• 1 January 1983
    • journal article
    • research article
    • Vol. 224 (3), 552-558
Abstract
The .alpha.-adrenoceptor subtype(s) on which intrathecally applied .alpha.-adrenergic agonists act to produce their antinociceptive effect were studied. The potencies of intrathecal (i.t.) prazosin or i.t. yohimbine to antagonize the elevations of thermal nociceptive threshold induced by i.t. 2-[2,6-diethyl-phenylamino]-2-imidazoline (ST-91), methoxamine or norepinephrine (NE) were determined in the rat. Tail-flick and hot plate tests were used to determine thermal nociceptive threshold. At the ID50 [median inhibitory dose] level, the .alpha.-2 selective antagonist yohimbine was significantly more potent than the .alpha.-1 selective antagonist prazosin at blocking the analgesia produced by the .alpha.-2 selective agonist ST-91, whereas prazosin was significantly more potent than yohimbine at antagonizing the analgesia produced by the .alpha.-1 selective agonist methoxamine or by the nonselective .alpha. agonist NE. Analgesic doses of methoxamine evoked a readily observable disturbance of motor and autonomic function, whereas such effects were not observed after analgesic doses of ST-91 or NE. Both i.t. methoxamine and i.t. ST-91 elevated thermal nociceptive threshold in rats depleted of lumbar spinal cord NE by pretreatment 7 days before with i.t. 6-hydroxydopamine. Stimulation of either 1 of 2 separate populations of postsynaptic spinal .alpha. adrenoceptors will apparently inhibit spinal nociceptive transmission. One of these populations appears to be composed of .alpha.-2 adrenoceptors. The subtype classification of the .alpha.-adrenoceptors composing the other population remains unclear.