کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2014280 1067151 2008 6 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Ketamine induces hyperactivity in rats and hypersensitivity to nicotine in rat striatal slices
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی زیست شیمی
پیش نمایش صفحه اول مقاله
Ketamine induces hyperactivity in rats and hypersensitivity to nicotine in rat striatal slices
چکیده انگلیسی
The symptoms of schizophrenia can be modeled in rats through blockade of ionotropic glutamate receptors, which induces changes in central dopamine circuits. These circuits also contain nicotinic acetylcholine receptors that are activated by nicotine. A role for nicotine in the etiology of schizophrenia is supported by clinical observations of high tobacco use rates in individuals experiencing the psychopathology. The present study investigated the effect of the ionotropic glutamate receptor antagonist ketamine on the function of striatal nicotinic acetylcholine receptors to understand better the potential role of these receptors in schizophrenia. Ketamine (0.1-300 µM) was ineffective to evoke [3H] overflow from rat striatal slices preloaded with [3H]dopamine. Application of psychotomimetic ketamine concentrations (1-10 µM) to striatal slices augmented nicotine-evoked [3H] overflow. Finally, rats received ketamine (30-50 mg/kg) injections for 30 days, to model the development of the disorder, and hyperactivity was observed, although repeated ketamine treatment did not significantly alter nicotine-evoked [3H]dopamine overflow. These data indicate that the function of nicotinic acetylcholine receptors that mediate dopamine release are altered by ketamine, and support a role for nicotinic acetylcholine receptors in schizophrenia pathology.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Pharmacology Biochemistry and Behavior - Volume 91, Issue 1, November 2008, Pages 71-76
نویسندگان
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