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Phencyclidine (PCP) and dizocilpine (MK801) exert time‐dependent effects on the expression of immediate early genes in rat brain
Author(s) -
Gao XueMin,
Hashimoto Takeshi,
Tamminga Carol A.
Publication year - 1998
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(199805)29:1<14::aid-syn2>3.0.co;2-e
Subject(s) - phencyclidine , nmda receptor , junb , dizocilpine , immediate early gene , psychotomimetic , pharmacology , glutamate receptor , neuroscience , gene expression , chemistry , medicine , biology , receptor , gene , biochemistry
The mRNA expression pattern for four different immediate early genes was examined dynamically in rat brain after administration of phencyclidine (PCP; 0.86 or 8.6 mg/kg) or MK801 (0.1 or 1.0 mg/kg). Following each treatment, the expression of cfos , cjun , junB , and zif268 mRNA changed distinctively and dynamically between 1 and 48 hours. cfos mRNA was induced in cortical areas at early times after either dose of PCP or of MK801; the change was especially prominent in cingulate and auditory cortices. zif268 mRNA showed an early (1 hour) activation and a delayed (24–48 hour) suppression after PCP and MK801 in neocortical areas. PCP also caused cjun and junB mRNA induction in cortical areas at early times, with a distribution and time course similar to its effects on cfos mRNA. No alterations in cfos , cjun , or junB mRNA were found in neocortical or hippocampal areas at any delayed time (>6 hours) after PCP treatment, whereas suppression of zif268 expression was prominent even at 48 hours post‐treatment. CPP, a competitive NMDA antagonist, showed a similar pattern of effects on cfos and zif268 mRNA expression. These functional consequences of a PCP‐ or MK801‐induced reduction in NMDA‐sensitive glutamate transmission may be relevant to an understanding of animal NMDA pharmacology and/or to clinical psychotomimetic side effects of antiglutamatergic treatments. Synapse 29:14–28, 1998. © 1998 Wiley‐Liss, Inc.