ISSN:
1432-1912
Keywords:
GABA
;
ACh release
;
GABA receptor
;
Gallbladder
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Summary We investigated the effect of GABA on the spontaneous efflux of 3H-acetylcholine (ACh) from the isolated guinea pig gallbladder loaded with 3H-choline. Application of GABA (10−5 M) caused a significant increase in the fractional rate of tritium efflux. This GABA-evoked efflux of ACh was inhibited by the perfusion of tetrodotoxin (10−6 M) and Ca-free medium. Nipecotic acid (10−4 M) did not affect the GABA-evoked release of ACh, indicating that ACh was not released by the entry of GABA into cholinergic nerve terminals. Bicuculline (10−6 M) and furosemide (10−6 M), the chloride ion channel blocker, inhibited the GABA-evoked ACh release. The application of muscimol (10−5 M), but not baclofen (10−5 M) also produced an increase in the fractional rate of ACh release. Thus, the GABA receptors involved in the increase of ACh release are bicuculline-sensitive. The GABA-evoked release of ACh was not altered by the perfusion with hexamethonium (10−5 M), thus indicating the presence of GABA receptors on the postganglionic cholinergic neurons. These findings suggest that bicuculline-sensitive GABA receptors probably coupled to a Cl− ionophore are present on postganglionic cholinergic neurons and are involved in the increase of ACh release in guinea pig gallbladder.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00518777
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