Involvement of the intralaminar parafascicular nucleus in muscarinic-induced antinociception in rats.

The thalamic contribution to cholinergic-induced antinociception was examined by microinjecting the acetylcholine (ACh) agonist carbachol into the intralaminar nucleus parafascicularis (nPf) of rats. Pain behaviors organized at spinal (spinal motor reflexes), medullary (vocalizations during shock), and forebrain (vocalization afterdischarges, VADs) levels of the neuraxis were elicited by noxious tailshock. Carbachol (0.5, 1, and 2 microg/side) administered into nPf produced dose-dependent elevations of vocalization thresholds, but failed to elevate spinal motor reflex threshold. Injections of carbachol into adjacent sites dorsal or ventral to nPf failed to alter vocalization thresholds. Elevations in vocalization thresholds produced by intra-nPf carbachol were reversed in a dose-dependent manner by local administration of the muscarinic receptor antagonist atropine (30 and 60 microg/side). These results provide the first direct evidence supporting the involvement of the intralaminar thalamus in muscarinic-induced antinociception. Results are discussed in terms of the contribution of nPf to the processing of the affective dimension of pain.