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Involvement of adenosine and glutamate receptors in the induction of c‐fos in the striatum by haloperidol
Author(s) -
Boegman R.J.,
Vincent S.R.
Publication year - 1996
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/(sici)1098-2396(199601)22:1<70::aid-syn8>3.0.co;2-f
Subject(s) - haloperidol , chemistry , striatum , nmda receptor , adenosine a2a receptor , dopamine receptor d2 , glutamate receptor , globus pallidus , dopamine , pharmacology , medicine , adenosine receptor , endocrinology , neuroscience , receptor , basal ganglia , biology , central nervous system , biochemistry , agonist
The psychostimulant drugs amphetamine and cocaine induce the expression of immediate early genes, such as c‐fos , in the striatum via D 1 dopamine receptor activation. This occurs primarily in the striato‐nigral neurons. Conversely, neuroleptic drugs, such as haloperidol, which block D 2 ‐type dopamine receptors, induce c‐fos expression in striatal neurons projecting to the globus pallidus. In order to gain insight into the neurochemical substrates of neuroleptic‐induced c‐fos expression, we examined the effects of adenosine A 2 and N‐methyl‐D‐aspartate (NMDA) receptor antagonists as well as inhibition of nitric oxide synthase, on haloperidol‐induced Fos immunoreactivity in the striatum. While blockade of D 1 receptors had no effect on haloperidol‐induced Fos expression, adenosine A 2 receptor antagonists decreased the number of neurons in the striatum expressing haloperidol‐induced Fos by half. NMDA receptor antagonists also potently blocked the induction of Fos immunoreactivity by haloperidol, while inhibition of nitric oxide synthase activity had no effect. These results indicate that in the presence of a dopamine D 2 antagonist, Fos expression in striato‐pallidal neurons is mediated in part through activation of A 2 receptors by adenosine, and via NMDA receptor activation by glutamate. © 1996 Wiley‐Liss, Inc.