The role of cholecystokinin in ganglionic transmission in the guinea‐pig gall‐bladder.
- 1 July 1991
- journal article
- Published by Wiley in The Journal of Physiology
- Vol. 439 (1) , 89-102
- https://doi.org/10.1113/jphysiol.1991.sp018658
Abstract
1. The effects of cholecystokinin (CCK) on intact guinea-pig gall-bladder ganglia were investigated with intracellular, single-electrode current- and voltage-clamp recording techniques. 2. Cholecystokinin octapeptide (CCK-8; 0.01-100 nM) increased the amplitude of the fast excitatory postsynaptic potential (EPSP) that was evoked by stimulation of interganglionic fibre tracts. In most cases, neurones that exhibited subthreshold EPSPs in normal Krebs solution fired action potentials in the presence of CCK-8. In a low Ca2+/high Mg2+ solution, CCK-8 caused a 3-fold increase in the amplitude of fast EPSPs. 3. The amplitude of the evoked excitatory postsynaptic current (EPSC) was increased by CCK-8 (0.01-100 nM) in a concentration-dependent manner. The effect was maximal at 1.0 nM. 4. Cholecystokinin octapeptide caused a 3-fold increase in the quantal content of the EPSP in a low Ca2+/high Mg2+ solution, but had no effect on the quantal size. 5. The specific CCK-A receptor antagonist, MK-329 (formerly L-364,718; 1.0 nM), reversibly blocked the facilitatory effect of CCK-8 on ganglionic transmission. However, the specific CCK-B receptor antagonist, L-365,260 (10 nM), did not alter the presynaptic facilitatory effect of CCK-8. 6. The response of gall-bladder neurones to exogenously applied ACh was not modified by CCK-8. 7. Application of CCK-8, by superfusion (0.001-100 nM) or by pressure microejection (100 microM), had no effect on the membrane potential, membrane conductance, action potential, or threshold of gall-bladder neurones. 8. Immunohistochemistry was employed to determine whether the actions of CCK could be elicited by release of the peptide from nerve terminals within the ganglionated plexus of the gall-bladder. Immunoreactivity for CCK was not detected in the ganglionated plexus of the gall-bladder, but CCK immunoreactivity was plentiful in control preparations of intestinal myenteric and submucosal plexuses. 9. These results show that CCK has a presynaptic facilitatory effect on fast synaptic transmission in guinea-pig gall-bladder ganglia, and that this effect is mediated by presynaptic CCK-A receptors. Furthermore, it appears that such an effect would normally occur in response to hormonal CCK, rather than CCK that is released from nerve terminals.Keywords
This publication has 25 references indexed in Scilit:
- Characterization of neuronal cholecystokinin receptor by L-364,718 in Auerbach's plexusEuropean Journal of Pharmacology, 1990
- A new potent and selective non-peptide gastrin antagonist and brain cholecystokinin receptor (CCK-B) ligand: L-365,260European Journal of Pharmacology, 1989
- Cholecystokinin octapeptide depolarizes guinea pig inferior mesenteric ganglion cells and facilitates nicotinic transmissionNeuroscience Letters, 1986
- Effects of cholecystokinin, caerulein and pentagastrin on electrical behavior of myenteric neuronsEuropean Journal of Pharmacology, 1985
- Distribution of certain peptide‐containing nerve fibres and endocrine cells in the gastrointestinal mucosa in five mammalian speciesJournal of Comparative Neurology, 1985
- The Effect of Vagotomy on Gallbladder Function and Bile Composition in ManAnnals of Surgery, 1982
- Effect of cholecystokinin and the octapeptide of cholecystokinin on the feline sphincter of Oddi and gallbladder. Mechanisms of action.Journal of Clinical Investigation, 1980
- Effect of the C-Terminal Octapeptide of Cholecystokinin on Guinea Pig Ileum and Gall-Bladder in vitroActa Physiologica Scandinavica, 1970
- Gall-bladder function after vagotomyBritish Journal of Surgery, 1969
- A SENSITIVE IN-VITRO METHOD FOR THE ASSAY OF CHOLECYSTOKININJournal of Endocrinology, 1969