-neuronal networks under normal conditions, and the amplitude was defined as the normal voltage threshold (VTh). Then the changes of the VTh of PC12 quasi-neuronal networks treated by

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Friederich, Patrick, and Bernd W. Urban. "Interaction of Intravenous Anesthetics with Human Neuronal Potassium Currents in Relation to Clinical Concentrations." Anesthesiology 91, no. 6 (1999): 1853. http://dx.doi.org/10.1097/00000542-199912000-00040.

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Background Neuronal voltage-dependent potassium (K) currents are crucial for various cellular functions, such as the integration of temporal information in the central nervous system. Data for the effects of intravenous anesthetics on human neuronal K currents are limited. It was the authors' aim to evaluate the concentration-related effects of three opioids (fentanyl, alfentanil, sufentanil) and seven nonopioids (thiopental, pentobarbital, methohexital, propofol, ketamine, midazolam, droperidol) used in clinical anesthesia on neuronal voltage-dependent K currents of human origin. Method K cur

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Couture, L., R. Élie, and P. A. Lavoie. "Effect of antidepressants on ATP-dependent calcium uptake by neuronal endoplasmic reticulum." Canadian Journal of Physiology and Pharmacology 79, no. 11 (2001): 946–52. http://dx.doi.org/10.1139/y01-074.

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This study investigated the effect of tricyclic and atypical antidepressants on adenosine triphosphate (ATP) dependent calcium uptake by the endoplasmic reticulum of lysed synaptosomes from rat brain cortex. Tricyclic antidepressants (imipramine, desipramine, clomipramine, amitriptyline) exhibited no effect in the lower range (0.06 to 2 µM) of drug concentrations, and a concentration-dependent inhibition of calcium uptake in the upper range (6 to 200 µM). A concentration-dependent inhibition was observed for atypical antidepressants (mianserin, desmethylmianserin, venlafaxine, desmethylvenlafa

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15

Friedlander, D. R., P. Milev, L. Karthikeyan, R. K. Margolis, R. U. Margolis, and M. Grumet. "The neuronal chondroitin sulfate proteoglycan neurocan binds to the neural cell adhesion molecules Ng-CAM/L1/NILE and N-CAM, and inhibits neuronal adhesion and neurite outgrowth." Journal of Cell Biology 125, no. 3 (1994): 669–80. http://dx.doi.org/10.1083/jcb.125.3.669.

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We have previously shown that aggregation of microbeads coated with N-CAM and Ng-CAM is inhibited by incubation with soluble neurocan, a chondroitin sulfate proteoglycan of brain, suggesting that neurocan binds to these cell adhesion molecules (Grumet, M., A. Flaccus, and R. U. Margolis. 1993. J. Cell Biol. 120:815). To investigate these interactions more directly, we have tested binding of soluble 125I-neurocan to microwells coated with different glycoproteins. Neurocan bound at high levels to Ng-CAM and N-CAM, but little or no binding was detected to myelin-associated glycoprotein, EGF recep

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Elfarnawany, Amira, and Faramarz Dehghani. "Time- and Concentration-Dependent Adverse Effects of Paclitaxel on Non-Neuronal Cells in Rat Primary Dorsal Root Ganglia." Toxics 11, no. 7 (2023): 581. http://dx.doi.org/10.3390/toxics11070581.

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Paclitaxel is a chemotherapeutic agent used to treat a wide range of malignant tumors. Although it has anti-tumoral properties, paclitaxel also shows significant adverse effects on the peripheral nervous system, causing peripheral neuropathy. Paclitaxel has previously been shown to exert direct neurotoxic effects on primary DRG neurons. However, little is known about paclitaxel’s effects on non-neuronal DRG cells. They provide mechanical and metabolic support and influence neuronal signaling. In the present study, paclitaxel effects on primary DRG non-neuronal cells were analyzed and their con

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17

Minoshima, Wataru, Kyoko Masui, Tomomi Tani, et al. "Deuterated Glutamate-Mediated Neuronal Activity on Micro-Electrode Arrays." Micromachines 11, no. 9 (2020): 830. http://dx.doi.org/10.3390/mi11090830.

