The aims of the present study were to investigate, using mouse whole stomach in vitro, the effects ofg-aminobutyric acid (GABA) and GABA receptor agonists on the spontaneous gastric tone, to examine thesubtypes of GABA receptors involved in the responses and to determine the possible site(s) of action.GABA induced gastric relaxation, which was antagonized by the GABAA-receptor antagonist, bicuculline,potentiated by phaclofen, GABAB-receptor antagonist, but not affected by 1,2,5,6-Tetrahydropyridin-4-yl methylphosphinic acid hydrate (TPMPA), GABAC-receptor antagonist. Muscimol,GABAA-receptor agonist, mimicked GABA effects inducing relaxation, which was significantly reduced bybicuculline, Nu-nitro-L-arginine methyl ester (L-NAME), inhibitor of NO synthase or apamin, inhibitor ofsmall conductance Ca2þ-dependent Kþ channels, which blocks the purinergic transmission in thispreparation. It was abolished by tetrodotoxin (TTX) or L-NAME plus apamin. Baclofen, a specific GABABreceptoragonist, induced an increase in the gastric tone, which was antagonized by phaclofenand abolished by TTX or atropine. Bicuculline, but not phaclofen or TPMPA, per se induced an increase ingastric tone, which was prevented by L-NAME. In conclusion, our results suggest that GABA is involvedin the regulation of mouse gastric tone, through modulation of intrinsic neurons. Activation of GABAAreceptorsmediates relaxation through neural release of NO and neurotransmitters, activating Ca2þ-dependent Kþ channels, likely purines, while activation of GABAB-receptors leads to contraction throughacetylcholine release.
|Numero di pagine||5|
|Stato di pubblicazione||Published - 2010|
All Science Journal Classification (ASJC) codes
- Cellular and Molecular Neuroscience