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Activation of arc , a Putative “Effector” Immediate Early Gene, by Cocaine in Rat Brain
Author(s) -
Fosnaugh Jennifer S.,
Bhat Ratan V.,
Yamagata Kanato,
Worley Paul F.,
Baraban Jay M.
Publication year - 1995
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.1471-4159.1995.64052377.x
Subject(s) - arc (geometry) , effector , immediate early gene , neuroscience , gene , biology , genetics , microbiology and biotechnology , gene expression , geometry , mathematics
As immediate early genes (IEGs) are thought to play a critical role in mediating stimulus‐induced neuronal plasticity, several laboratories have characterized the IEG response induced by cocaine to help define the changes in gene expression that may underlie its long‐lasting behavioral effects. Although activation of several transcription factor IEGs has been described, little is known about which “effector” IEGs, if any, are also induced. In the present study, we have examined whether cocaine administration affects expression of a recently identified “effector” IEG, referred to as arc ( a ctivity‐ r egulated, c ytoskeleton‐associated). This IEG encodes a protein with homology to spectrin that appears to be associated with the actin cytoskeleton. Using in situ hybridization, we have found that systemic cocaine administration elicits a robust, transient rise in arc mRNA levels in striatum, which is suppressed by D 1 dopamine receptor blockade, reserpine treatment, or striatal 6‐hydroxydopamine lesions. D 2 receptor antagonists triggered arc expression when administered alone. Immunohistochemical studies indicated that Arc protein induced by cocaine is expressed in neuronal cell bodies and dendrites. As Arc appears to be a component of the neuronal cytoskeleton, it may be involved in structural alterations underlying neuronal plasticity triggered by cocaine.