ROLE OF THE PARAFASCICULAR THALAMIC NUCLEUS AND N-METHYL-D-ASPARTATE TRANSMISSION IN THE D-1-DEPENDENT CONTROL OF IN-VIVO ACETYLCHOLINE-RELEASE IN RAT STRIATUM

We investigated the involvement of glutamatergic neurotransmission in the modulation of D-1 receptor-mediated stimulation of acetylcholine o utflow in dorsal striatum in freely moving rats, and the relative role s of the thalamostriatal and corticostriatal pathways in this regulati on using in vivo microdialysis. The selective n-methyl-D-aspartate non -competitive antagonist dizocilpine maleate (0.1 mg/kg i.p.), but not the kainate/quisqualate receptor antagonist, 6,7-dinitroquinoxaline-2, 3-dione (3 mu g per side i.c.v.), completely prevented the rise in str iatal extracellular acetylcholine elicited by maximal effective doses of the full D-1 agonist SKF 82958 (3 mg/kg s.c.) and of the dopamine r eleaser d-amphetamine (2 mg/kg s.c.). Acute bilateral electrolytic les ions of the parafascicular nucleus of the thalamus prevented the stimu lation of striatal acetylcholine output by SKF 82958 and d-amphetamine but only slightly reduced basal acetylcholine release. In contrast ac ute interruption of the corticostriatal pathway did not alter the effe ct of the two dopaminergic drugs although it markedly reduced basal st riatal acetylcholine release. Lesions of the parafascicular thalamic n ucleus, or a low dose of dizocilpine maleate (0.1 mg/kg i.p.), also pr evented the acetylcholine-increasing effect of the neuroleptic remoxip ride (10 mg/kg s.c.), an effect known to be D-1 receptor dependent. Th e results suggest that striatal projections arising from the parafasci cular thalamic nucleus and utilizing N-methyl-D-aspartate receptors pl ay a critical role in the D-1-mediated stimulation of acetylcholine re lease in dorsal striata.