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Volume 16, Number 13,
Issue of July 1, 1996
pp. 4231-4239
Copyright ©1996 Society for Neuroscience
Amphetamine and Dopamine-Induced Immediate Early Gene Expression
in Striatal Neurons Depends on Postsynaptic NMDA Receptors and
Calcium
Received Jan. 22, 1996; revised April 9, 1996; accepted April 11, 1996.
Christine Konradi,
Jean-Christophe Leveque, and
Steven E. Hyman
Molecular and Developmental Neuroscience Laboratory and Department
of Psychiatry, Massachusetts General Hospital and Harvard Medical
School, Boston, Massachusetts 02114
Amphetamine and cocaine induce the expression of both immediate
early genes (IEGs) and neuropeptide genes in rat striatum. Despite the
demonstrated dependence of these effects on D1
dopamine receptors, which activate the cyclic AMP pathway, there are
several reports that amphetamine and cocaine-induced IEG expression can
be inhibited in striatum in vivo by NMDA receptor
antagonists. We find that in vivo, the NMDA receptor
antagonist MK-801 inhibits amphetamine induction of c-fos
acutely and also prevents downregulation of IEG expression with chronic
amphetamine administration. Such observations raise the question of
whether dopamine/glutamate interactions occur at the level of
corticostriatal and mesostriatal circuitry or within striatal neurons.
Therefore, we studied dissociated striatal cultures in which midbrain
and cortical presynaptic inputs are removed. In these cultures, we find
that dopamine- or forskolin-mediated IEG induction requires
Ca2+ entry via NMDA receptors but not via L-type
Ca2+ channels. Moreover, blockade of NMDA
receptors diminishes the ability of dopamine to induce phosphorylation
of the cyclic AMP responsive element binding protein CREB. Although
these results do not rule out a role for circuit-level
dopamine/glutamate interactions, they demonstrate a requirement at the
cellular level for interactions between the cyclic AMP and NMDA
receptor pathways in dopamine-regulated gene expression in striatal
neurons.
Key words:
dopamine;
amphetamine;
NMDA;
striatum;
immediate
early genes;
Fos;
CREB
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