Héry F, Bourgoin S, Hamon M, Ternaux J P, Glowinski J
Naunyn Schmiedebergs Arch Pharmacol. 1977 Jan;296(2):91-7. doi: 10.1007/BF00508459.
The effects of various cholinergic agonists and antagonists on the spontaneous release of newly synthetized 3H-5-HT were examined in rat hypothalamic slices. 3H-5-HT was measured in incubating medium at the end of a 30 min incubation carried out with L-3H-tryptophan in the presence of the various drugs tested. ACh (10(-5) M) in the presence of eserine (2 X 10(-4) M), and carbachol (10(-5) M) stimulated the release of 3H-5-HT. In contrast, oxotremorine (10(-5) M) reduced the 3H-amine release. The effect of carbachol was blocked by two nicotinic blockers, mecamylamine (10(-6) M) and d-tubocurarine (10(-6) M). It was not reduced by the muscarinic antagonists, atropine (10(-6) M) and scopolamine (10(-6) M). In fact, each of two antagonists added alone to the incubating medium enhanced 3H-5-HT release. The scopolamine (10(-6) M) stimulating effect on 3H-5-HT release was suppressed by d-tubocurarine (10(-6) M). Finally, the inhibiting effect of oxotremorine on 3H-5-HT release was not prevented by d-tubocurarine (10(-6) M) but was in the presence of atropine (10(-6) M) or scopolamine (10(-6) M). In the concentrations used in the release study, the cholinergic agonists and antagonists had no effect on the total formation of 3H-5-HT and 3H-5-HIAA from L-3H-tryptophan and on the accumulation of L-3H-tryptophan in tissues. In these concentrations, except for eserine, they did not affect the uptake of exogenous 3H-5-HT in hypothalamic synaptosomes (P2 fraction). These results suggest that cholinergic receptors of the muscarinic and nicotinic type are involved in the control of 3H-5-HT release; since the stimulation of the muscarinic and nicotonic cholinergic receptors resulted in an inhibition and an activation of 3H-5-HT release, respectively. As in the case of peripheral noradrenergic and central dopaminergic neurons the cholinergic receptors could be localized on serotoninergic terminals.
在大鼠下丘脑切片中，研究了各种胆碱能激动剂和拮抗剂对新合成的3H - 5 -羟色胺（3H - 5 - HT）自发释放的影响。在用L - 3H -色氨酸在各种受试药物存在的情况下进行30分钟孵育结束时，测定孵育培养基中的3H - 5 - HT。乙酰胆碱（ACh，10(-5) M）在毒扁豆碱（2×10(-4) M）存在下，以及卡巴胆碱（10(-5) M）刺激了3H - 5 - HT的释放。相反，氧化震颤素（10(-5) M）减少了3H -胺的释放。卡巴胆碱的作用被两种烟碱受体阻断剂美加明（10(-6) M）和d -筒箭毒碱（10(-6) M）阻断。它未被毒蕈碱拮抗剂阿托品（10(-6) M）和东莨菪碱（10(-6) M）减弱。实际上，单独添加到孵育培养基中的两种拮抗剂中的每一种都增强了3H - 5 - HT的释放。东莨菪碱（10(-6) M）对3H - 5 - HT释放的刺激作用被d -筒箭毒碱（10(-6) M）抑制。最后，氧化震颤素对3H - 5 - HT释放的抑制作用未被d -筒箭毒碱（10(-6) M）阻止，但在阿托品（10(-6) M）或东莨菪碱（10(-6) M）存在时被阻止。在释放研究中使用的浓度下，胆碱能激动剂和拮抗剂对L - 3H -色氨酸合成3H - 5 - HT和3H - 羟吲哚乙酸（3H - 5 - HIAA）的总量以及L - 3H -色氨酸在组织中的积累没有影响。在这些浓度下，除毒扁豆碱外，它们不影响下丘脑突触体（P2部分）对外源性3H - 5 - HT的摄取。这些结果表明，毒蕈碱型和烟碱型胆碱能受体参与了3H -
