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The K ‐Opioid Agonist, U‐69593, Decreases Acute Amphetamine‐Evoked Behaviors and Calcium‐Dependent Dialysate Levels of Dopamine and Glutamate in the Ventral Striatum
Author(s) -
Gray Alex M.,
Rawls Scott M.,
Shippenberg Toni S.,
McGinty Jacqueline F.
Publication year - 1999
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.1471-4159.1999.0731066.x
Subject(s) - dopamine , striatum , amphetamine , medicine , endocrinology , glutamate receptor , chemistry , agonist , biology , receptor
: The effect of a k ‐opioid receptor agonist on acute amphetamine‐induced behavioral activation and dialysate levels of dopamine and glutamate in the ventral striatum were investigated. Amphetamine (2.5 mg/kg i.p.) evoked a substantial increase in rearing, sniffing, and hole‐poking behavior as well as dopamine and glutamate levels in the ventral striatum of awake rats. U‐69593 (0.32 mg/kg s.c.) significantly decreased the amphetamine‐evoked increase in behavior and dopamine and glutamate levels in the ventral striatum. Reverse dialysis of the selective k ‐opioid receptor antagonist, nor ‐binaltorphimine, into the ventral striatum antagonized the effects of U‐69593 on amphetamine‐induced behavior and dopamine and glutamate levels. Reverse dialysis of low calcium (0.1 m M ) into the ventral striatum decreased basal dopamine, but not glutamate, dialysate levels by 91% 45 min after initiation of perfusion. Strikingly, 0.1 m M calcium perfusion significantly reduced the 2.5 mg/kg amphetamine‐evoked increase in dopamine and glutamate levels in the ventral striatum, distinguishing a calcium‐dependent and a calcium‐independent component of release. U‐69593 did not alter the calcium‐independent component of amphetamine‐evoked dopamine and glutamate levels. These data are consistent with the view that a transsynaptic mechanism augments the increase in dopamine and glutamate levels in the ventral striatum evoked by a moderately high dose of amphetamine and that stimulation of k ‐opioid receptors suppresses the calcium‐dependent component of amphetamine’s effects.