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Specific enhancement of neuronal responses to catecholamine by p‐tyramine
Author(s) -
Jones Roland S. G.
Publication year - 1981
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.490060106
Subject(s) - iontophoresis , excitatory postsynaptic potential , caudate nucleus , acetylcholine , dopamine , glutamate receptor , chemistry , long term potentiation , neuroscience , neurotransmitter , neurotransmission , biogenic amine , pharmacology , biology , central nervous system , inhibitory postsynaptic potential , biochemistry , receptor
Extracellular recording and iontophoresis techniques were used to study the interactions of the trace amine, p‐tyramine (p‐TA) with putative neurotransmitters on single neurones in the cerebral cortex and caudate nucleus of the rat. p‐TA, when applied with weak iontophoretic currents which did not result in any change in neuronal firing rate, caused a pronounced potentiation of depressant responses to iontophoretically applied dopamine (DA). Depressant responses of cortical neurones to noradrenaline were also markedly potentiated by weak background applications of p‐TA. This potentiating action of p‐TA was related to the amount of the trace amine applied and was apparently specific for catecholamines, since depressant responses to 5‐hydroxytryptamine and γ‐aminobutyric acid were unaffected. Excitatory responses to iontophoretically applied glutamate were also unaltered by weak applications of p‐TA. Excitatory responses of most neurones to acetylcholine (ACh) were also unaffected by p‐TA in the cortex and caudate nucleus. However, responses to ACh of a small number of cells in both brain areas were reduced in size during weak applications of p‐TA. It is suggested that p‐TA may act as a modulator of neurotransmission, particularly that mediated by DA in the central nervous system.