Effects of cerebral lesions on binding sites for calcitonin and calcitonin gene-related peptide in the rat nucleus accumbens and ventral tegmental area

Abstract

Binding site densities of [ 125I]-labelled salmon calcitonin and human calcitonin gene-related peptide were investigated in the rat nucleus accumbens and ventral tegmental area by means of quantitative autoradiography following selective brain lesions. [ 125I]salmon calcitonin and [ 125I]human calcitonin gene-related peptide binding sites were highly concentrated in the accumbens, whereas the ventral tegmental area only contained [ 125I]salmon calcitonin binding sites. Unilateral injection of 6-hydroxydopamine into the ventral tegmental area did not alter [ 125I]salmon calcitonin and [ 125I]human calcitonin gene-related peptide binding site densities in the ipsilateral accumbens, while it produced a significant decrease in [ 125I]salmon calcitonin binding sites in the lesioned ventral tegmental area (−50%). In contrast, following unilateral injection of quinolinic acid into the accumbens, the densities of [ 125I]salmon calcitonin and [ 125I]human calcitonin gene-related peptide binding sites were significantly decreased in the lesioned accumbens (−57% and −56%, respectively), while [ 125I]salmon calcitonin binding site densities were not modified in the ipsilateral ventral tegmental area. The present study clearly suggests that [ 125I]salmon calcitonin and [ 125I]human calcitonin gene-related peptide binding sites are located on intrinsic neurons but not on the dopaminergic nerve terminals in the accumbens. Moreover, a certain proportion of [ 125I]salmon calcitonin binding sites could be present on dopaminergic cell bodies in the ventral tegmental area.