Stimulation of receptors of XXXX modulates the release of @entity8586 -like immunoreactivity from slices of @entity35 neostriatum.

@entity6341 @entity1246 @entity53958 @entity1027 @entity1022 @entity13981 @entity11359 @entity8586 @entity35 @entity1772
Slices of @entity35 dorsal neostriatum were incubated in Krebs-Henseleit medium and the release of @entity8586 -like immunoreactivity (CCK-IR) was induced by @entity13981 or high concentrations of K+. It was investigated whether drugs which act at receptors for @entity1246 ( @entity1246 ) affected the release. The GABAA-receptor agonists @entity6341 and @entity11359 enhanced the @entity13981 -induced release of CCK-IR. This effect was abolished by the GABAA-receptor antagonist, @entity1027 . When used alone, @entity1027 decreased the release. The GABAB-receptor agonist, @entity1772 , decreased the @entity13981 -induced release of CCK-IR. The stereoisomer @entity1772 , which has low intrinsic activity, had no effect when used alone, but antagonized the effect of @entity1772 as did @entity53958 , another antagonist at GABAB-receptors. When the release of CCK-IR was stimulated by K+ (40 mM) in the presence of @entity1022 , it was no longer affected by GABAA-receptor agonists or antagonists. Thus, their sites of action were probably not in the immediate vicinity of the nerve-endings which release CCK-IR. Under these conditions, stimulation of GABAB-receptors still reduced the release of CCK-IR. Therefore, it is concluded that these receptors are in the immediate vicinity of or even on the terminals which release CCK-IR.