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The excitatory synaptic transmission is mediated by glutamate (GLU) in neuronal networks of the mammalian brain. In addition to the synaptic GLU, extra-synaptic GLU is known to modulate the neuronal activity. In neuronal networks, GLU uptake is an important role of neurons and glial cells for lowering the concentration of extracellular GLU and to avoid the excitotoxicity. Monitoring the spatial distribution of intracellular GLU is important to study the uptake of GLU, but the approach has been hampered by the absence of appropriate GLU analogs that report the localization of GLU. Deuterium-lab

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18

Taninishi, Hideki, Yoshimasa Takeda, Motomu Kobayashi, Toshihiro Sasaki, Minako Arai, and Kiyoshi Morita. "Effect of Nitrous Oxide on Neuronal Damage and Extracellular Glutamate Concentration as a Function of Mild, Moderate, or Severe Ischemia in Halothane-anesthetized Gerbils." Anesthesiology 108, no. 6 (2008): 1063–70. http://dx.doi.org/10.1097/aln.0b013e318173f684.

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Background The effect of nitrous oxide on ischemic neuronal damage was quantitatively evaluated by use of logistic regression curves. Methods Seventy-two gerbils were anesthetized with 1% halothane and randomly assigned to receive 70% nitrous oxide or 70% nitrogen. Forebrain ischemia was performed for 3, 5, or 7 min, and direct-current potential in the hippocampal CA1 region was recorded. Histologic outcome was evaluated 5 days later. Relations of neuronal damage with ischemic duration and duration of ischemic depolarization were determined by logistic regression curves. In some animals, extra

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Halnes, Geir, Ivar Østby, Klas H. Pettersen, Stig W. Omholt, and Gaute T. Einevoll. "Electrodiffusive Model for Astrocytic and Neuronal Ion Concentration Dynamics." PLoS Computational Biology 9, no. 12 (2013): e1003386. http://dx.doi.org/10.1371/journal.pcbi.1003386.

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20

Barreto, Ernest, and John R. Cressman. "Ion concentration dynamics as a mechanism for neuronal bursting." Journal of Biological Physics 37, no. 3 (2011): 361–73. http://dx.doi.org/10.1007/s10867-010-9212-6.

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21

Rössler, Oliver G., Lars Steinmüller, Klaus M. Giehl, and Gerald Thiel. "Role of c-Jun concentration in neuronal cell death." Journal of Neuroscience Research 70, no. 5 (2002): 655–64. http://dx.doi.org/10.1002/jnr.10447.

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22

Fang, Mengke, Li Chen, and Shengqiang Lu. "Effect of Levobupivacaine Hydrochloride-Loaded Nanospheres on Delayed Cerebral Vasospasm Following Subarachnoid Hemorrhage in Rabbits." Journal of Biomedical Nanotechnology 20, no. 9 (2024): 1487–95. http://dx.doi.org/10.1166/jbn.2024.3904.

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This research was aimed to analyze the mechanism of action of levobupivacaine hydrochloride-loaded nanospheres on delayed cerebral vasospasm following subarachnoid hemorrhage (SAH). Levobupivacaine hydrochloride-loaded nanospheres (LevoBPV Hcl/PLGA) were prepared using the solvent evaporation methodology, with the raw material as a control. The blood drug concentrations were detected by HPLC after subcutaneous and subarachnoid administration in experimental rabbits. Forty New Zealand white rabbits were randomly assigned into Sham group, SAH group, LevoBPV Hcl group (10 mg/kg), and LevoBPV Hcl/

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Thauerer, Bettina, Simon Geisler, Dietmar Fuchs, and Gabriele Baier-Bitterlich. "Modulation of phenylalanine and tyrosine concentrations by ischemia and guanosine in neuronal PC12 cells." Pteridines 24, no. 3 (2013): 245–50. http://dx.doi.org/10.1515/pterid-2013-0036.

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AbstractSurvival of neurons is dependent on the presence of trophic and non-trophic factors. We have previously observed the protective capacity of purine nucleosides in hypoxic neuronal cell cultures. Guanosine appeared especially interesting with respect to its remarkable neurite-stimulating aptitude. Here we report the effect of ischemic stress and guanosine on the concentration of the essential amino acids phenylalanine and tyrosine, in culture supernatants of PC12 cells. In ischemic neuronal cultures, a substantial rise of phenylalanine and tyrosine levels was observed, indicating inhibit

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de Wet, Sholto, Asandile Mangali, Richard Batt, et al. "The Highs and Lows of Memantine—An Autophagy and Mitophagy Inducing Agent That Protects Mitochondria." Cells 12, no. 13 (2023): 1726. http://dx.doi.org/10.3390/cells12131726.

