Abstract
Inhibition of the spinal nociceptive tail-flick (TF) reflex by focal electrical stimulation in the caudal medulla was examined and characterized in lightly pentobarbital-anesthetized rats. Systematic mapping studies revealed that inhibition of the TF reflex was produced at low intensities of stimulation (12.5–25 microA) only from the lateral reticular nucleus (LRN). Areas dorsal and medial to the LRN required higher intensities of stimulation to produce descending inhibition of the TF reflex, likely reflecting spread of current to the LRN at these higher intensities of stimulation (50–100 microA). At threshold inhibitory intensities of stimulation in the LRN, changes in blood pressure were not produced. Strength-duration characterization of stimulation and the microinjection of glutamate into the LRN at the same site where focal electrical stimulation was effective suggest that the descending inhibition produced arises from activation of cell bodies in the LRN. The intrathecal administration of a variety of pharmacological antagonists revealed the descending inhibition produced by stimulation in the LRN to be mediated at least in part by spinal alpha 2-adrenoceptors. These findings, together with previous observations, suggest a role for the LRN in the centrifugal modulation of spinal nociceptive transmission.