Amann R, Hankins M W, Dray A
Sandoz Institute for Medical Research, London, U.K.
Neurosci Lett. 1988 Feb 15;85(1):125-30. doi: 10.1016/0304-3940(88)90441-7.
Neuropeptide K (NPK) induced a slow depolarization in principal ganglion cells of the guinea pig inferior mesenteric ganglion (IMG) in vitro. This effect was due to a postsynaptic action and prevented by pre-exposure of the IMG to neurokinin A (NKA) or substance P (SP). The non-cholinergic slow postsynaptic excitatory potential (s-EPSP) evoked by ureteric nerve stimulation was depressed during NPK, SP or NKA application. Calcitonin gene-related peptide (CGRP) applied in concentrations up to 10 microM had no effect on the membrane potential in 90% of IMG cells nor did it influence the s-EPSP. We suggest that NPK may depolarize IMG neurones via similar mechanisms/in a similar fashion, to other tachykinins and that the s-EPSP, induced by stimulation of the afferent ureteric nerve fibres, is mediated by a tachykinin whereas there is little indication/evidence for an involvement of CGRP.
神经肽K(NPK)在体外可使豚鼠肠系膜下神经节(IMG)的主要神经节细胞发生缓慢去极化。这种效应是由突触后作用引起的,并且可通过IMG预先暴露于神经激肽A(NKA)或P物质(SP)而被阻止。在应用NPK、SP或NKA期间,输尿管神经刺激诱发的非胆碱能缓慢突触后兴奋性电位(s-EPSP)受到抑制。浓度高达10微摩尔的降钙素基因相关肽(CGRP)对90%的IMG细胞的膜电位没有影响,也不影响s-EPSP。我们认为,NPK可能通过与其他速激肽相似的机制/以相似的方式使IMG神经元去极化,并且由输尿管传入神经纤维刺激诱发的s-EPSP是由速激肽介导的,而几乎没有迹象/证据表明CGRP参与其中。