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Memantine is an FDA-approved, non-competitive NMDA-receptor antagonist that has been shown to have mitochondrial protective effects, improve cell viability and enhance clearance of Aβ42 peptide. Currently, there are uncertainties regarding the precise molecular targets as well as the most favourable treatment concentrations of memantine. Here, we made use of an imaging-based approach to investigate the concentration-dependent effects of memantine on mitochondrial fission and fusion dynamics, autophagy and mitochondrial quality control using a neuronal model of CCCP-induced mitochondrial injury

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Čižas, Paulius, Aistė Jekabsonė, Vilmantė Borutaitė, and Ramunė Morkūnienė. "Prevention of Amyloid-Beta Oligomer-Induced Neuronal Death by EGTA, Estradiol, and Endocytosis Inhibitor." Medicina 47, no. 2 (2011): 15. http://dx.doi.org/10.3390/medicina47020015.

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Background and objective. Alzheimer’s disease is a progressive neurodegenerative disease that is biochemically characterized by the accumulation of amyloid beta (Aβ) peptides in the brain. The current hypothesis suggests that Aβ oligomers rather than fibrillar aggregates are the most toxic species of Aβ though the mechanisms of their neurotoxicity are unclear. The authors have previously shown that small Aβ1–42 oligomers at around 1 μM concentration caused rapid (in 24 h) neuronal death in cerebellar granule cell (CGC) cultures. In this study, we aimed to investigate whether protracted (up to

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Le Foll, Christelle, Boman G. Irani, Christophe Magnan, Ambrose A. Dunn-Meynell, and Barry E. Levin. "Characteristics and mechanisms of hypothalamic neuronal fatty acid sensing." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 297, no. 3 (2009): R655—R664. http://dx.doi.org/10.1152/ajpregu.00223.2009.

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We assessed the mechanisms by which specialized hypothalamic ventromedial nucleus (VMN) neurons utilize both glucose and long-chain fatty acids as signaling molecules to alter their activity as a potential means of regulating energy homeostasis. Fura-2 calcium (Ca2+) and membrane potential dye imaging, together with pharmacological agents, were used to assess the mechanisms by which oleic acid (OA) alters the activity of dissociated VMN neurons from 3- to 4-wk-old rats. OA excited up to 43% and inhibited up to 29% of all VMN neurons independently of glucose concentrations. In those neurons exc

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Borroni, Virginia, Constanza Kamerbeek, María F. Pediconi та Francisco J. Barrantes. "Lovastatin Differentially Regulates α7 and α4 Neuronal Nicotinic Acetylcholine Receptor Levels in Rat Hippocampal Neurons". Molecules 25, № 20 (2020): 4838. http://dx.doi.org/10.3390/molecules25204838.

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Neuronal α7 and α4β2 are the predominant nicotinic acetylcholine receptor (nAChR) subtypes found in the brain, particularly in the hippocampus. The effects of lovastatin, an inhibitor of cholesterol biosynthesis, on these two nAChRs endogenously expressed in rat hippocampal neuronal cells were evaluated in the 0.01–1 µM range. Chronic (14 days) lovastatin treatment augmented cell-surface levels of α7 and α4 nAChRs, as measured by fluorescence microscopy and radioactive ligand binding assays. This was accompanied in both cases by an increase in total protein receptor levels as determined by Wes

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Hinojosa, María G., Ana I. Prieto, Clara Muñoz-Castro, et al. "Cytotoxicity and Effects on the Synapsis Induced by Pure Cylindrospermopsin in an E17 Embryonic Murine Primary Neuronal Culture in a Concentration- and Time-Dependent Manner." Toxins 14, no. 3 (2022): 175. http://dx.doi.org/10.3390/toxins14030175.

