Thyroid Function, Body Temperature Regulation and Growth in Rats With Hypothalamic Lesions12

Electrolytic lesions of the hypothalamus were produced in 73 male rats. When compared with 64-sham-operated controls, certain rats with lesions had thyroid inhibition (decreased I131 uptake and release rate), persistent hyperthormia, diabetes insipidus, tosticular atrophy and growth disturbance. Functional and neuroanatomical studies indicated that thyroid dysfunction, hyperthermia, diabetes insipidus and testicular atrophy were all independent consequences of localized brain injury. A temperature regulating center was localized to the pre-optic area; this partially overlapped the TSH regulating area which lies between the paraventricular nucleus and the median eminence. Gonad atrophy was caused by infundibular damage. As measured by rate of increase in body length (nose-tail) and by tibial length at death, growth was significantly impaired by certain hypothalamic lesions. No specific neural localization of the lesion responsible for poor growth could be made but it was noted that the most striking effects occurred with large median eminence lesions that had involved the primary portal plexus or stalk and had caused severe diabetes insipidus. India ink perfusion showed that the pituitaries were generally well vascularized. Hyperthermia and thyroid dysfunction were probably not the cause of the growth reduction since either or both of these abnormalities occurred in rats with normal growth rate.