scholarly journals 2‐(4‐methyl‐thiazol‐5‐yl) ethyl nitrate maleate‐potentiated GABA A receptor response in hippocampal neurons

2018 ◽  
Vol 24 (12) ◽  
pp. 1231-1240 ◽  
Author(s):  
Xiao‐Mei Jiang ◽  
Wei‐Ping Wang ◽  
Zhi‐Hui Liu ◽  
Hua‐Jing Yin ◽  
Hao Ma ◽  
...  
Keyword(s):  
Hippocampal Neurons ◽  
Gaba A ◽  
Receptor Response

Effects of Neurosteroid and Benz[ e ]indene Enantiomers on GABA A Receptors in Cultured Hippocampal Neurons and Transfected HEK-293 Cells

1996 ◽  
Vol 35 (9-10) ◽  
pp. 1161-1168 ◽  
Author(s):  
C.F ZORUMSKI ◽  
L.L WITTMER ◽  
K.E ISENBERG ◽  
HU YUEFEI ◽  
D.F COVEY
Keyword(s):  
Hippocampal Neurons ◽  
Hek 293 ◽  
Gaba A ◽  
Hek 293 Cells ◽  
293 Cells ◽  
Cultured Hippocampal Neurons

scholarly journals Conductance of GABA A Channels Activated by Pentobarbitone in Hippocampal Neurons from Newborn Rats

2003 ◽  
Vol 552 (1) ◽  
pp. 13-22 ◽  
Author(s):  
Mansoureh Eghbali ◽  
Bryndis Birnir ◽  
Peter W. Gage
Keyword(s):  
Hippocampal Neurons ◽  
Newborn Rats ◽  
Gaba A

Embryonic Rat Hippocampal Neurons and GABA A Receptor Subunit-Transfected Non-neuronal Cells Release GABA Tonically

1998 ◽  
Vol 164 (3) ◽  
pp. 239-251 ◽  
Author(s):  
A.Y. Valeyev ◽  
A.E. Schaffner ◽  
P. Skolnick ◽  
V.S. Dunlap ◽  
G. Wong ◽  
...  
Keyword(s):  
Hippocampal Neurons ◽  
Neuronal Cells ◽  
Receptor Subunit ◽  
Gaba A

scholarly journals Role of L-Type Voltage-Gated Calcium Channels in Epileptiform Activity of Neurons

2021 ◽  
Vol 22 (19) ◽  
pp. 10342
Author(s):  
Denis P. Laryushkin ◽  
Sergei A. Maiorov ◽  
Valery P. Zinchenko ◽  
Sergei G. Gaidin ◽  
Artem M. Kosenkov
Keyword(s):  
Calcium Channels ◽  
Hippocampal Neurons ◽  
Epileptiform Activity ◽  
Gaba A ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channels ◽  
Effective Doses ◽  
High Doses ◽  
Paroxysmal Depolarization Shift

Epileptic discharges manifest in individual neurons as abnormal membrane potential fluctuations called paroxysmal depolarization shift (PDS). PDSs can combine into clusters that are accompanied by synchronous oscillations of the intracellular Ca2+ concentration ([Ca2+]i) in neurons. Here, we investigate the contribution of L-type voltage-gated calcium channels (VGCC) to epileptiform activity induced in cultured hippocampal neurons by GABA(A)R antagonist, bicuculline. Using KCl-induced depolarization, we determined the optimal effective doses of the blockers. Dihydropyridines (nifedipine and isradipine) at concentrations ≤ 10 μM demonstrate greater selectivity than the blockers from other groups (phenylalkylamines and benzothiazepines). However, high doses of dihydropyridines evoke an irreversible increase in [Ca2+]i in neurons and astrocytes. In turn, verapamil and diltiazem selectively block L-type VGCC in the range of 1–10 μM, whereas high doses of these drugs block other types of VGCC. We show that L-type VGCC blockade decreases the half-width and amplitude of bicuculline-induced [Ca2+]i oscillations. We also observe a decrease in the number of PDSs in a cluster and cluster duration. However, the pattern of individual PDSs and the frequency of the cluster occurrence change insignificantly. Thus, our results demonstrate that L-type VGCC contributes to maintaining the required [Ca2+]i level during oscillations, which appears to determine the number of PDSs in the cluster.

