The antinociception of opiates is mediated through the activation of opioid receptors in several mid brain and brain stem areas. This paper reports that the forebrain area termed area tempestas (AT), first identified as a convulsant trigger area, is also a component of the endogenous pain suppression system. Unilateral AT application of DAMGO, morphine and U-50,488H in rats at doses in the nanogram range produced marked and dose-dependent increases in the latency to respond to nociceptive stimuli. A lower effect is found after application of DPDPE and DADLE. Antinociception is more evident in the hot plate than in the tail flick test. In the former test, the effect was restricted to the paws contralateral to the hemisphere of injection. Unilateral AT application of naltrexone (4 ng) reduced in the contralateral paws the antinociceptive effect that the bilateral AT application of morphine (20 ng/hemisphere) had induced in both body sides. Unilateral application of naltrexone, (20 ng) ICI 154, 129 (20 ng) and Win 44,441-3 (8 ng) antagonized the antinociceptive effect elicited by the systemic injection of morphine (2.5 mg/kg s), DPDPE (20 mg/kg s) and U-50,488H (20 mg/kg s), respectively. In the hot plate test, the antagonism was found in the paws ipsilateral and contralateral to the hemisphere of injection of the antagonists.
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