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Cylindrospermopsin (CYN) is a cyanotoxin whose incidence has been increasing in the last decades. Due to its capacity to exert damage at different levels of the organism, it is considered a cytotoxin. Although the main target organ is the liver, recent studies indicate that CYN has potential toxic effects on the nervous system, both in vitro and in vivo. Thus, the aim of the present work was to study the effects of this cyanotoxin on neuronal viability and synaptic integrity in murine primary cultures of neurons exposed to environmentally relevant concentrations (0–1 µg/mL CYN) for 12, 24, and

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Loginova, Maria, Tatiana Mishchenko, Maria Savyuk, et al. "Double-Edged Sword of Vitamin D3 Effects on Primary Neuronal Cultures in Hypoxic States." International Journal of Molecular Sciences 22, no. 11 (2021): 5417. http://dx.doi.org/10.3390/ijms22115417.

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The use of vitamin D3 along with traditional therapy opens up new prospects for increasing the adaptive capacity of nerve cells to the effects of a wide range of stress factors, including hypoxia-ischemic processes. However, questions about prophylactic and therapeutic doses of vitamin D3 remain controversial. The purpose of our study was to analyze the effects of vitamin D3 at different concentrations on morpho-functional characteristics of neuron–glial networks in hypoxia modeling in vitro. We showed that a single administration of vitamin D3 at a high concentration (1 µM) in a normal state

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Kratzer, Stephan, Hedwig Irl, Corinna Mattusch та ін. "Tranexamic Acid Impairs γ-Aminobutyric Acid Receptor Type A–mediated Synaptic Transmission in the Murine Amygdala". Anesthesiology 120, № 3 (2014): 639–49. http://dx.doi.org/10.1097/aln.0000000000000103.

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Abstract Background: Tranexamic acid (TXA) is commonly used to reduce blood loss in cardiac surgery and in trauma patients. High-dose application of TXA is associated with an increased risk of postoperative seizures. The neuronal mechanisms underlying this proconvulsant action of TXA are not fully understood. In this study, the authors investigated the effects of TXA on neuronal excitability and synaptic transmission in the basolateral amygdala. Methods: Patch clamp recordings and voltage-sensitive dye imaging were performed in acute murine brain slices. Currents through N-methyl-d-aspartate,

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Ichinose, Fumito, Paul L. Huang, and Warren M. Zapol. "Effects of Targeted Neuronal Nitric Oxide Synthase Gene Disruption and Nitro sup G -L-Arginine Methylester on the Threshold for Isoflurane Anesthesia." Anesthesiology 83, no. 1 (1995): 101–8. http://dx.doi.org/10.1097/00000542-199507000-00013.

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Background Considerable evidence suggests that nitric oxide plays a role in synaptic transmission in the central and peripheral nervous system. Nonselective inhibition of nitric oxide synthase by nitroG-L-arginine methylester (L-NAME) reduces the minimum alveolar concentration of halothane anesthesia. The effects of selective neuronal nitric oxide synthase inhibition on the anesthetic requirements in mice congenitally deficient in neuronal nitric oxide synthase (knockout mice) were examined. Methods Isoflurane minimum alveolar concentration and righting reflex ED50 (RRED50) were determined in

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Ma, Y., RB Campenot, and FD Miller. "Concentration-dependent regulation of neuronal gene expression by nerve growth factor." Journal of Cell Biology 117, no. 1 (1992): 135–41. http://dx.doi.org/10.1083/jcb.117.1.135.

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NGF is a neurotrophic protein that promotes the survival, growth, and differentiation of developing sympathetic neurons. To directly determine the effects of different concentrations of NGF on neuronal gene expression, we examined mRNAs encoding the p75 low-affinity NGF (LNGF) receptor, T alpha 1 alpha-tubulin (T alpha 1), and tyrosine hydroxylase (TH) in pure cultures of rat sympathetic neurons from postnatal day 1 superior cervical ganglia. Studies of the timecourse of gene expression during 2 wk in culture indicated that a 5-d incubation period would be optimal for the concentration-effect

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Ábrahám, István M., Peter Meerlo, and Paul GM Luiten. "Concentration Dependent Actions of Glucocorticoids on Neuronal Viability and Survival." Dose-Response 4, no. 1 (2006): dose—response.0. http://dx.doi.org/10.2203/dose-response.004.01.004.abraham.

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Voipio, J., W. F. Boron, S. W. Jones, U. Hopfer, J. A. Payne, and K. Kaila. "Comment on "Local impermeant anions establish the neuronal chloride concentration"." Science 345, no. 6201 (2014): 1130. http://dx.doi.org/10.1126/science.1252978.

