Neurokinin3 receptor regulation of acetylcholine release from myenteric plexus.

This study sought to characterize the action of neurokinin B (NKB) and senktide, a selective synthetic agonist for NK3 receptors, on the myenteric plexus of the guinea pig small intestine. Both peptides stimulated a dose-dependent release of [3H]-acetylcholine (ACh). The mean effective dose values were 1 x 10(-9) for NKB and 3 x 10(-11) M for senktide.

Evidence for an involvement of eicosanoids in neurokinin3-receptor mediated acetylcholine release from myenteric neurons.

The release of acetylcholine (ACh) from myenteric plexus evoked by 5-hydroxytryptamine (5-HT) and senktide (a selective neurokinin3 (NK3) agonist) was depressed by mepacrine, an inhibitor for phospholipase A2 activity. Release of ACh was stimulated by arachidonic acid; this release was partially depressed by nordihydroguaiaretic acid (NDGA), which inhibits lipoxygenase activity. NDGA failed to modify the ACh secretion elicited by 5-HT.

Modulation of submucosal cholinergic neurons by 5-hydroxytryptamine and neuropeptides.

Release of [3H]acetylcholine ([3H]ACh) was examined in a submucous plexus preparation obtained from the guinea pig small intestine in vitro. Constant-current field stimulation evoked ACh output; this output was dependent on the stimulus frequency applied. Maximal release was observed at 10 Hz; this release was blocked by tetrodotoxin (1 x 10(-6) M) or in Ca2(+)-free buffer.

Stimulation of acetylcholine release from myenteric neurons of guinea pig small intestine by forskolin and cyclic AMP.

Forskolin, an activator of adenylate cyclase, was used to examine the regulation of [3H]acetylcholine (ACh) release by cyclic AMP (cAMP)-related mechanisms in myenteric plexus-longitudinal muscle preparations of guinea pig small intestine. Forskolin evoked a dose-related increase in [3H]ACh release. Both dibutyryl-cAMP and 8-Br-cAMP significantly elevated [3H]ACh secretion.

Evidence for galanin as an inhibitory neuropeptide on myenteric cholinergic neurons in the guinea pig small intestine.

The effect of galanin on the [3H]ACh release from myenteric plexus-longitudinal muscle strips of the guinea pig small intestine was studied. While galanin did not alter the basal spontaneous efflux of ACh, it significantly depressed the ACh release evoked by electrical stimulation or caused by VIP and substance P. These results suggest an important neuromodulatory role for galanin in the enteric nervous system.