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Vol. 281, Issue 2, 699-706, 1997
Department of Neuroscience, Finch University of Health Sciences/The
Chicago Medical School, North Chicago, Illinois
It is well established that behavioral sensitization to psychomotor
stimulants is associated with adaptations in the mesoaccumbens dopamine
(DA) system. We showed previously that the responsiveness of ventral
tegmental area (VTA) DA neurons to glutamate was significantly enhanced
in amphetamine- and cocaine-pretreated rats tested after 3 days of
withdrawal, which suggests that adaptations in excitatory amino acid
transmission also contribute to sensitization. The purpose of the
present study was to determine the subtype of excitatory amino acid
receptor responsible for this effect and to examine its persistence
during withdrawal. Extracellular single cell recording and
microiontophoresis were used to investigate possible alterations in the
ability of glutamate agonists
[(S)-
-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA), N-methyl-D-aspartate (NMDA), and
(1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (1S,3R-t-ACPD)] to stimulate the
firing of VTA DA neurons after 3 days of withdrawal from repeated
administration of saline, cocaine or amphetamine. Current-response
curves showed that responses to iontophoretic AMPA, but not NMDA or
1S,3R-t-ACPD were
significantly enhanced in cocaine- or amphetamine-pretreated rats in
that neurons entered into a state of apparent depolarization block at
significantly lower iontophoretic currents. When rats were tested for
responsiveness to iontophoretic glutamate after 14 days of withdrawal,
there was no significant difference between cocaine- or amphetamine- and saline-pretreated rats with respect to glutamate current-response curves. These results suggest that increased responsiveness of AMPA
receptors on VTA DA neurons may contribute to sensitization at early
withdrawal times, but that this alteration, like others described
within the VTA, is transient.
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