Tsunoo A, Konishi S, Otsuka M
Neuroscience. 1982;7(9):2025-37. doi: 10.1016/0306-4522(82)90117-8.
Electrophysiological and neurochemical experiments were carried out to examine a possible transmitter role substance P in the prevertebral ganglia of the guinea-pig. When potentials were recorded intracellularly from neurons of the isolated ganglia, stimulation of the pre- or postganglionic nerves elicited a non-cholinergic slow excitatory postsynaptic potential (EPSP). This synaptic potential was compared with the effects of substance P. Brief application of substance P caused a depolarization of the ganglion cells with a similar time course to that of the non-cholinergic slow EPSP. Changes in membrane resistance during the substance P-induced depolarization resembled those associated with the non-cholinergic slow EPSP. During the substance P-induced depolarization the non-cholinergic slow EPSP was markedly depressed. Attempts were made to determine the origin of the fibers eliciting the non-cholinergic slow EPSP. In the inferior mesenteric ganglia isolated together with preganglionic nerves that retained intact connections with spinal nerve roots, dorsal root stimulation evoked a non-cholinergic slow EPSP but not a cholinergic fast EPSP in the ganglion cells, whereas ventral root stimulation caused only cholinergic fast EPSPs. Following the prolonged treatment with capsaicin, the non-cholinergic slow EPSP was greatly depressed or abolished. Radioimmunoassay revealed that after ligation or section of pre- or postganglionic nerves an accumulation of substance P occurred in the proximal stumps of the interrupted nerves. Stimulation with high potassium medium evoked a release of immunoreactive substance P from the prevertebral ganglia and the release was calcium-dependent. The present findings suggests that axon collaterals of certain visceral primary efferents form synapses with principal cells in the prevertebral ganglia and release substance P as a transmitter for the non-cholinergic slow EPSP.
进行了电生理和神经化学实验，以研究P物质在豚鼠椎前神经节中可能作为递质的作用。当从分离的神经节神经元进行细胞内电位记录时，刺激节前或节后神经会引发非胆碱能慢兴奋性突触后电位（EPSP）。将这种突触电位与P物质的作用进行了比较。短暂施加P物质会使神经节细胞去极化，其时间进程与非胆碱能慢EPSP相似。P物质诱导去极化期间膜电阻的变化类似于与非胆碱能慢EPSP相关的变化。在P物质诱导的去极化期间，非胆碱能慢EPSP明显受到抑制。试图确定引发非胆碱能慢EPSP的纤维的起源。在与保留与脊神经根完整连接的节前神经一起分离的肠系膜下神经节中，刺激背根会在神经节细胞中引发非胆碱能慢EPSP，但不会引发胆碱能快EPSP，而刺激腹根只会引起胆碱能快EPSP。用辣椒素长期处理后，非胆碱能慢EPSP大大降低或消失。放射免疫测定显示，在结扎或切断节前或节后神经后，P物质在中断神经的近端残端中积累。用高钾培养基刺激会引起椎前神经节释放免疫反应性P物质，且这种释放是钙依赖性的。目前的研究结果表明，某些内脏初级传出纤维的轴突侧支与椎前神经节中的主细胞形成突触，并释放P物质作为非胆碱能慢EPSP的递质。
