Lukomskaia N Ia, Bol'shakov V Iu, Samoĭlova M V
Zh Evol Biokhim Fiziol. 1988 Sep-Oct;24(5):668-78.
Organophosphorus inhibitor of acetylcholinesterase (AChE) armin (1 x 10(-6) M) induced a variety of pre- and postsynaptic effects resulting from the AChE inhibition and subsequent accumulation of acetylcholine (ACh) in the synaptic cleft. The intensity of postsynaptic effects (level of neuron depolarization, degree of action potential depression) was shown to be different in the ganglia of frog and rabbit. This could be explained by differences in the total amount of ACh released in response to nerve stimulation as well as at rest. Both muscarinic and nicotinic cholinoreceptors were involved in the process of sustained depolarization of the neurons in the rabbit superior cervical ganglion after AChE inhibition. In frog ganglion neurons the nicotinic receptors did not participate in depolarization evidently due to their fast desensitization. The activation of presynaptic muscarinic receptors resulted in decrease of ACh released by nerve stimulation seems to weaken depolarization and blockade of synaptic transmission in sympathetic ganglia treated by AChE inhibitors.
乙酰胆碱酯酶（AChE）抑制剂阿米菌素（1×10⁻⁶ M）通过抑制AChE以及随后突触间隙中乙酰胆碱（ACh）的积累，诱导了多种突触前和突触后效应。结果表明，突触后效应的强度（神经元去极化水平、动作电位抑制程度）在青蛙和兔子的神经节中有所不同。这可以通过神经刺激以及静息时释放的ACh总量的差异来解释。在AChE抑制后，毒蕈碱型和烟碱型胆碱能受体均参与了兔颈上神经节神经元的持续去极化过程。在青蛙神经节神经元中，烟碱型受体显然没有参与去极化，这是由于它们快速脱敏。突触前毒蕈碱型受体的激活导致神经刺激释放的ACh减少，这似乎会削弱AChE抑制剂处理的交感神经节中的去极化和突触传递阻滞。
