Abstract

Experiments were conducted to determine if both electrical and chemical stimulation of the ventromedial hypathalamic nucleus (VMH) could activate brown adipose tissue (BAT) thermogenesis. Age-matched, room-acclimated (21 °C) and cold-acclimated (4 °C for 3 weeks prior to testing) male Sprague-Dawley rats were given unilateral electrical or chemical stimulation to the VMH by way of a ‘chemotrode apparatus’. The devised ‘chemotrode’ allowed both electrical stimulation (insulated piano wire stimulating electrode) and chemical stimulation (23 gauge stainless steel intracranial cannula of equal length) to be performed at the same VMH site using a common 19 gauge stainless steel outer guide tube. The first unilateral VMH electrical stimulation (0.5 ms pulse, 50 Hz and 120 μA for 30 s) caused no significant rise in interscapular brown adipose tissue temperature (T bat ) colonic (T c) or tail surface temperatures (T t), compared to respective prestimulation control values in rats acclimated to 21 °C. In the 4 °C-acclimated group the first VMH electrical stimulation caused a significant rise in IBAT temperature. l-Glutamate administration to the same VMH site (60 nmol in 600 nl volume) also caused a significant increase in IBAT temperature in the 4 °C but not the 21 °C-acclimated rats. The rise in IBAT temperature following the l-glutamate injection to the 4 °C-acclimated group was similar to that found following the first electrical stimulation to this group. Interestingly, a second unilateral electrical stimulation of the VMH to 4 °C-acclimated rats could not evoke a similar increase in IBAT temperature suggesting that overall l-glutamate was acting in vivo as an excitotoxin. The results indicate that both unilateral chemical and electrical stimulation of the VMH of 4 °C but not 21 °C acclimated, anesthetized male Sprague-Dawley rats can evoke significant rises in IBAT temperature, indicative of activation of BAT thermogenesis by this CNS site. These results infer that cold acclimation causes facilitation of BAT thermogenesis peripherally and/or centrally such that subsequent electrical or chemical stimulation of the VMH can then evoke significant rises in IBAT temperature in those animals.

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