title: Escitalopram increases cortical nitric oxide synthase (NOS) in rat brain during ethanol withdrawal.
abstract: The effect of escitalopram on ethanol withdrawal syndrome (EWS) and involvement of nitric oxide system in rats was investigated. Male Wistar rats divided into five experimental groups of eight animals each: (a) control group; (b) EWS (saline) group; (c) escitalopram 2.5 mg group; (d) escitalopram 5mg group and (e) escitalopram 10 mg group. Ethanol dependence was induced in rats by ethanol-containing liquid diet and ethanol withdrawal was precipitated by replacing ethanol free diet. Ethanol receiving rats in individual groups were decapitated on 21st day of ethanol ingestion and at sixth hour of ethanol withdrawal. Brains were removed and dissected. Five regions of the brain were dissected: the frontal cortex, cerebellum, striatum, hippocampus and hypothalamus. Immunohistochemical NOS staining was performed. The NOS staining intensity in cortex and hypothalamus regions were significantly lower in EWS group than control group. During EWS period, in rats given 2.5 and 10 mg/kg escitalopram, the staining intensity in cortex, striatum and hippocampus were found to be 11.492, 8.519 and 11.234, respectively, and was statistically different than the control group. The hippocampal NOS staining intensity was found to be significantly decreased with 2.5 mg/kg escitalopram, whereas the cortex, striatum and hippocampal staining intensity were increased significantly with 5 mg/kg. In 10 mg/kg escitalopram group, staining properties were not different than those of the control group. Our results suggest that NOS decreases during ethanol withdrawal in cortex and hypothalamus of rat brain and treatment with escitalopram reverses the enzyme density in cortex but not hypothalamus.
authors.affiliation: Maltepe University, Faculty of Medicine, Department of Pharmacology and Clinical Pharmacology, Maltepe 34845, Istanbul, Turkey. esras@maltepe.edu.tr
authors.forename: Esra
authors.initials: E
authors.lastname: Saglam
authors.forename: Lora Esberk
authors.initials: LE
authors.lastname: Ates
authors.forename: Hakan
authors.initials: H
authors.lastname: Kayir
authors.forename: Turgay
authors.initials: T
authors.lastname: Celik
authors.forename: Berna
authors.initials: B
authors.lastname: Terzioglu
authors.forename: Tayfun
authors.initials: T
authors.lastname: Uzbay
mesh_terms: D000818:Animals; D001921:Brain / Q000187:drug effects / Q000201:enzymology*; D002531:Cerebellum / Q000187:drug effects / Q000201:enzymology; D015283:Citalopram / Q000494:pharmacology*; D003342:Corpus Striatum / Q000187:drug effects / Q000201:enzymology; D000431:Ethanol / Q000009:adverse effects*; D005625:Frontal Lobe / Q000187:drug effects / Q000201:enzymology; D006624:Hippocampus / Q000187:drug effects / Q000201:enzymology; D007031:Hypothalamus / Q000187:drug effects / Q000201:enzymology; D007150:Immunohistochemistry; D008297:Male; D052248:Nitric Oxide Synthase Type I / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D017367:Selective Serotonin Reuptake Inhibitors / Q000494:pharmacology*; D018709:Statistics, Nonparametric; D013375:Substance Withdrawal Syndrome / Q000201:enzymology*
chemical_list: D015283:Citalopram; D000431:Ethanol; D052248:Nitric Oxide Synthase Type I; D017367:Selective Serotonin Reuptake Inhibitors