Brunelli M, Castellucci V, Kandel E R
Science. 1976 Dec 10;194(4270):1178-81. doi: 10.1126/science.186870.
The neural changes accompanying sensitization of the gill-withdrawal reflex in Aplysia are associated with presynaptic facilitation at monosynaptic connections between sensory neurons and motor cells. To analyze the molecular mechanisms underlying the facilitation, the pharmacological actions of serotonin, octopamine, and dopamine were examined. Only serotonin enhanced synaptic transmission between the sensory and the motor neurons. A serotonin antagonist, cinanserin, reversibly blocked the synaptic facilitation. The action of serotonin may be mediated by adenosime 3',5'-monophosphate (cyclic AMP). Exposing the ganglion to dibutyryl cyclic AMP or injecting cyclic AMP into the cell body enhances the synaptic action of a sensory neuron. The mechanism of presynaptic facilitation, therefore, may include activation of one or more serotonergic neurons, which enhance the release of a neurotransmitter by increasing the intracellular concentration of cyclic AMP in the terminals of the sensory neurons.
海兔鳃收缩反射敏感化过程中伴随的神经变化与感觉神经元和运动细胞之间单突触连接的突触前易化有关。为了分析易化作用背后的分子机制，研究了5-羟色胺、章鱼胺和多巴胺的药理作用。只有5-羟色胺能增强感觉神经元和运动神经元之间的突触传递。5-羟色胺拮抗剂辛那色林能可逆地阻断突触易化。5-羟色胺的作用可能由3',5'-环磷酸腺苷（环化腺苷酸）介导。将神经节暴露于二丁酰环化腺苷酸或将环化腺苷酸注入细胞体可增强感觉神经元的突触作用。因此，突触前易化的机制可能包括激活一个或多个5-羟色胺能神经元，这些神经元通过增加感觉神经元末梢细胞内环化腺苷酸的浓度来增强神经递质的释放。
