| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2005: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2004: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2003: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Research Abstract |
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 both the rate of whole-body oxygen consumption (VO2) and the body core (colonic) temperature of urethane-chloralose-anesthetized, artificially ventilated rats. 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 plus 4 mg/kg vecuronium bromide, I.V.) prevented the GABA-induced EMG activity but had no significant effect on the GABA-induced thermogenesis. However, pretreatment with the β-adrenoceptor propranolol (5 mg/kg, 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 ℃ water also elicited thermogenic, tachycardic, and EMG responses. Bilateral microinjections of the GABA_A 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 cold-induced thermogenesis requires GABA and GABA_A receptors in the POA.
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