Smith D O
Department of Physiology, University of Wisconsin, Madison 53706.
Neurosci Lett. 1992 Jan 20;135(1):5-9. doi: 10.1016/0304-3940(92)90123-o.
Acetylcholine efflux at the rat neuromuscular junction was assayed following blockage of ACh transport into synaptic vesicles by 2-(4-phenylpiperidino) cyclohexanol (AH5183). [2H4]Choline was used as a labeled precursor. AH5183 completely blocked ACh efflux from the cytosolic compartment but had comparatively less effect on release from the unlabeled vesicular pool. Tissue [2H4]ACh levels increased after AH5183 addition due to cytosolic ACh retention. Thus, ACh in the non-vesicular pool (calculated to be 34% of the total ACh) may efflux solely via the AH5183-sensitive ACh transporter inserted into the terminal membrane. ACh released from the vesicular fraction was about 100-fold more than could be accounted for by miniature end-plate potentials; possible causes of this overestimate are discussed.
在用2-(4-苯基哌啶基)环己醇(AH5183)阻断乙酰胆碱(ACh)转运至突触囊泡后，测定大鼠神经肌肉接头处的ACh流出。[2H4]胆碱用作标记前体。AH5183完全阻断了胞质区室的ACh流出，但对未标记囊泡池的释放影响相对较小。添加AH5183后，由于胞质ACh滞留，组织[2H4]ACh水平升高。因此，非囊泡池中的ACh(计算占总ACh的34%)可能仅通过插入终末膜的对AH5183敏感的ACh转运体流出。从囊泡部分释放的ACh比微小终板电位所解释的量多约100倍；讨论了这种高估的可能原因。
