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Mice were treated with N-2-chloroethyl-N-ethyl-2-bromobenzylamine hydrochloride (DSP4), which causes severe noradrenaline (NA) depletions in brain regions and the spinal cord, or vehicle i.p. They were tested 14 days later for antinociception induced by intrathecal injections of different doses of NA. A potentiation of the NA effect upon pain sensitivity was observed, with both an increase in the magnitude and duration of the antinociceptive responses. Upon biochemical analysis of spinal cords, it was found that DSP4-treated mice had a 80% depletion of NA, whereas dopamine and 5-hydroxytryptamine were unaffected. Radioligand binding of [3H]clonidine in membranes prepared from spinal cord, showed no differences in density of alpha 2-adrenoceptors, but the affinity had been increased, probably explaining the supersensitivity.
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