Isobolographic Analysis of the Interactions between Midazolam and Propofol at GABAAReceptors in Embryonic Mouse Neurons 

1998 ◽  
Vol 89 (6) ◽  
pp. 1444-1454 ◽  
Author(s):  
Laura C. McAdam ◽  
John F. MacDonald ◽  
Beverley A. Orser
Keyword(s):  
Hippocampal Neurons ◽  
Clinical Effects ◽  
Gamma Aminobutyric Acid ◽  
Response Curves ◽  
Additive Interaction ◽  
Embryonic Mouse ◽  
Gaba A ◽  
Isobolographic Analysis ◽  
Low Concentrations ◽  
Patch Clamp Method

Background Clinical studies suggest that midazolam and propofol interact synergistically to induce hypnosis, but these drugs do not interact synergistically to prevent movement in response to noxious stimuli. The mechanisms underlying these interactions are not certain but may occur at the level of the gamma-aminobutyric acid A (GABA(A)) receptor. Methods The authors evaluated the interactions between propofol and midazolam in modulating GABA(A) receptor activity in embryonic hippocampal neurons. The effects of midazolam and propofol on peak current evoked by submaximal concentrations of GABA were studied using the patch clamp method. Isobolographic analysis was undertaken by constructing concentration-response curves for midazolam and propofol alone and then evaluating the potency of combinations of midazolam and propofol. In other experiments, the concentration of GABA was increased and flurazepam was substituted for midazolam. Results Isobolographic analysis confirmed that midazolam and propofol interact synergistically to enhance currents evoked by low concentrations of GABA (1 microM). However, when the concentration of GABA was increased to 3 microM, the interaction was additive. The interaction between flurazepam and propofol was also additive for enhancement of currents evoked by 3 microM GABA. Conclusions The interaction between midazolam and propofol was critically dependent on the concentration of GABA: Synergism was evident at low concentrations of GABA, but an additive interaction was apparent when the concentration of GABA was increased. Changes in GABA(A) receptor function may underlie the synergistic interaction between propofol and midazolam for clinical effects such as hypnosis. The clinical implication of the results is that the benefits of synergism observed at one concentration ratio of these drugs may not be apparent at another.

Nitrous Oxide-induced Enhancement of γ-Aminobutyric Acid-A-mediated Chloride Currents in Acutely Dissociated Hippocampal Neurons 

1998 ◽  
Vol 88 (2) ◽  
pp. 473-480 ◽  
Author(s):  
Misa Dzoljic ◽  
Bert Van Duijn
Keyword(s):  
Nitrous Oxide ◽  
Hippocampal Neurons ◽  
Prolonged Exposure ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
General Anesthetics ◽  
Patch Clamp Recording ◽  
Gaba A ◽  
Ca1 Region ◽  
Tube Application

Background Because the synaptic inhibition in the human brain is largely mediated by gamma-aminobutyric acid (GABA), the GABA receptor is of primary interest for the study of the working mechanism of general anesthetics. This article examines the interaction between this type of ion channel and nitrous oxide (N2O). Methods Patch clamp recording techniques were applied to investigate the effects of N2O on GABA(A) receptor channels in a whole-cell configuration at room temperature. Acutely dissociated rat hippocampal cells from the CA1 region were used. Rapid application of the agonist muscimol and anesthetics (N2O, pentobarbital, and ethanol) was accomplished using a Y tube application system. Peak chloride (Cl-) currents were measured. Results Short-term application of muscimol (5-30 microM) with dissolved N2O (80%, approximately 22.5 mM) increased the Cl- current (approximately 140%) compared with muscimol alone. This effect is comparable with results the authors obtained with ethanol (800 mM) and pentobarbital (100 microM). Prolonged exposure (9 min) to N2O further increased Cl- currents by an additional 50%. Concentrations of N2O lower than 12 mM did not show an enhancement of this current, whereas application of N2O alone did not result in any Cl- conductance. Conclusions These results indicate that N2O can enhance GABA(A) channel-mediated Cl- currents by modulating the effect of the specific GABA(A) agonist; it is not active by itself.

