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Differential Sensitivity to Blockade by 4‐Aminopyridine of Presynaptic Receptors Regulating [ 3 H]Acetylcholine Release from Rat Hippocampus
Author(s) -
Fredholm Bertil B.
Publication year - 1990
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1990.tb01973.x
Subject(s) - chemistry , carbachol , acetylcholine , 4 aminopyridine , agonist , muscarinic acetylcholine receptor , adenosine , cholinergic , endocrinology , medicine , neurotransmitter , adenosine receptor , receptor , potassium channel , biochemistry , biology
The inhibitory effect of an adenosine analogue, R ‐ N 6 ‐phenylisopropyl adenosine ( R ‐PIA), of the cholinergic agonist carbachol, and of morphine on 3 H efflux from [ 3 H]choline‐labeled field‐stimulated rat hippocampal slices was compared with that produced by two inhibitors of N‐and L‐type Ca 2+ channels, ω‐conotoxin (CgTx; conotoxin GVIA) and cadmium chloride. 4‐Aminopyridine (4‐AP) caused a dose‐dependent increase in evoked transmitter release, with a maximal effect (an almost threefold increase) at 100 μ M . 4‐AP (100 μ M ) did not affect the actions of CgTx, cadmium chloride, and R ‐PIA but almost abolished the effect of carbachol and morphine. The present results indicate that presynaptic muscarinic and opiate receptors reduce acetylcholine release by a mechanism that is somewhat different from that used by adenosine A 1 receptors. Furthermore, the results indicate that presynaptic A 1 receptors on hippocampal cholinergic neurons do not primarily regulate 4‐AP‐dependent potassium channels, but that they might act directly on a Ca 2+ conductance.