Mangan P S, Cometa A K, Friesen W O
Department of Biology, University of Virginia, Charlottesville 22901.
J Comp Physiol A. 1994 Dec;175(6):723-36. doi: 10.1007/BF00191844.
Serotonin enhances the expression of swimming in the medicinal leech Hirudo medicinalis. These two reports examine the physiological causes underlying this modulation. The initial paper (Mangan et al. 1994) demonstrated that serotonin enhanced the participation of inhibitory swim motor neurons (MNs) in the generation of the swimming rhythm in the isolated nerve cord. In experiments reported here, we examined whether synaptic interactions between neurons of the swim circuit are altered by serotonin. Following exposure to 50 microM serotonin, pairwise intracellular recording revealed the presence of a time-dependent synaptic decrement. Synaptic decrement was characterized by: 1) a substantial decline in synaptic inhibition (half-decay time about 0.4 s) during constant presynaptic excitation; 2) a reduced half-time of recovery from synaptic inhibition; and 3) a strong dependence on the presynaptic neuron's membrane potential. We found little alteration in the physiology of synaptic transmission involving MNs following amine depletion in leech nerve cords. We propose that alterations in synaptic interactions resulting from exposure to elevated serotonin levels, coupled with the changes in MN cellular properties described earlier, are crucial to the increased efficacy of MNs in participating in generating and expressing the leech swimming rhythm.
血清素增强药用蚂蟥(Hirudo medicinalis)的游泳行为表达。这两篇报告研究了这种调节作用背后的生理原因。第一篇论文(Mangan等人,1994年)表明,血清素增强了抑制性游泳运动神经元(MNs)在离体神经索游泳节律产生过程中的参与度。在本文报道的实验中,我们研究了血清素是否会改变游泳回路神经元之间的突触相互作用。暴露于50微摩尔血清素后,细胞内成对记录显示存在时间依赖性的突触递减。突触递减的特征为:1)在恒定的突触前兴奋期间,突触抑制显著下降(半衰期约为0.4秒);2)突触抑制恢复的半衰期缩短;3)强烈依赖于突触前神经元的膜电位。我们发现,蚂蟥神经索中胺耗竭后,涉及MNs的突触传递生理变化不大。我们提出,暴露于升高的血清素水平导致的突触相互作用改变,再加上之前描述的MN细胞特性变化,对于MNs参与产生和表达蚂蟥游泳节律的效能增加至关重要。