Zafirov D H, Palmer J M, Nemeth P R, Wood J D
Brain Res. 1985 Nov 18;347(2):368-71. doi: 10.1016/0006-8993(85)90201-x.
Iontophoretic injection of cyclic adenosine monophosphate (cAMP) into the somas of ganglion cells in the myenteric plexus of guinea pig small intestine mimicked the slow excitatory postsynaptic potentials that occur in these neurons. These effects were: (1) membrane depolarization. (2) decreased membrane conductance, (3) augmented excitability with increased probability of spontaneous spike discharge and increased spike discharge during depolarizing current pulses, (4) anodal break excitation, (5) suppression of hyperpolarizing afterpotentials. The same effects were produced by application of membrane-permeable analogs of cAMP in the bathing medium. The phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine, potentiated the effects of the analogs. The results suggest that the biochemical basis for long-lasting excitatory neuromodulation in myenteric neurons is activation of adenylate cyclase and elevation of intraneuronal cAMP.
将环磷酸腺苷（cAMP）离子电渗注入豚鼠小肠肌间神经丛神经节细胞的胞体，可模拟这些神经元中出现的缓慢兴奋性突触后电位。这些效应包括：（1）膜去极化；（2）膜电导降低；（3）兴奋性增强，自发动作电位发放概率增加，去极化电流脉冲期间动作电位发放增加；（4）阳极断电兴奋；（5）超极化后电位受到抑制。在浴液中应用cAMP的膜通透性类似物也产生了相同的效应。磷酸二酯酶抑制剂3-异丁基-1-甲基黄嘌呤增强了这些类似物的效应。结果表明，肌间神经元中持久兴奋性神经调制的生化基础是腺苷酸环化酶的激活和神经元内cAMP的升高。
