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SLEEP AND TEMPERATURE REGULATION

Cold-induced thermogenesis mediated by GABA in the preoptic area of anesthetized rats

National Institute of Health and Nutrition, Shinjuku 162-8636, Japan

Submitted 3 January 2004 ; accepted in final form 11 March 2004

Bilateral microinjections of GABA (300 mM, 100 nl) or the GABA_A receptor agonist muscimol (100 µM, 100 nl) into the preoptic area (POA) of the hypothalamus increased the rate of whole body O₂ consumption (O₂) 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 pancuronium bromide + 4 mg/kg vecuronium bromide iv) prevented GABA-induced EMG activity but had no significant effect on GABA-induced thermogenesis. However, pretreatment with the -adrenoceptor propranolol (5 mg/kg iv) greatly attenuated the GABA-induced increase in O₂ and tachycardic responses. Accordingly, the GABA-induced increase in O₂ 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 GABA_A receptor antagonist bicuculline (500 µM, 100 nl), but not the vehicle saline, into the POA blocked these skin cooling-induced responses. These results suggest that GABA and GABA_A receptors in the POA mediate cold information arising from the skin for eliciting cold-induced thermogenesis.

thermoafferent; neurotransmitter; nonshivering thermogenesis

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