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Opioid inhibition of synaptic transmission in the guinea‐pig myenteric plexus
Author(s) -
Cherubini E.,
Morita K.,
North R.A.
Publication year - 1985
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1985.tb11079.x
Subject(s) - acetylcholine , hyperpolarization (physics) , excitatory postsynaptic potential , chemistry , neurotransmission , myenteric plexus , enkephalin , membrane potential , biophysics , cholinergic , postsynaptic potential , neuroscience , reversal potential , opioid , endocrinology , inhibitory postsynaptic potential , pharmacology , medicine , electrophysiology , biology , patch clamp , biochemistry , receptor , stereochemistry , immunohistochemistry , nuclear magnetic resonance spectroscopy
1 Intracellular recordings were made from neurones in the myenteric plexus of the guinea‐pig ileum. Presynaptic nerves were excited by a focal stimulating electrode on an interganglionic strand. 2 Fast excitatory postsynaptic potentials (e.p.s.ps) were depressed in amplitude by morphine and [Met 5 ]enkephalin in the concentration range of l nM‐l μM. Nicotinic depolarizations evoked by exogenously applied acetylcholine (ACh) were not affected by these opioids. 3 Hyperpolarization of the presynaptic fibres probably contributed to the depression of the fast e.p.s.p. because fast e.p.s.ps evoked by low stimulus voltages were more depressed than those evoked by high stimulus voltages and fast e.p.s.ps resulting from activation of a single presynaptic fibre were blocked in a non‐graded manner. 4 Opioids depressed the slow e.p.s.p. in those neurones in which they did not change the resting membrane potential. 5 The slow e.p.s.p. was increased in amplitude in those neurones hyperpolarized by opioids. Depolarizations resulting from application of barium, substance P or ACh were also enhanced by opioids. Equivalent circuit models in which opioids increase, and substance P or ACh decrease, the same potassium conductance could account for this enhancement. 6 The actions of opioids were prevented or reversed by naloxone (l nM‐l μM). 7 It is concluded that morphine and enkephalin inhibit the release of ACh and a non‐cholinergic transmitter from fibres of the myenteric plexus, and that this may involve a hyperpolarization of presynaptic fibres. Additionally, opioids can interact postsynaptically with other substances which affect membrane potassium conductances.