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Luhmann, H. J., S. Kirischuk, and W. Kilb. "Comment on "Local impermeant anions establish the neuronal chloride concentration"." Science 345, no. 6201 (2014): 1130. http://dx.doi.org/10.1126/science.1255337.

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Shimizu, Akira, Jiani Wang, Ken-Ichiro Tsutsui, and Toshio Iijima. "Odor concentration dependent neuronal activities in the anterior piriform cortex." Neuroscience Research 68 (January 2010): e388. http://dx.doi.org/10.1016/j.neures.2010.07.1721.

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Leyrer-Jackson, Jonna M., Erin K. Nagy, Lauren E. Hood, Jason M. Newbern, Cassandra D. Gipson, and M. Foster Olive. "Ethanol has concentration-dependent effects on hypothalamic POMC neuronal excitability." Alcohol 86 (August 2020): 103–12. http://dx.doi.org/10.1016/j.alcohol.2020.04.001.

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Neerland, Bjørn Erik, Nathalie Bodd Halaas, Ane Victoria Idland, et al. "Fatty Acid-Binding Protein 3 in Cerebrospinal Fluid of Hip Fracture Patients with Delirium." Journal of Alzheimer's Disease 77, no. 1 (2020): 183–90. http://dx.doi.org/10.3233/jad-200364.

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Background: Delirium is associated with dementia and thus biomarkers reflecting neurodegeneration are of interest. Fatty acid-binding protein 3 (FABP3) is a cytoplasmic neuronal protein that has been isolated from the brain. It is released following brain injury and concentrations in cerebrospinal fluid (CSF) are also higher in neurodegenerative disorders such as Alzheimer’s disease (AD). Objective: To examine the relationship between CSF FABP3 concentration and delirium in hip fracture patients compared to a group of cognitively normal controls. Methods: CFS FABP3 concentration was measured i

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Bikson, Marom, Rahul S. Ghai, Scott C. Baraban, and Dominique M. Durand. "Modulation of Burst Frequency, Duration, and Amplitude in the Zero-Ca2+ Model of Epileptiform Activity." Journal of Neurophysiology 82, no. 5 (1999): 2262–70. http://dx.doi.org/10.1152/jn.1999.82.5.2262.

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Incubation of hippocampal slices in zero-Ca2+ medium blocks synaptic transmission and results in spontaneous burst discharges. This seizure-like activity is characterized by negative shifts (bursts) in the extracellular field potential and a K+ wave that propagates across the hippocampus. To isolate factors related to seizure initiation, propagation, and termination, a number of pharmacological agents were tested. K+ influx and efflux mechanisms where blocked with cesium, barium, tetraethylammonium (TEA), and 4-aminopyridine (4-AP). The effect of the gap junction blockers, heptanol and octanol

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Qaid, Entesar Yaseen Abdo, Rahimah Zakaria, Nurul Aiman Mohd Yusof, et al. "Tualang Honey prevents neuronal damage in medial prefrontal cortex (mPFC) through enhancement of cholinergic system in male rats following exposure to normobaric hypoxia." Bangladesh Journal of Medical Science 20, no. 1 (2021): 122–29. http://dx.doi.org/10.3329/bjms.v20i1.50356.

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Background: Medial prefrontal cortex (mPFC) is considered to be involved in human cognition to mPFCin terms of learning and memory. Hypoxia is one of the crucial factors causing secondary damage incerebral hemorrhage and traumatic brain injury. However, the underlying mechanisms and possibletherapeutic approach to prevent neuronal damage has not been attempted yet. Therefore, the present studyaimed to investigate the role of Tualang honey on medial prefrontal cortical neuronal morphology andcholinergic markers such as acetylcholine (ACh) and acetylcholinesterase (AChE) following exposure to no

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Kaku, Yasuhiko, Yasuhiro Yonekawa, Tetsuya Tsukahara, Nobuyoshi Ogata, Tetsuya Kimura, and Takashi Taniguchi. "Alterations of a 200 kDa Neurofilament in the Rat Hippocampus after Forebrain Ischemia." Journal of Cerebral Blood Flow & Metabolism 13, no. 3 (1993): 402–8. http://dx.doi.org/10.1038/jcbfm.1993.54.

