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Effects of Amphetamine on Carrier‐Mediated and Electrically Stimulated Dopamine Release in Slices of Rat Caudate Putamen and Nucleus Accumbens
Author(s) -
Iravani M. M.,
Kruk Z. L.
Publication year - 1995
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 - 10.1046/j.1471-4159.1995.64031161.x
Subject(s) - nucleus accumbens , amphetamine , caudate nucleus , dopamine , putamen , chemistry , neuroscience , medicine , endocrinology , biology
The effects of (+)‐amphetamine on carrier‐mediated and electrically stimulated dopamine release were investigated using fast cyclic voltammetry in rat brain slices incorporating the nucleus accumbens, and in the caudate putamen. In the caudate putamen, dopamine release either increased with increasing frequency of local electrical stimulation (hot spots) or did not increase significantly (cold spots); dopamine release increased with increasing frequency of electrical stimulation in the nucleus accumbens. Local pressure application of (+)‐amphetamine from a micropipette caused dopamine efflux at all sites examined, and this was not affected by sulpiride, indicating that efflux of dopamine caused by (+)‐amphetamine is not regulated by dopamine D 2 autoreceptors. (+)‐Amphetamine reduced single‐pulse electrically stimulated dopamine release at all sites; sulpiride reversed this decrease, indicating that endogenous dopamine released by (+)‐amphetamine activates dopamine D 2 autoreceptors. In nucleus accumbens and hot spots, (+)‐amphetamine did not affect 20‐pulse 50‐Hz‐stimulated dopamine release, whereas in cold spots it potentiated 20‐pulse 50‐Hz‐stimulated dopamine release. We conclude that (+)‐amphetamine modifies electrically stimulated dopamine release by uptake inhibition or by indirect activation of D 2 autoreceptors; the precise mechanism is determined by site and duration of electrical stimulation.