Glutamate uptake in mice bred for ethanol withdrawal severity

被引:0
|
作者
Jennifer F. Buckman
C. K. Meshul
Deborah A. Finn
Aaron Janowsky
机构
[1] Department of Behavioral Neuroscience,
[2] Oregon Health Sciences University and Research Service,undefined
[3] Portland Veteran’s Administration Medical Center,undefined
[4] Portland,undefined
[5] OR 97201,undefined
[6] USA,undefined
[7] Departments of Behavioral Neuroscience and Pathology,undefined
[8] Oregon Health Sciences University and Research Service,undefined
[9] Portland Veteran’s Administration Medical Center,undefined
[10] Mail Code RD-29,undefined
[11] 3710 SW US Veterans Hospital Road,undefined
[12] Portland,undefined
[13] OR 97201,undefined
[14] USA e-mail: meshulc@ohsu.edu,undefined
[15] Departments of Behavioral Neuroscience,undefined
[16] Psychiatry,undefined
[17] and Physiology and Pharmacology,undefined
[18] Oregon Health Sciences University and Research Service,undefined
[19] Portland Veteran’s Administration Medical Center,undefined
[20] Portland,undefined
[21] OR 97201,undefined
[22] USA,undefined
来源
Psychopharmacology | 1999年 / 143卷
关键词
Key words Glutamate; Convulsion; Ethanol; Hippocampus;
D O I
暂无
中图分类号
学科分类号
摘要
Rationale: Withdrawal seizure-prone and withdrawal seizure-resistant mice were selectively bred to exhibit differences in handling-induced convulsion severity during ethanol withdrawal. The glutamatergic system has been implicated in seizure activity as well as ethanol withdrawal symptoms. Objective: This study assessed L-[3H]glutamate uptake into hippocampal synaptosomes prepared from withdrawal seizure-prone and- resistant mice. Methods:Glutamate uptake was characterized following repeated handling-induced convulsions, during acute intoxication, and during peak withdrawal following chronic ethanol exposure. Results: Hippocampal synaptosomal L-[3H]glutamate uptake did not differ between convulsion- and ethanol-naive withdrawal seizure-prone and- resistant mice. Furthermore, exposure to convulsions or to a hypnotic dose of ethanol (4 g/kg) did not alter L-[3H]glutamate uptake. However, withdrawal from 72 h of ethanol exposure significantly increased L-[3H]glutamate uptake in both mouse lines as compared to their respective ethanol-naive controls. Conclusions:These data suggest that glutamate uptake is influenced by chronic ethanol exposure similarly in both withdrawal seizure-prone and- resistant mice. The observed increases in glutamate uptake during withdrawal may be associated with compensatory mechanisms triggered by chronic intoxication and are independent of the selected differences for withdrawal severity.
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页码:174 / 182
页数:8
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