Actions of neuropeptide K and calcitonin gene-related peptide on inferior mesenteric ganglion cells — Tachykinin interactions with non-cholinergic potentials evoked by ureteric nerve stimulation

doi:10.1016/0304-3940(88)90441-7

Neuroscience Letters

Volume 85, Issue 1, 15 February 1988, Pages 125-130

https://doi.org/10.1016/0304-3940(88)90441-7 Get rights and content

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 μM 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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Cited by (4)

Patterns of innervation of sympathetic vascular neurons by peptide- containing primary sensory fibers
1999, Brain Research
The purpose of this study was to determine whether there is a specific organization of the primary sensory innervation on to identified vascular neurons in the inferior mesenteric ganglion (IMG) in guinea-pig. Retrograde tracers were placed intraluminally in inferior mesenteric artery (IMA) or inferior mesenteric vein (IMV) in vitro to identify ganglionic neurons as arterial, venous or unlabeled neurons. The distribution of primary sensory nerve fibers containing calcitonin gene-related peptide (CGRP), neuronal nitric oxide synthase (NOS) and substance P immunoreactivity (SP-IR) was compared before and after treatment with capsaicin. In control animals the density of immunoreactivity varied both with the transmitter and the type of neuron innervated. The density of immunoreactivity for all the three substances was reduced by capsaicin treatment. The degree of reduction of immunoreactivity in the fibers varied with the transmitter and the type of neuron. The density of CGRP and SP immunoreactive fibers was greatest around unlabeled neurons; 78% of the CGRP fibers were of primary sensory origin and all of the SP fibers were primary sensory. Around arterial neurons 44% of the CGRP fibers were of primary sensory origin and around venous 68% were primary sensory. NOS positive innervation around venous neurons was denser than around arterial neurons and all of it was completely (97%) eliminated by capsaicin, indicating that it was solely of primary sensory origin. We conclude that the primary sensory fibers innervating the IMG are differentially distributed to arterial and venous neurons and that the pattern of distribution is characteristic for each sensory neurotransmitter.
Characterization of the peripheral action of neuropeptide K on the rat cardiovascular system
1992, European Journal of Pharmacology
The effects of neuropeptide K (NPK) were measured on mean arterial pressure (MAP) and heart rate (HR) after i.v. injection in urethane-anesthetized rats. NPK (6.5 and 32.5 nmol/kg) produced sustained decreases in MAP and elicited increases in HR. Whereas the NPK-induced tachycardia lasted more than 30 min at 32.5 nmol/kg, a latent and long-lasting bradycaria appeared from 20 min after injection of 6.5 nmol/kg. The initial tachycardia was converted to bradycardia by metoprolol but remained unaffected by hexamethonium, atropine and naloxone. These four treatments, however, prevented the bradycardiac response to NPK at 30 min. Whereas phentolamine, idazoxan, bilateral adrenalectomy and chemical sympathectomy with 6-hydroxydopamine (6-OHDA) preserved the initial tachycardia induced by NPK, they converted the decrease in HR to a tachycardiac response at 30 min. The vasodepressor response to NPK was significantly enhanced by bilateral adrenalectomy, chemical sympathectomy and metoprolol but remained unaffected by all other treatments. Neither the MAP nor the HR responses to NPK were affected by indomethacin. These results suggest that NPK can accelerate HR through non-reflex activation of the sympathoadrenal system. The secondary bradycardia induced by NPK may be due to a vagal reflex while the vasodepressor response to NPK is probably attributable to a direct action mediated by specific receptors on arterial blood vessels. Thus, NPK is considered as the most potent biologically active tachykinin so far described on the rat cardiovascular system.
Myogenic and neurogenic factors in the control of pyeloureteral motility and ureteral peristalsis
1998, Pharmacological Reviews
Neurones in the chicken ureter are innervated by substance P- and calcitonin gene-related peptide-containing nerve fibres: Immunohistochemical and electrophysiological evidence
1997, Journal of Comparative Neurology

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Actions of neuropeptide K and calcitonin gene-related peptide on inferior mesenteric ganglion cells — Tachykinin interactions with non-cholinergic potentials evoked by ureteric nerve stimulation

Abstract

Peptides

Neurosci. Lett.

Regul. Pept.

Brain Res.

Eur. J. Pharmacol.

Neuroscience

Neuroscience