Consequences of monosodium glutamate or goldthioglucose arcuate nucleus lesions on ethanol-induced locomotion.

Abstract

It has been suggested that the endogenous opioid system, especially beta-endorphins, may play an important role in the behavioral effects of ethanol. The main site of beta-endorphin synthesis in the brain is the hypothalamic arcuate nucleus (ARC). In the present study, we used the neurotoxins monosodium glutamate (MSG) or goldthioglucose (GTG) to produce a selective ARC lesion and to assess its effects on the locomotion observed after ethanol administration. The results show that MSG or GTG pre-treatment produces a blockade of the increased locomotion produced by the injection of low and moderate doses of ethanol (0.5 and 1.5 g/kg, respectively). These effects were observed in the absence of any change in blood ethanol levels. On the other hand, MSG (but not GTG) pre-treatment enhanced the locomotor depression produced by higher doses of this alcohol (2.5 g/kg). Finally, caffeine (10 mg/kg)-induced locomotion was unaffected by the aforementioned neurotoxic agents. Thus, taken together, the present results suggest that MSG and GTG administration produce a blockade of the stimulating effects of ethanol on locomotion in mice and thus provides further support for a role of the ARC in the behavioral effects observed after ethanol administration.