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Amphetamine‐evoked c‐ fos mRNA expression in the caudate‐putamen: the effects of DA and NMDA receptor antagonists vary as a function of neuronal phenotype and environmental context
Author(s) -
Ferguson Susan M.,
Norton Camille S.,
Watson Stanley J.,
Akil Huda,
Robinson Terry E.
Publication year - 2003
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.1471-4159.2003.01815.x
Subject(s) - amphetamine , nmda receptor , c fos , medicine , dopamine , endocrinology , dynorphin , population , striatum , context (archaeology) , glutamate receptor , biology , immediate early gene , chemistry , gene expression , receptor , neuroscience , opioid , opioid peptide , biochemistry , gene , paleontology , environmental health
Dopamine (DA) and glutamate neurotransmission is thought to be critical for psychostimulant drugs to induce immediate early genes (IEGs) in the caudate‐putamen (CPu). We report here, however, that the ability of DA and glutamate NMDA receptor antagonists to attenuate amphetamine‐evoked c‐ fos mRNA expression in the CPu depends on environmental context. When given in the home cage, amphetamine induced c‐ fos mRNA expression predominately in preprodynorphin and preprotachykinin mRNA‐containing neurons (Dyn‐SP+ cells) in the CPu. In this condition, all of the D1R, D2R and NMDAR antagonists tested dose‐dependently decreased c‐ fos expression in Dyn‐SP+ cells. When given in a novel environment, amphetamine induced c‐ fos mRNA in both Dyn‐SP+ and preproenkephalin mRNA‐containing neurons (Enk+ cells). In this condition, D1R and non‐selective NMDAR antagonists dose‐dependently decreased c‐ fos expression in Dyn‐SP+ cells, but neither D2R nor NR2B‐selective NMDAR antagonists had no effect. Furthermore, amphetamine‐evoked c‐ fos expression in Enk+ cells was most sensitive to DAR and NMDAR antagonism; the lowest dose of every antagonist tested significantly decreased c‐ fos expression only in these cells. Finally, novelty‐stress also induced c‐ fos expression in both Dyn‐SP+ and Enk+ cells, and this was relatively resistant to all but D1R antagonists. We suggest that the mechanism(s) by which amphetamine evokes c‐ fos expression in the CPu varies depending on the stimulus (amphetamine vs. stress), the striatal cell population engaged (Dyn‐SP+ vs. Enk+ cells), and environmental context (home vs. novel cage).