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We studied the feeding rhythms and feeding patterns of adult Long-Evans rats treated with monosodium glutamate (MSG) in their early post-natal period. This treatment is known to induce neuronal degeneration in the arcuate nucleus (ARC), a major hypothalamic site implicated in the regulation of feeding. Neonatal rats were treated intraperitoneally with MSG or saline (controls) alone on the first days of life. At age of 6 months, male control and male MSG rats were placed in our automatic feeding system, and the structure of feeding behavior and diurnal feeding rhythms were analysed. On a 24 hours basis, MSG rats ate less than control rats (-24%). This hypophagia resulted from a mild diurnal hyperphagia (+6%) and a pronounced nocturnal hypophagia (-34%). This hypophagia was the main consequence of a decrease of meal size in MSG rats (-37%) and was associated with an increase in meal duration (+52%). It was also associated with a total disappearance of the two feeding peaks that normally occur at light and dark onset in the rat (-90% 2 h after dark onset and -49% 2 h before light onset). These results indicate that neonatal treatment with MSG induces important changes in feeding patterns and feeding rhythms in the adulthood. These changes might be related to the disappearance of neurotransmitters located in the arcuate nucleus.

The presence of a nitric oxide synthetase (NOS) was demonstrated in the rat brain. It has been demonstrated recently that NOS-inhibitors reduce food intake in mammals and this suggest that nitric oxide (NO) might be a physiological mediator involved in the mechanisms controlling feeding behavior. Actually, there is no information about the acute central and peripheral effects of NOSinhibitors on feeding behavior in obese an lean Zucker rats. That is why we investigated the acute dose-dependent activity of NG-Nitro-Arginine-Methyl-Ester (L-NAME) on food intake and feeding behavior in these rats. When given peripherally in the obese rats, L-NAME produced a dosedependent decrease in food intake (p < 0.001). The calculated MED and the ED 50 were 0.50 mg/kg IP and 3.46 mg/kg IP, respectively. These effects could not be reproduced in the lean Zucker rats whatever the dose used (p = 0.59). The anorectic properties of L-NAME were wery well translated into the microstructure of the feeding behavior. Time spent to eat (p < 0.001), meal duration (p < 0.01) and meal number (p < 0.001) were reduced in the obese rats. Interestingly, L-NAME produced the same effects in the lean rats, but meal size increased in a compensatory manner. Central administration of L-NAME reproduced the same effects in the obese rats, but lean rats still remained insensitive. Central aminergic and/or peptidergic defects associated with the expression of hyperphagia might explain the differences observed between these lean and the obese animals. These results indicate a role of nitric oxide in the expression of hyperphagia and show that it might be a physiological mediator involved in the mechanisms controlling feeding behavior.