Developmental effects of ventromedial hypothalamic lesions on spontaneous activity, quinine finickiness, and reactivity to shock in the male rat

Abstract

The purpose of the present investigation was to examine the effects of time, feeding procedure, and VMH lesions on spontaneous activity, quinine finickiness, and reactivity to shock in male rats. Further, the effects of VMH lesions and yoked feeding procedures on certain aspects of the neuro-endocrine system and neurohypophysial-gonodal axis were examined in an attempt to elucidate the roles of these two systems in the regulation of activity in the VMH subject. The experimental groups consisted of normal rats feeding ad lib, normal rats yoke-fed, rats with VMH lesions feeding ad lib, and yoke-fed rats with VMH lesions. Repeated measures were taken for all groups on spontaneous activity, QHCL finickiness, and shock reactivity for 28 days following surgery. Physiological measures were taken after 28 days of behavioral testing and included adrenal weights, reproductive organ weights, and carcass analysis. The results of the study suggested the following conclusions: 1) the quinine finickiness data were not clearly in support of a developmental hypothesis of quinine aversion. Reasons for this failure were explored and discussed; 2) the shock threshold data were not conclusive but in general did not support a developmental hypothesis of stimulus reactivity; 3) running wheel activity is a regulatory mechanism; 4) increases in body weight and depot fat do not account for observed decreases in activity following VMH lesions; 5) hypoactivity may contribute an increase in adiposity but it is certainly not sufficient to produce the degree of adiposity seen in VMH subjects; 6) increases in adiposity are not directly related to decreased gonadal functioning and hypothalamic hypoactivity does not depend on decreased gonadal activity; 7) the relationship between adrenals and activity is unclear and deserves further study; 8) changes in activity following surgery are probably a direct effect of neural pathway interruption and are related to hyperphagia only insofar as running is a metabolic regulatory mechanism.