Keller E, Cummins J T, von Hungen K
Subst Alcohol Actions Misuse. 1983;4(6):383-92.
Chronic ethanol treatment effects a decrease in K+-stimulated endogenous glutamate release and an increase in glutamate levels in rat frontal cortex. This treatment also increases (3H)-glutamate uptake in striatal and hippocampal slices. No uptake changes were observed in either cortical slices or synaptosomes. Ethanol withdrawal increases K+-stimulated glutamate release in cortex and hippocampus and glutamate levels in cortex, striatum and hippocampus. (3H)-glutamate uptake is increased in striatum of withdrawn animals. Thus, regional variations were observed with regard to both effect and degree of effect. Because in vitro and acute ethanol treatments had no effect on uptake or release, these changes probably result from activated feedback mechanisms that attempt to compensate for ethanol's action on brain systems rather than direct effects on membrane structure. Combined level-release data suggest an effect of ethanol on glutamate distribution in cortex and striatum. Combined uptake and release data indicate a correlation between diminished glutamate synaptic activity and the addicted state, and between heightened glutamate synaptic activity and the withdrawn state.
慢性乙醇处理会导致大鼠额叶皮质中钾离子刺激的内源性谷氨酸释放减少，谷氨酸水平升高。这种处理还会增加纹状体和海马切片中（3H）-谷氨酸的摄取。在皮质切片或突触体中均未观察到摄取变化。乙醇戒断会增加皮质和海马中钾离子刺激的谷氨酸释放以及皮质、纹状体和海马中的谷氨酸水平。戒断动物的纹状体中（3H）-谷氨酸摄取增加。因此，在效应和效应程度方面均观察到区域差异。由于体外和急性乙醇处理对摄取或释放均无影响，这些变化可能是由激活的反馈机制引起的，该机制试图补偿乙醇对脑系统的作用，而非对膜结构的直接影响。综合水平-释放数据表明乙醇对皮质和纹状体中谷氨酸分布有影响。综合摄取和释放数据表明，谷氨酸突触活性降低与成瘾状态之间以及谷氨酸突触活性增强与戒断状态之间存在相关性。
