Hyperphagia and obesity produced by midbrain lesions in the rat: A comparison with hypothalamic hyperphagia and obesity

Abstract

Bilateral electrolytic lesions were made in female Wistar rats to compare the characteristics of the obesity produced by lesioning the mesencephalon (MES) with those produced by lesioning the ventromedial hypothalamus (VMH). The hyperphagia following VMH lesions was immediate but it developed more slowly in the rats with MES lesions and in several rats there was an initial aphagia. Three weeks after lesioning, however, both groups weighed the same but major differences were found in response to various challenges. The appetite suppressant effect of d -amphetamine hydrochloride (1.5 mg/kg) as well as the circadian rhythm of eating and the response to a quinine adulterated (quinine monohydrochloride 0.25%) diet were not identical in the two groups of animals. MES-Lesioned rats ate much less food than either the VMH-lesioned rats or the controls when a screen baffle was placed over their food jars and increases in their body weights were observed to be diet-dependent. Fat deposition in MES-lesioned rats was almost entirely in the intrascapular area in contrast to fat deposition commonly observed in obese VMH-lesioned rats where it is mostly in the abdominal area. The results of these experiments provide further support to the observations that midbrain and hypothalamic hyperphagias are not identical.