Abstract
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.
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