This experiment tested the effects of an intracerebroventricular injection of prostaglandin E1 on the sympathetic activation and the thermogenic changes in rats with ibotenate lesions of the ventromedial hypothalamus. Under pentobarbital anesthesia, twelve Sprague-Dawley male rats were lesioned bilaterally in the ventromedial hypothalamus with an injection of ibotenic acid (30 nmol into each side). Sham lesions were carried out in other twelve control rats. After 48 h, all animals were anesthetized with ethyl-urethane. The firing rate of the sympathetic nerves innervating the interscapular brown adipose tissue and the colonic and interscapular brown adipose tissue temperatures were monitored before and after an intracerebroventricular injection of prostaglandin E1 (500 ng) or saline. Prostaglandin E1 induced an increase in the firing rate of sympathetic nerves and the colonic and interscapular brown adipose tissue temperatures. These effects were reduced by the ventromedial hypothalamic lesion. Since ibotenic acid destroys cell bodies, the findings indicate that neurons of the ventromedial hypothalamus play a considerable role in the control of sympathetic activation and the thermogenic changes during prostaglandin E1 hyperthermia., M. Monda, A. Sullo, V. De Luca, A. Viggiano., and Obsahuje bibliografii
Interscapular brown adipose tissue (IBAT) activity is controlled by sympathetic nervous system, and factors that influence thermogenesis appear to be centrally connected to the sympathetic outflow to IBAT. Cold exposure produces a rise in BAT temperature, which is associated with an increased thyroid activity, elevated serum levels of 3,5,3’-triiodothyronine (T3), and an increased rate of T3 production. This study evaluated the effect of swimming training on 5’-triiodothyronine deiodinase (5’-D) activity in IBAT under normal environmental conditions and after short (30 min) cold exposure (TST stimulation test). 5’-D activity is lower in trained rats at basal condition, and TST increases 5’-D in IBAT of both untrained and trained rats. However, this increase is lower in trained rats. Training reduces the deiodinating activity in normal environmental conditions as well as after short cold exposure. Probably, other compensatory mechanisms of heat production are active in trained rodents.