Abstract

After the microinjection of morphine (5 μg/0.5 μl) into the periaqueductal gray resulted in an increase in the hot-plate and tail-flick response latency of the unanesthetized rat, the α-adrenergic antagonists yohimbine, rauwolscine and corynanthine were given intrathecally. This treatment resulted in a dose-dependent reversal of the inhibition of the thermally evoked tail-flick reflex. The relative potency of these stereoisomers was: yohimbine=rauwolscine>corynanthine. Given the reported affinity of these agonists for the α 2 (yohimbine/rauwolscine) and α 1 (corynanthine) receptors, these observations suggest that the spinopetal noradrenergic systems are acting on α 2-adrenergic receptors. Prazosin, an agent with several orders of magnitude higher affinity for the α 1than theα 2-receptor , was at best only equiactive with yohimbine. None of the intrathecal treatments produced a significant reversal of the effects of periaqueductal gray morphine on the hot-plate response. This suggests that the activation of spinopetal noradrenergic pathways alone cannot account for the suppression by morphine in the periaqueductal gray of this response which is organized at the supraspinal level.

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