scholarly journals Could α5-GABA-A receptor activation be used as a target for managing medulloblastomas?

CNS Oncology ◽  
2014 ◽  
Vol 3 (4) ◽  
pp. 245-247 ◽  
Author(s):  
Soma Sengupta ◽  
Shyamal D Weeraratne ◽  
Yoon-Jae Cho ◽  
Scott L Pomeroy
Keyword(s):  
Receptor Activation ◽  
Gaba A

scholarly journals Gonadal hormone‐independent sex differences in GABA A receptor activation in rat embryonic hypothalamic neurons

2020 ◽  
Vol 177 (13) ◽  
pp. 3075-3090 ◽  
Author(s):  
Franco R. Mir ◽  
Carlos Wilson ◽  
Lucas E. Cabrera Zapata ◽  
Luis G. Aguayo ◽  
María Julia Cambiasso
Keyword(s):  
Sex Differences ◽  
Receptor Activation ◽  
Gonadal Hormone ◽  
Hypothalamic Neurons ◽  
Gaba A

scholarly journals An Allosteric Coagonist Model for Propofol Effects on α1β2γ2L γ-Aminobutyric Acid Type A Receptors

2012 ◽  
Vol 116 (1) ◽  
pp. 47-55 ◽  
Author(s):  
Dirk Ruesch ◽  
Elena Neumann ◽  
Hinnerk Wulf ◽  
Stuart A. Forman
Keyword(s):  
Type A ◽  
Receptor Activation ◽  
Convincing Evidence ◽  
Receptor Activity ◽  
Aminobutyric Acid ◽  
Single Class ◽  
Gaba A ◽  
Direct Activation ◽  
Receptor Sites ◽  
Acid Type

Background Propofol produces its major actions via γ-aminobutyric acid type A (GABA(A)) receptors. At low concentrations, propofol enhances agonist-stimulated GABA(A) receptor activity, and high propofol concentrations directly activate receptors. Etomidate produces similar effects, and there is convincing evidence that a single class of etomidate sites mediate both agonist modulation and direct GABA(A) receptor activation. It is unknown if the propofol binding site(s) on GABA(A) receptors that modulate agonist-induced activity also mediate direct activation. Methods GABA(A) α1β2γ2L receptors were heterologously expressed in Xenopus oocytes and activity was quantified using voltage clamp electrophysiology. We tested whether propofol and etomidate display the same linkage between agonist modulation and direct activation of GABA(A) receptors by identifying equiefficacious drug solutions for direct activation. We then determined whether these drug solutions produce equal modulation of GABA-induced receptor activity. We also measured propofol-dependent direct activation and modulation of low GABA responses. Allosteric coagonist models similar to that established for etomidate, but with variable numbers of propofol sites, were fitted to combined data. Results Solutions of 19 μM propofol and 10 μM etomidate were found to equally activate GABA(A) receptors. These two drug solutions also produced indistinguishable modulation of GABA-induced receptor activity. Combined electrophysiological data behaved in a manner consistent with allosteric coagonist models with more than one propofol site. The best fit was observed when the model assumed three equivalent propofol sites. Conclusions Our results support the hypothesis that propofol, like etomidate, acts at GABA(A) receptor sites mediating both GABA modulation and direct activation.

Regulation of endogenous dopamine release in amphibian retina by gamma-aminobutyric acid and glycine

1994 ◽  
Vol 11 (5) ◽  
pp. 1003-1012 ◽  
Author(s):  
Jeffrey H. Boatright ◽  
Nara M. Rubim ◽  
P. Michael Iuvone
Keyword(s):  
Receptor Agonist ◽  
Dopamine Release ◽  
Receptor Activation ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Gaba A ◽  
Endogenous Dopamine ◽  
Endogenous Dopamine Release ◽  
Inhibitory Tone

AbstractEndogenous dopamine release in the retina of the African clawed frog (Xenopus laevis) increases in light and decreases in darkness. The roles of the inhibitory amino acid transmitters gamma-aminobutyric acid (GABA) and glycine in regulating this light/dark difference in dopamine release were explored in the present study. Exogenous GABA, the GABA-A receptor agonist muscimol, the GABA-B receptor agonist baclofen, and the GABA-C receptor agonist cis-aminocrotonic acid (CACA) suppressed light-evoked dopamine overflow from eyecups. The effects of GABA-A and -B receptor agonists were selectively reversed by their respective receptor-specific antagonists, whereas the effect of CACA was reversed by the competitive GABA-A receptor antagonist bicuculline. The benzodiazepine diazepam enhanced the effect of muscimol on light-evoked dopamine release. Both GABA-A and -B receptor antagonists stimulated dopamine release in light or darkness. Bicuculline was more potent in light than in darkness. These data suggest that retinal dopaminergic neurons are inhibited by GABA-A and -B receptor activation in both light and darkness but that GABA-mediated inhibitory tone may be greater in darkness than in light.Exogenous glycine inhibited light-stimulated dopamine release in a concentration-dependent and strychnine-sensitive manner. However, strychnine alone did not increase dopamine release in light or darkness, nor did it augment bicuculline-stimulated release in darkness. Additionally, both strychnine and 7-chlorokynurenate, an antagonist of the strychnine-insensitive glycine-binding site of the N-methyl-D-aspartate subtype of glutamate receptor, suppressed light-evoked dopamine release. Thus, the role of endogenous glycine in the regulation of dopamine release remains unclear.

Presynaptic regulation of spinal cord tachykinin signaling via GABA B but not GABA A receptor activation

Neuroscience ◽  
2001 ◽  
Vol 103 (3) ◽  
pp. 725-737 ◽  
Author(s):  
R.C Riley ◽  
J.A Trafton ◽  
S.I Chi ◽  
A.I Basbaum
Keyword(s):  
Spinal Cord ◽  
Receptor Activation ◽  
Gaba A ◽  
Presynaptic Regulation

Biphasic action of axonal GABA-A receptors on presynaptic calcium influx

2011 ◽  
Vol 105 (6) ◽  
pp. 2931-2936 ◽  
Author(s):  
Brandon M. Stell
Keyword(s):  
Action Potential ◽  
Cerebellar Cortex ◽  
High Speed ◽  
Calcium Influx ◽  
Receptor Activation ◽  
Aminobutyric Acid ◽  
Parallel Fibers ◽  
Gaba A ◽  
Biphasic Effect ◽  
Presynaptic Calcium

Although ionotropic γ-aminobutyric acid A receptors (GABAARs) have long been known to exist on the axons of many different cells, their effect on axon excitability and synaptic transmission remains controversial. Here, using high-speed Ca2+ imaging, it is shown that they induce a biphasic effect in parallel fibers of the cerebellar cortex. Multicellular measurements indicate a facilitation of action potential (AP)-evoked Ca2+ transients, which is subsequently followed by depression. However, the receptor activation does not increase influx of Ca2+ into individual fibers but instead, increases the probability of AP generation. These results provide a description of the effect of presynaptic GABAAR activation and explain why reports of the effect of their activation have been so varied.

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