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Alteration in the concentration of a 200 kDa neurofilament (NF200) in the rat hippocampus after forebrain ischemia and its relationship to hippocampal neuronal death were studied with an anti-200 kDa neurofilament antibody, using immunohistochemical and immunoblotting techniques. In rats subjected to 8 min of transient forebrain ischemia, hematoxylin-eosin staining showed survival of most of the neurons in the hippocampal CA1 region at 1 day and loss of more than 75% of the neurons at 7 days after ischemia. Immunoblotting showed that the concentration of NF200 in the hippocampal homogenate ten

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LEIPER, James M., Joanne SANTA MARIA, Ann CHUBB, et al. "Identification of two human dimethylarginine dimethylaminohydrolases with distinct tissue distributions and homology with microbial arginine deiminases." Biochemical Journal 343, no. 1 (1999): 209–14. http://dx.doi.org/10.1042/bj3430209.

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Methylarginines inhibit nitric oxide synthases (NOS). Cellular concentrations of methylarginines are determined in part by the activity of dimethylarginine dimethylaminohydrolase (DDAH; EC 3.5.3.18). We have cloned human DDAH and identified and expressed a second novel DDAH isoform (DDAH I and II respectively). DDAH I predominates in tissues that express neuronal NOS. DDAH II predominates in tissues expressing endothelial NOS. These results strengthen the hypothesis that methylarginine concentration is actively regulated and identify molecular targets for the tissue and cell-specific regulatio

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Brandes, Ivo F., Edward J. Zuperku, Astrid G. Stucke, Francis A. Hopp, Danica Jakovcevic, and Eckehard A. E. Stuth. "Isoflurane Depresses the Response of Inspiratory Hypoglossal Motoneurons to Serotonin In Vivo." Anesthesiology 106, no. 4 (2007): 736–45. http://dx.doi.org/10.1097/01.anes.0000264750.93769.99.

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Background Endogenous serotonin (5-HT) provides important excitatory drive to inspiratory hypoglossal motoneurons (IHMNs). In vitro studies show that activation of postsynaptic 5-HT receptors decreases a leak K+ channel conductance and depolarizes hypoglossal motoneurons (HMNs). In contrast, volatile anesthetics increase this leak K+ channel conductance, which causes neuronal membrane hyperpolarization and depresses HMN excitability. Clinical studies show upper airway obstruction, indicating HMN depression, even at subanesthetic concentrations. The authors hypothesized that if anesthetic activ

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Giffard, Rona G., John H. Weiss, Raymond A. Swanson, and Dennis W. Choi. "Secobarbital Attenuates Excitotoxicity but Potentiates Oxygen—Glucose Deprivation Neuronal Injury in Cortical Cell Culture." Journal of Cerebral Blood Flow & Metabolism 13, no. 5 (1993): 803–10. http://dx.doi.org/10.1038/jcbfm.1993.102.

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We examined the effects of secobarbital and other sedative-hypnotic barbiturates on the neuronal death induced by exposure to excitatory amino acids or deprivation of oxygen or glucose in mouse cortical cell cultures. N-Methyl-d-aspartate (NMDA), α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate, and kainate toxicities were attenuated in a concentration-dependent fashion by high concentrations of secobarbital or thiopental. Antagonism of NMDA toxicity was not overcome by increasing NMDA concentration and not mimicked by γ-aminobutyrate. Despite these antiexcitotoxic actions, secobarbital exacer

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Baker, R. Roy, and H. Y. Chang. "The acylation of 1-acyl-sn-glycero-3-phosphate by neuronal nuclei and microsomal fractions of immature rabbit cerebral cortex." Biochemistry and Cell Biology 68, no. 3 (1990): 641–47. http://dx.doi.org/10.1139/o90-091.

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The acylation of 1-acyl-sn-glycero-3-phosphate to form phosphatidic acid was studied using a neuronal nuclear fraction N1 and microsomal fractions P3, R (rough), S (smooth), and P (neuronal microsomes from nerve cell bodies) isolated from cerebral cortices of 15-day-old rabbits. The assays contained this lysophospholipid, ATP, CoA, MgCl2, NaF, dithiothreitol, and radioactive palmitate, oleate, or arachidonate. Of the subfractions, N1 and R had the highest specific activities (expressed per micromole phospholipid in the fraction). The rates with oleate were two to four times the values seen for

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Monyer, Hannelore, and Dennis W. Choi. "Glucose Deprivation Neuronal Injury in vitro is Modified by Withdrawal of Extracellular Glutamine." Journal of Cerebral Blood Flow & Metabolism 10, no. 3 (1990): 337–42. http://dx.doi.org/10.1038/jcbfm.1990.62.

