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Neurotensin modulates differently potassium, veratridine and 4‐aminopyridine‐evoked release of dopamine in rat striatal slices
Author(s) -
Boireau A.,
Miquet JM,
Olivier V.
Publication year - 1993
Publication title -
fundamental and clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.655
H-Index - 73
eISSN - 1472-8206
pISSN - 0767-3981
DOI - 10.1111/j.1472-8206.1993.tb00224.x
Subject(s) - veratridine , neurotensin , dopamine , chemistry , 4 aminopyridine , neurotransmitter , depolarization , potassium , endocrinology , medicine , ouabain , biophysics , pharmacology , neuropeptide , potassium channel , sodium , receptor , biology , biochemistry , sodium channel , organic chemistry
Summary— We have studied the effects of neurotensin (NT) on the release of [ 3 H]dopamine ([ 3 H]DA) evoked by terminal depolarization with either K+, veratridine or 4‐aminopyridine (4‐AP). NT (1–1000 nM) induced a net potentiation (up to 170%) of the K+ (25 mM) ‐evoked release of [ 3 H]DA. The capacity of NT to potentiate the effect of K+ ions decreased as the K+ concentration rose from 25 to 50 mM and totally disappeared at this high K+ concentration. NT (100 nM; 1000 nM) had no significant effect on the veratridine (1.5; 5μM) or 4‐AP (20 μM) ‐evoked release of [ 3 H]DA. The relevance of these experimental models of DA release to physiological transmitter release remains to be established. Those data highlight the complexity of the modulation of evoked neurotransmitter release by pharmacological agents.