scholarly journals GABA Depolarizes Neuronal Progenitors of the Postnatal Subventricular Zone Via GABA A Receptor Activation

2003 ◽  
Vol 550 (3) ◽  
pp. 785-800 ◽  
Author(s):  
D. D. Wang ◽  
D. D. Krueger ◽  
A. Bordey
2020 ◽  
Vol 177 (13) ◽  
pp. 3075-3090 ◽  
Author(s):  
Franco R. Mir ◽  
Carlos Wilson ◽  
Lucas E. Cabrera Zapata ◽  
Luis G. Aguayo ◽  
María Julia Cambiasso

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

2012 ◽  
Vol 116 (1) ◽  
pp. 47-55 ◽  
Author(s):  
Dirk Ruesch ◽  
Elena Neumann ◽  
Hinnerk Wulf ◽  
Stuart A. Forman

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.


1994 ◽  
Vol 11 (5) ◽  
pp. 1003-1012 ◽  
Author(s):  
Jeffrey H. Boatright ◽  
Nara M. Rubim ◽  
P. Michael Iuvone

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.


Neuroscience ◽  
2001 ◽  
Vol 103 (3) ◽  
pp. 725-737 ◽  
Author(s):  
R.C Riley ◽  
J.A Trafton ◽  
S.I Chi ◽  
A.I Basbaum

2008 ◽  
Vol 11 (1) ◽  
pp. 187-200 ◽  
Author(s):  
Fabienne Agasse ◽  
Liliana Bernardino ◽  
Bruno Silva ◽  
Raquel Ferreira ◽  
Sofia Grade ◽  
...  

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