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Cultured cortical neurons deprived of glucose in a defined solution containing 2 m M glutamine became acutely swollen and went on to degenerate over the next day; this neuronal loss could be substantially attenuated by an N-methyl-D-aspartate (NMDA) antagonist. Removal of extracellular glutamine produced two effects: an increase in overall neuronal injury and a decrease in the protective effect of an NMDA antagonist. Both effects of glutamine removal were glutamine concentration dependent (EC50 for both ∼300 μ M) and not reversed by substitution of equimolar concentrations of alanine or argini

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O'Connor, Daniel T., Justine H. Cervenka, Richard A. Stone та ін. "Dopamine β-Hydroxylase Immunoreactivity in Human Cerebrospinal Fluid: Properties, Relationship to Central Noradrenergic Neuronal Activity and Variation in Parkinson's Disease and Congenital Dopamine β-Hydroxylase Deficiency". Clinical Science 86, № 2 (1994): 149–58. http://dx.doi.org/10.1042/cs0860149.

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1. Dopamine β-hydroxylase is stored and released with catecholamines by exocytosis from secretory vesicles in noradrenergic neurons and chromaffin cells. Although dopamine β-hydroxylase enzymic activity is measurable in cerebrospinal fluid, such activity is unstable, and its relationship to central noradrenergic neuronal activity in humans is not clearly established. To explore the significance of cerebrospinal fluid dopamine β-hydroxylase, we applied a homologous human dopamine β-hydroxylase radioimmunoassay to cerebrospinal fluid, in order to characterize the properties and stability of cere

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Cymerys, Joanna, Andrzej Kowalczyk, Katarzyna Mikołajewicz, Anna Słońska, and Małgorzata Krzyżowska. "Nitric Oxide Influences HSV-1-Induced Neuroinflammation." Oxidative Medicine and Cellular Longevity 2019 (February 11, 2019): 1–17. http://dx.doi.org/10.1155/2019/2302835.

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Herpes simplex virus type 1 (HSV-1) has the ability to replicate in neurons and glial cells and to produce encephalitis leading to neurodegeneration. Accumulated evidence suggests that nitric oxide (NO) is a key molecule in the pathogenesis of neurotropic virus infections. NO can exert both cytoprotective as well as cytotoxic effects in the central nervous system (CNS) depending on its concentration, time course exposure, and site of action. In this study, we used anin vitromodel of HSV-1-infected primary neuronal and mixed glial cultures as well as an intranasal model of HSV-1 in BALB/c mice

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Hoshino, Osamu, Meihong Zheng, and Kazuo Watanabe. "Improved Perceptual Learning by Control of Extracellular GABA Concentration by Astrocytic Gap Junctions." Neural Computation 30, no. 1 (2018): 184–215. http://dx.doi.org/10.1162/neco_a_01027.

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Learning of sensory cues is believed to rely on synchronous pre- and postsynaptic neuronal firing. Evidence is mounting that such synchronicity is not merely caused by properties of the underlying neuronal network but could also depend on the integrity of gap junctions that connect neurons and astrocytes in networks too. In this perspective, we set out to investigate the effect of astrocytic gap junctions on perceptual learning, introducing a model for coupled neuron-astrocyte networks. In particular, we focus on the fact that astrocytes are rich of GABA transporters (GATs) which can either up

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Swingland, James T., Pascal F. Durrenberger, Richard Reynolds, et al. "Mean expression of the X-chromosome is associated with neuronal density." Frontiers in Neuroscience 6 (November 12, 2012): 161. https://doi.org/10.3389/fnins.2012.00161.

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<strong>Background: </strong>Neurodegenerative diseases are characterized by key features such as loss of neurons, astrocytosis, and microglial activation/proliferation. These changes cause differences in the density of cell types between control and disease subjects, confounding results from gene expression studies. Chromosome X (ChrX) is known to be specifically important in the brain. We hypothesized the existence of a chromosomal signature of gene expression associated with the X-chromosome for neurological conditions not normally associated with that chromosome. The hypothesis was in

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