scholarly journals Reduced neurosteroid potentiation of GABA A receptors in epilepsy and depolarized hippocampal neurons

2020 ◽  
Vol 7 (4) ◽  
pp. 527-542 ◽  
Author(s):  
Suchitra Joshi ◽  
William H. Roden ◽  
Jaideep Kapur ◽  
Laura A. Jansen
Keyword(s):  
Hippocampal Neurons ◽  
Gaba A

Halothane Depresses Glutamatergic Neurotransmission to Brain Stem Inspiratory Premotor Neurons in a Decerebrate Dog Model

2003 ◽  
Vol 98 (4) ◽  
pp. 897-905 ◽  
Author(s):  
Astrid G. Stucke ◽  
Edward J. Zuperku ◽  
Viseslav Tonkovic-Capin ◽  
Mislav Tonkovic-Capin ◽  
Francis A. Hopp ◽  
...  
Keyword(s):  
Ampa Receptors ◽  
Gamma Aminobutyric Acid ◽  
Glutamatergic Neurotransmission ◽  
Neuronal Responses ◽  
Gaba A ◽  
Mechanically Ventilated ◽  
Receptor Response ◽  
Premotor Neurons ◽  
Glutamate Agonists ◽  
Synaptic Mechanisms

Background Inspiratory bulbospinal neurons in the caudal ventral medulla are premotor neurons that drive phrenic motoneurons and ultimately the diaphragm. Excitatory drive to these neurons is mediated by N-methyl-d-aspartate (NMDA) receptors and alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) receptors and modulated by an inhibitory gamma-aminobutyric acid(A) (GABA(A))ergic input. The authors investigated the effect of halothane on these synaptic mechanisms in decerebrate dogs. Methods Studies were performed in decerebrate, vagotomized, paralyzed, and mechanically ventilated dogs during hypercapnic hyperoxia. The effect of 1 minimum alveolar concentration (MAC) halothane on extracellularly recorded neuronal activity was measured during localized picoejection of the GABA(A) receptor blocker bicuculline and the glutamate agonists AMPA and NMDA. Complete blockade of the GABA(A)ergic mechanism by bicuculline allowed differentiation between the effects of halothane on overall GABA(A)ergic inhibition and on overall glutamatergic excitation. The neuronal responses to exogenous AMPA and NMDA were used to estimate the anesthetic effect on postsynaptic glutamatergic neurotransmission. Results Halothane, 1 MAC, depressed the spontaneous activity of 21 inspiratory neurons by 20.6 +/- 18.0% (mean +/- SD; P = 0.012). Overall glutamatergic excitation was depressed 15.4 +/- 20.2% (P = 0.001), while overall GABA(A)ergic inhibition did not change. The postsynaptic responses to exogenous AMPA and NMDA were also depressed by 18.6 +/- 35.7% (P = 0.03) and 22.2 +/- 26.2% (P = 0.004), respectively. Conclusion Halothane, 1 MAC, depressed the activity of inspiratory premotor neurons by a reduction of glutamatergic excitation. Overall inhibitory drive did not change. The postsynaptic AMPA and NMDA receptor response was significantly reduced. These findings contrast with studies in expiratory premotor neurons in which overall inhibition was significantly increased by halothane and there was no reduction in the postsynaptic glutamate receptor response.

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