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Vol. 281, Issue 2, 972-982, 1997
Department of Anatomy and Cell Biology, East Carolina University
School of Medicine, Greenville, North Carolina
Neuropeptide and immediate early gene expression in striatonigral
neurons of the normosensitive striatum is induced by mixed D1/D2 receptor agonists and indirect dopamine
agonists, such as cocaine and amphetamine. Both D1 and
D2 receptor antagonists block these events. In contrast,
the partial D1 agonist, SKF-38393, does not evoke
striatonigral gene expression in intact rats. These findings have
contributed to the idea that both D1 and D2
receptors must be stimulated to evoke gene expression in striatonigral
neurons. How these "D1/D2 interactions" are
accomplished is unclear in light of the controversy over whether
striatonigral neurons express both D1 and D2
receptors. This study addresses these issues by demonstrating that in
intact rats 1) a full D1 receptor agonist, SKF-82958,
induced behavioral activity and preprodynorphin (PPD) and substance P
(SP) gene expression in medium spiny neurons in the dorsal, and
especially, in the ventral striatum, 2) either a D1
antagonist, SCH-23390, or a D2 antagonist, eticlopride,
blocked these effects, 3) the muscarinic antagonist, scopolamine,
augmented PPD and SP mRNA expression induced by SKF-82958 and prevented the ability of eticlopride to block SKF-82958-induced PPD and SP mRNAs
and 4) the SKF-82958-induced increase in preproenkephalin mRNA in
striatopallidal neurons was blocked by SCH-23390 or scopolamine but not
by eticlopride. These data indicate that endogenous acetylcholine attenuates D1 receptor-stimulated PPD/SP gene expression in
medium spiny neurons, mediates D1 receptor-stimulated
preproenkephalin gene expression in striatopallidal neurons and
contributes to D2 receptor involvement in
D1-stimulated PPD/SP gene expression.
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