Abstract

The lateral reticular nucleus (LRN) has been identified as an area in the caudal medulla involved in the centrifugal modulation of spinal nociceptive transmission and withdrawal reflexes. The data presented in this report further support a role for the LRN in the modulation of nociceptive responses. It was confirmed in the present study that focal electrical stimulation in the LRN inhibits the nociceptive tail-flick (TF) reflex at low intensities of stimulation in lightly pentobarbital-anesthetized rats. Aversive effects, however, were typically produced at similar and higher intensities of stimulation in the LRN in the same rats in the awake state. It was also determined that an inhibitory modulation of nociceptive responses organized both spinally and supraspinally could be activated independently by muscarinic cholinergic or opioid mechanisms in the LRN. Microinjection of morphine into the LRN in conscious rats produced an antinociception in both TF and hot plate (HP) tests which could be attenuated significantly by naloxone, but not atropine, previously microinjected into the same site in the LRN. Carbachol microinjected into the LRN also produced an antinociception which was attenuated significantly by atropine but not naloxone previously microinjected into the same site in the LRN. In contrast, the microinjection of clonidine or norepinephrine into the LRN either did not affect or shortened significantly response latencies in the TF and HP tests. These results further establish that the LRN contributes to the modulation of nociception. Opioid and cholinergic influences in the LRN appear to independently activate inhibition of responding to nociceptive stimuli organized either spinally or supraspinally, although descending inhibition was most clearly activated. An action at α 2 adrenececeptors in the LRN, conversely, produces an hyperalgesia as reflected by shortened latencies to respond in TF and HP tests.

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