Premium
Activator Protein‐1 Binding Activities in Discrete Regions of Rat Brain After Acute and Chronic Administration of Methamphetamine
Author(s) -
Ishihara Takeshi,
Akiyama Kazufumi,
Kashihara Kenichi,
Ujike Hiroshi,
Hamamura Takashi,
Okada Shoshiro,
Kuroda Shigetoshi
Publication year - 1996
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.1471-4159.1996.67020708.x
Subject(s) - meth , methamphetamine , nucleus accumbens , striatum , abstinence , saline , medicine , chemistry , eticlopride , self administration , endocrinology , pharmacology , sch 23390 , central nervous system , receptor , antagonist , dopamine , psychiatry , polymer , monomer , organic chemistry , acrylate
The activator protein‐1 (AP‐1) binding activities increased in three brain regions (striatum, nucleus accumbens, and cingulate cortex) after a single methamphetamine (METH) injection to rats. Pretreatment with SCH 23390, but not (−)‐eticlopride, significantly inhibited the enhanced AP‐1 binding activities induced by acute METH administration. The magnitude of enhancement of AP‐1 binding activities 3 h after the last dose of chronic METH administration (4 mg/kg once daily for 14 days) was significantly attenuated as compared with those 3 h after a single METH administration. The AP‐1 binding activities after a 1‐, but not 4‐, week abstinence from chronic administration of METH were still significantly higher than those of the saline‐treated controls. A METH challenge after a 4‐week abstinence period induced significantly lower AP‐1 binding activities in rats chronically injected with METH than in rats chronically injected with saline. The supershift assay revealed that the levels of Jun family protein, but not Fos‐related antigen, increased significantly in the striatum and nucleus accumbens of chronically METH‐treated rats after a 1‐week abstinence. These results suggest that chronic METH administration leads to delayed decay of the induced AP‐1 binding activities and Jun component levels after abstinence for up to 1 week but results in no change in or decreases these activities and attenuates METH challenge‐induced AP‐1 binding activities after abstinence for 4 weeks.