Neurotransmitter release mechanisms in sympathetic and parasympathetic nerve terminals

1993 ◽  
Vol 21 (2) ◽  
pp. 416-420
Author(s):  
Timothy J. Searl ◽  
Thomas C. Cunnane
Keyword(s):  
Neurotransmitter Release ◽  
Nerve Terminals ◽  
Parasympathetic Nerve ◽  
Release Mechanisms

Amitriptyline and imipramine inhibit the release of acetylcholine from parasympathetic nerve terminals in the rat iris

1984 ◽  
Vol 62 (7) ◽  
pp. 857-859 ◽  
Author(s):  
J. S. Richardson ◽  
T. G. Mattio ◽  
E. Giacobini
Keyword(s):  
Nerve Terminals ◽  
Dependent Manner ◽  
Parasympathetic Nerve ◽  
Drug Concentrations ◽  
Release Of Acetylcholine ◽  
Rat Iris ◽  
Anticholinergic Side Effects ◽  
Dose Dependent ◽  
Drug Free

The electrically stimulated release of [3H]acetylcholine from the parasympathetic nerve terminals of the rat iris in vitro is increased in a dose-dependent manner by scopolamine but is decreased by the tricyclic antidepressants amitriptyline and imipramine. The increased release in the presence of scopolamine seems to be due to the blockade of a presynaptic muscarinic autoreceptor that, in the drug-free state, inhibits the release of acetylcholine. However, at drug concentrations that should have comparable antimuscarinic potency, the antidepressants inhibit the release of acetylcholine. This suggests that the anticholinergic side effects of the antidepressants may be due to the reduced release of acetylcholine from parasympathetic nerve terminals as well as a possible direct postsynaptic muscarinic receptor blocking action. Whatever the mechanism of this action, the antidepressants do not have the same effect as scopolamine at the presynaptic muscarinic autoreceptor in the rat iris.

scholarly journals Signalling by CGRP and Adrenomedullin in the Cerebellum and Other Systems

2001 ◽  
Vol 1 ◽  
pp. 11-11
Author(s):  
David Poyner ◽  
Heather Cater ◽  
Nick Hartell ◽  
Alex Conner ◽  
Debbie Hay ◽  
...  
Keyword(s):  
Tyrosine Kinases ◽  
Transmitter Release ◽  
Neurotransmitter Release ◽  
Cultured Cells ◽  
Signalling Pathways ◽  
Nerve Terminals ◽  
Parallel Fibre ◽  
Isolated Tissues ◽  
Stimulation Of

The best characterised signalling pathway activated by both CGRP and adrenomedullin is stimulation of adenylate cyclase via Gs. However, it is clear that in some circumstances the peptides can activate other signal transduction pathways, e.g., increases in intracellular calcium. Many of these signalling pathways can be observed in cultured cells but it is important also to examine isolated tissues to discover the full repertoire of transduction events. In the rat cerebellum there are receptors that respond to both CGRP and adrenomedullin. These seem to be located postsynaptically on Parallel Fibre nerve terminals and modulate transmission to Purkinje cells. Adrenomedullin acts via cAMP, apparently to augment neurotransmitter release. By contrast, CGRP decreases transmitter release, via a non-cAMP mediated pathway. We are currently examining the role of NO and tyrosine kinases in the responses to these peptides.

Analysis of neurotransmitter release mechanisms by photolysis of caged Ca2+ in an autaptic neuron culture system

2012 ◽  
Vol 7 (7) ◽  
pp. 1351-1365 ◽  
Author(s):  
Andrea Burgalossi ◽  
SangYong Jung ◽  
Kwun-nok Mimi Man ◽  
Ramya Nair ◽  
Wolf J Jockusch ◽  
...  
Keyword(s):  
Neurotransmitter Release ◽  
Culture System ◽  
Neuron Culture ◽  
Release Mechanisms

Simulation of In Vitro-Like Electrical Activities in Urinary Bladder Smooth Muscle Cells

2017 ◽  
Vol 33 ◽  
pp. 45-51
Author(s):  
Chitaranjan Mahapatra ◽  
Rohit Manchanda
Keyword(s):  
Smooth Muscle ◽  
Urinary Bladder ◽  
Neurotransmitter Release ◽  
Compartment Model ◽  
Bladder Smooth Muscle ◽  
Parasympathetic Nerve ◽  
Stochastic Nature ◽  
Urinary Bladder Smooth Muscle ◽  
Electrical Activities

Urinary bladder smooth muscle (UBSM) generates spontaneous electrical activities due to stochastic nature of purinergic neurotransmitter release from the parasympathetic nerve. The stochastic nature of the purinergic neurotransmitter release was represented by a simplified ‘point-conductance’ model to mimic in vitro-like electrical activities in UBSM cell. The point-conductance was represented by the independent synaptic conductance described by the stochastic random-walk processes and injected into a single-compartment model of mouse UBSM cell. This model successfully evoked irregular spontaneous depolarizations (SDs) and spontaneous action potential (sAP) as the properties of in vitro-like electrical activities in UBSM cells. The model mimics the T- and L-type Ca2+ ion channel blocker by setting their respective conductance to zero. We also found that the point-conductance model modulates the sAP properties by adding background activity.

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