Weston J, Greenfield S A
Neuroscience. 1986 Apr;17(4):1079-88. doi: 10.1016/0306-4522(86)90078-3.
Acetylcholinesterase is released from both axon terminals and dendrites of nigrostriatal neurons. The relationship of this phenomenon to: (1) activation of receptors, and (2) firing rate, has been examined. In the first series of experiments, apomorphine or acetylcholine were infused into substantiae nigrae of urethane anaesthetized rats, via push-pull cannulae. In the ipsilateral striatum, the release of acetylcholinesterase was modified in a fashion reminiscent of the changes in firing rate induced by these drugs in nigrostriatal cells. Thus, application of acetylcholine into the substantia nigra induced an increase, while apomorphine induced a decrease in the release of acetylcholinesterase from the striatum. However, in the substantia nigra, the release of acetylcholinesterase did not follow this pattern: acetylcholine reduced local release, while apomorphine caused no change. In the second part of this study we studied the relationship between firing rate of nigrostriatal cells and the release of acetylcholinesterase. Two compounds known to block neuronal impulse flow were infused into the substantia nigra. These drugs were tetrodotoxin (a Na+ channel blocker), or gamma-hydroxybutyrate (a drug which blocks impulse flow specifically in dopaminergic cells). Both compounds reduced the release of acetylcholinesterase in the ipsilateral striatum. However, locally in the substantia nigra there was no decrease in release of the enzyme. In fact, following administration of gamma-hydroxybutyrate, there was a large Ca2+ dependent increase in release of acetylcholinesterase in the substantia nigra. These results suggest that release of acetylcholinesterase in the striatum may be linked to the discharge frequency of nigrostriatal neurons. On the other hand, release of acetylcholinesterase from the substantia nigra, which probably occurs from dendrites, is independent of Na+ mediated action potentials. This release may instead be associated with specific dendritic Ca2+ conductances.
乙酰胆碱酯酶从黑质纹状体神经元的轴突终末和树突中释放。已对这一现象与以下两点的关系进行了研究：（1）受体激活；（2）放电频率。在第一系列实验中，通过推挽式套管将阿扑吗啡或乙酰胆碱注入经乌拉坦麻醉的大鼠黑质。在同侧纹状体中，乙酰胆碱酯酶的释放以一种类似于这些药物在黑质纹状体细胞中诱导的放电频率变化的方式被改变。因此，将乙酰胆碱注入黑质会导致增加，而阿扑吗啡会导致纹状体中乙酰胆碱酯酶的释放减少。然而，在黑质中，乙酰胆碱酯酶的释放并不遵循这种模式：乙酰胆碱减少了局部释放，而阿扑吗啡则没有变化。在本研究的第二部分，我们研究了黑质纹状体细胞的放电频率与乙酰胆碱酯酶释放之间的关系。将两种已知可阻断神经元冲动传导的化合物注入黑质。这些药物是河豚毒素（一种钠通道阻滞剂）或γ-羟基丁酸（一种专门阻断多巴胺能细胞中冲动传导的药物）。两种化合物都减少了同侧纹状体中乙酰胆碱酯酶的释放。然而，在黑质局部，该酶的释放并没有减少。事实上，在给予γ-羟基丁酸后，黑质中乙酰胆碱酯酶的释放有大量依赖于钙离子的增加。这些结果表明，纹状体中乙酰胆碱酯酶的释放可能与黑质纹状体神经元的放电频率有关。另一方面，黑质中乙酰胆碱酯酶的释放可能来自树突，它独立于钠介导的动作电位。这种释放可能反而与特定的树突钙离子电导有关。
