Dixon D, Atwood H L
J Neurobiol. 1985 Nov;16(6):409-24. doi: 10.1002/neu.480160602.
Measurements of resting potential and action potential in presynaptic branches of the excitatory motor axon to the crayfish opener muscle were made with intracellular microelectrodes during application of serotonin (10(-9)-10(-3) M). A 5-min exposure to 10(-6) M serotonin produced enhancement of excitatory junction potentials (EJPs) lasting about 1 h. The membrane potential of the presynaptic terminal was depolarized by about 5 mV; the depolarization subsided within 1/2 h. Concomitant reduction in amplitude of the presynaptic action potential, not accompanied by spike broadening, was observed. The presynaptic depolarization, and the enhancement of EJPs, were dependent on the presence of extracellular sodium but not extracellular calcium. A possible mechanism for serotonin's effect involves initial entry of sodium into the nerve terminal, with consequent increased availability of intracellular calcium. The subsequent long-lasting phase of EJP enhancement may result from an additional effect on the metabolism of the nerve terminal.
在应用血清素(10⁻⁹ - 10⁻³ M)期间,用细胞内微电极测量了小龙虾开肌兴奋性运动轴突突触前分支的静息电位和动作电位。暴露于10⁻⁶ M血清素5分钟会使兴奋性突触后电位(EJP)增强,持续约1小时。突触前终末的膜电位去极化约5 mV;去极化在半小时内消退。观察到突触前动作电位幅度随之降低,但不伴有锋电位展宽。突触前去极化和EJP增强依赖于细胞外钠的存在,而非细胞外钙。血清素作用的一种可能机制涉及钠最初进入神经终末,从而使细胞内钙的可用性增加。EJP增强的后续持久阶段可能是对神经终末代谢的额外作用导致的。