Brain research
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Extracellular and intracellular recordings were made from within the dorsal horn of 10 anaesthetised and gallamine triethiodide-paralysed cats. Inhibition of background and residual noxious-evoked discharge by cooling and warming was demonstrated in 7 out of 33 nociceptor-driven dorsal horn neurones. Five units were inhibited by warming of the noxious mechanical excitatory receptive field. ⋯ Cooling (32-20 degrees C) excited two units; warming (32-43 degrees C) also excited two units. Heating above 43 degrees C excited 8 units; cold below 20 degrees C excited 3 units. The units inhibited by thermal stimulation may provide some neuronal basis for thermal analgesia.
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The lateral reticular nucleus (LRN) and locus coeruleus-subcoeruleus (LC/SC), brainstem structures which overlap the A1 and A6 noradrenergic nuclei respectively, have been implicated in descending modulation of spinal nociceptive transmission. The present studies were designed to examine the role of norepinephrine (NE) in the mediation of inhibition of the nociceptive tail flick reflex produced by focal electrical stimulation in the LRN and LC/SC. Spinal NE was depleted by intrathecal administration of 6-hydroxydopamine (6-OHDA; 20 micrograms) and the threshold electrical stimulation in the LRN and the LC/SC necessary to inhibit the tail flick reflex in lightly pentobarbital-anesthetized rats was determined 9 and 14 days later. ⋯ Binding of [3H]rauwolscine to lumbar spinal cord revealed an elevation in the estimated Bmax without a change in the estimated Kd of the high affinity binding component 9 days following 6-OHDA administration. This study demonstrates that spinal adrenoceptor denervation supersensitivity develops rapidly following intrathecal administration of 6-OHDA and compensates for the selective destruction of spinal noradrenergic nerve terminals. Thus, the absence of effect of NE depletion on the tail flick inhibitory stimulation threshold in the LRN and the LC/SC does not argue against the hypothesis that spinopetal NE-containing neurons in these brainstem loci are involved in modulation of spinal nociceptive transmission.