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Abstract
Spinopetal pathways may be activated by a variety of brainstem manipulations including
microinjections of morphine which are known to modulate spinal nociceptive processing.
Based on the ability of these manipulations to release spinal noradrenalin; the ability
to reverse the antinociceptive effects by intrathecal adrenergic antagonists and the
fact that intrathecal injections of noradrenalin mimic the antinociceptive effect,
it appears that the descending modulation may be mediated by descending noradrenergic
systems. Examination of the spinal receptor systems with intrathecally administered
agents indicates that spinal alpha, but not beta adrenergic receptor agonists produce
a powerful analgesia as measured on a variety of reflex and operant measures in mouse,
rat, cat, primate and man. On the basis of agonist and antagonist structure-activity
relationships it appears that a significant effect can be produced in the absence
of any detectable effect on motor function by the occupation of spinal alpha 2 receptors.
Distinguishable alpha 1 receptors also appear "analgetically-coupled," but their effects
are uniformly contaminated by signs of cutaneous hyperreflexia at doses required to
produce analgesia. The ordering of potency with which intrathecal adrenergic antagonists
reverse the effects of intrathecal noradrenalin is indistinguishable from that of
the reversal by these intrathecal agents of the antinociceptive effects evoked by
brainstem morphine. This suggests that the population of spinal receptors acted upon
by exogenously administered adrenergic agonists and endogenously released noradrenaline
have indistinguishable characteristics.