Parafascicular thalamic nucleus deafferentation reduces c-fos expression induced by dopamine D-l receptor stimulation in rat striatum

We investigated the role played by the parafascicular thalamostriatal pathw ay, one of the major excitatory inputs to the striatum, in the D-l receptor induction of c-fos messenger RNA expression in the rat striatum. The full D-l receptor agonist, SKF-82958 (0.05, 0.1, 0.5 and 1 mg/kg, s.c., 30 min), dose-dependently induced c-Sos messenger RNA in naive rat striatum as dete rmined by northern blot analysis. One day following electrolytic lesion of the parafascicular thalamostriatal nucleus, striatal c-fos signal by itself was not altered but the stimulated expression of c-fos was strongly decrea sed. Sections of sham-operated and acute-lesioned dorsal striata of vehicle - or SKF-82958-treated rats were processed for in situ hybridization histoc hemistry at the single-cell level with an RNA probe for c-fos. The basal ex pression of striatal c-fos was poorly detectable in sham and lesioned group s. Sections of dorsal striata from sham-operated rats treated with SKF-8295 8 showed two types of labeled neurons for c-fos: the lightly and the very d ensely labeled neurons which are few in number. Thalamic lesion strongly re duced SKF-82958 stimulated expression of c-fos RNA in both types of labeled cells. The frequency distribution of c-Sos labeling per neuron in dorsal s triata of lesioned rats treated with SKF-82958 was shifted to the left, and its median was lower than in the sham-operated striata treated with the D- l receptor agonist. The results provide evidence that the excitatory projections from the paraf ascicular nucleus of the thalamus, thought to operate primarily through the N-methyl-D-aspartate receptors, exert a facilitatory control over D-l rece ptor-induced c-fos gene expression specifically in the dorsal striatum. (C) 2001 IBRO. Published by Elsevier Science Ltd. All rights reserved.