GABAC receptors mediate slow membrane potentials in neurons of the rat major pelvic ganglia.

Content Provider	Semantic Scholar
Author	Munakata, Yasuhiko Tsurusaki, Masakatsu Akasu, Takashi
Copyright Year	1998
Abstract	Effects of gamma-aminobutyric acid (GABA) on the neuronal membrane of the rat major pelvic ganglia (MPG) were studied using intracellular recording techniques, in vitro. Application of GABA (100 microM) to MPG neurons induced a depolarization (GABAd) associated with a decreased membrane input resistance and a slow hyperpolarization (s-GABAh) associated with an increased membrane input resistance. The GABA depolarization had two phases, a fast depolarization (f-GABAd) and a subsequent slow depolarization (s-GABAd). Bicuculline (60 microM) blocked the f-GABAd but not the s-GABAd and s-GABAh. Picrotoxin (100 microM) blocked all the GABA responses. Imidazole-4-acetic acid (I4AA, 100 microM), a GABAc receptor antagonist, depressed the s-GABAd and s-GABAh, but did not block the f-GABAd. Cis-4-aminocrotonic acid (CACA), a GABAc receptor agonist, produced a depolarization followed by a hyperpolarization in MPG neurons. I4AA (100 microM) depressed the CACA-induced responses. It was concluded that GABAA receptors mediate the f-GABAd and that GABAc receptors mediate the s-GABAd and s-GABAh, in neurons of the rat MPG.
Starting Page	199
Ending Page	214
Page Count	16
File Format	PDF HTM / HTML
Alternate Webpage(s)	https://www.jstage.jst.go.jp/article/kurumemedj1954/45/4/45_4_295/_pdf
PubMed reference number	9914715v1
Volume Number	45
Issue Number	4
Journal	The Kurume medical journal
Language	English
Access Restriction	Open
Subject Keyword	4-aminocrotonic acid Basal Ganglia Diseases Bicuculline Depressive disorder MPG gene Membrane Potentials N(4)-chloroacetylcytosine arabinoside Picrotoxin Tissue membrane gamma-Aminobutyric Acid imidazole-4-acetic acid
Content Type	Text
Resource Type	Article