Manning B P, Mawe G M
Department of Anatomy and Neurobiology, The University of Vermont College of Medicine, Burlington, Vermont 05405, USA.
Am J Physiol Gastrointest Liver Physiol. 2001 Aug;281(2):G357-64. doi: 10.1152/ajpgi.2001.281.2.G357.
Intracellular recording techniques were used to test whether tachykinins could be mediators of slow excitatory postsynaptic potentials (EPSPs) in guinea pig sphincter of Oddi (SO) ganglia. Application of the tachykinin substance P (SP) onto SO neurons caused a prolonged membrane depolarization that was reminiscent of the slow EPSP in these cells. Pressure ejection of the neurokinin 3 (NK3) receptor-specific agonist senktide caused a similar depolarization; however, no responses were detected on application of NK1 or NK2 receptor agonists. The NK3 receptor antagonist SR-142801 (100 nM) significantly inhibited both SP-induced depolarization and the stimulation-evoked slow EPSP, as did NK3 receptor desensitization with senktide. Capsaicin, which causes the release of SP from small-diameter afferent fibers, induced a depolarization that was similar to the evoked slow EPSP in both amplitude and duration. The capsaicin-induced depolarization was significantly attenuated in the presence of SR-142801. These data indicate that tachykinins, released from extrinsic afferent fibers, act via NK3 receptors to provide slow excitatory synaptic input to SO neurons.
采用细胞内记录技术来检测速激肽是否可能是豚鼠Oddi括约肌（SO）神经节中慢兴奋性突触后电位（EPSP）的介质。将速激肽P物质（SP）施加于SO神经元会引起膜电位的长时间去极化，这与这些细胞中的慢EPSP相似。神经激肽3（NK3）受体特异性激动剂senktide的压力喷射引起了类似的去极化；然而，施加NK1或NK2受体激动剂时未检测到反应。NK3受体拮抗剂SR - 142801（100 nM）显著抑制了SP诱导的去极化和刺激诱发的慢EPSP，用senktide使NK3受体脱敏也有同样的效果。辣椒素可使小直径传入纤维释放SP，它诱导的去极化在幅度和持续时间上均与诱发的慢EPSP相似。在存在SR - 142801的情况下，辣椒素诱导的去极化显著减弱。这些数据表明，从外在传入纤维释放的速激肽通过NK3受体起作用，为SO神经元提供慢兴奋性突触输入。
