Luz S, Pinchasi I, Michaelson D M
FEBS Lett. 1983 Nov 28;164(1):9-12. doi: 10.1016/0014-5793(83)80007-6.
Activation of Torpedo presynaptic muscarinic acetylcholine (ACh) receptors with the agonist oxotremorine (20 microM) results in the inhibition of Ca2+-dependent release of endogenous ACh from Torpedo synaptosomes. This effect is reversed by the muscarinic antagonist atropine (1 microM) which, by itself, has no effect. In contrast, under the same conditions the amount of newly synthesized radiolabeled [3H]ACh released is not affected by muscarinic ligands. These findings suggest that presynaptic muscarinic inhibition in the Torpedo is due to interference with the mobilization of ACh from a storage pool.
用激动剂氧化震颤素(20微摩尔)激活电鳐突触前毒蕈碱型乙酰胆碱(ACh)受体,会抑制内源性ACh从电鳐突触体中依赖Ca2+的释放。这种效应可被毒蕈碱拮抗剂阿托品(1微摩尔)逆转,而阿托品本身无作用。相比之下,在相同条件下,新合成的放射性标记[3H]ACh的释放量不受毒蕈碱配体的影响。这些发现表明,电鳐中的突触前毒蕈碱抑制作用是由于干扰了ACh从储存池的动员。