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1 National Institute of Health and Nutrition, Shinjuku, Japan
* To whom correspondence should be addressed. E-mail: osaka{at}nih.go.jp.
Bilateral microinjections of GABA (300 mM, 100 nl) or the GABAA receptor agonist muscimol (100 µM, 100 nl) into the preoptic area (POA) of the hypothalamus increased both the rate of whole-body oxygen consumption (VO2) and the body core (colonic) temperature of urethane-chloralose-anesthetized, artificially ventilated rats. The most sensitive site was the dorsomedial POA at the level of the anterior commissure. The GABA-induced thermogenesis was accompanied by a tachycardic response and electromyographic (EMG) activity recorded from the femoral or neck muscles. Pretreatment with muscle relaxants (1 mg kg-1 pancuronium bromide plus 4 mg kg-1 vecuronium bromide, I.V.) prevented the GABA-induced EMG activity but had no significant effect on the GABA-induced thermogenesis. However, pretreatment with the
-adrenoceptor propranolol (5 mg kg-1, I.V.) greatly attenuated the GABA-induced increase in VO2 and tachycardic responses. Accordingly, the GABA-induced increase in VO2 reflected mainly nonshivering thermogenesis. On the other hand, cooling of the shaved back of the rat by contact with a plastic bag containing 28 °C water also elicited thermogenic, tachycardic, and EMG responses. Bilateral microinjections of the GABAA receptor antagonist bicuculline (500 µM, 100 nl), but not those of vehicle saline, into the POA blocked these skin cooling-induced responses. These results suggest that GABA and GABAA receptors in the POA mediate cold information arising from the skin for eliciting cold-induced thermogenesis.
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