Quantification of in vivo spiperone binding in the rat striatum after lesions produced by kainate or decortication.

The potential of in vivo spiperone binding as a tool for the detection and quantitative analysis of striatal dopamine (DA) receptor alterations was studied in rat brain lesioned in several ways. Two weeks after kainate (KA) injection a significantly higher radioactivity accumulation was observed in the lesioned striatum than in the contralateral structure after a tracer dose of [3H]spiperone. The difference was maximal 2 days after surgery and it was present for at least 4 weeks while it was reversed 11 weeks after KA injection. The radioactivity uptake (tracer dose of [3H]spiperone) measured 2 weeks after surgery could be specifically prevented in both KA-lesioned and contralateral striatum by haloperidol and N-n-propylnorapomorphine while non-dopaminergic drugs were almost without effect. More than 80% of the radioactivity accumulation was saturable in both contralateral (unlesioned) and KA-lesioned striatum, leaving a slightly higher non-saturable radioactivity level in the latter. One week after unilateral ablation of the cerebral cortex overlying the striatum only minor bilateral differences in striatal radioactivity content were found after a tracer dose of [3H]spiperone. No differences were present after 6-OHDA lesion of the nigrostriatal pathway. Striatal DA receptor densities (Bmax) were determined from the dose-dependency of total striatal spiperone accumulation. This relationship was assessed using cerebellar spiperone accumulation instead of dose. Thus a Bmax of about 75 fmol X mg-1 tissue was found in the striatum of control (unoperated) rats and contralateral to the striatal KA lesion while 2 weeks after surgery it was approximately 33 fmol X mg-1 in the KA-lesioned striatum. One week after unilateral decortication Bmax values of about 50 and 65 fmol X mg-1 were found ipsi- and contralaterally to the lesion respectively.