The expression of the calcium binding protein calretinin in the rat striatum: Effects of dopamine depletion and L-DOPA treatment

Citation
A. Mura et al., The expression of the calcium binding protein calretinin in the rat striatum: Effects of dopamine depletion and L-DOPA treatment, EXP NEUROL, 164(2), 2000, pp. 322-332
Citations number
62
Categorie Soggetti
Neurosciences & Behavoir
Journal title
EXPERIMENTAL NEUROLOGY
ISSN journal
00144886 → ACNP
Volume
164
Issue
2
Year of publication
2000
Pages
322 - 332
Database
ISI
SICI code
0014-4886(200008)164:2<322:TEOTCB>2.0.ZU;2-P
Abstract
The activity of the striatum is regulated by glutamate and dopamine neurotr ansmission. Consequent to striatal dopamine depletion the corticostriatal e xcitatory input is increased, which in turn can raise intracellular calcium levels. We investigated changes in the neuronal expression of the calcium binding protein calretinin related to dopamine depletion and L-DOPA adminis tration. Immunohistochemical methods were used to assess calretinin in the striatum of rats with unilateral lesions of the nigrostriatal system. In th ese animals we observed a loss of the patchy distribution of calretinin fib ers. Moreover, after dopaminergic depletion we detected two new, not previo usly described, calretinin cell types, the presence of which could be relat ed to morphological changes induced by loss of a dopaminergic input. We als o found an increase in the number of calretinin-labeled cells in the striat um ipsilateral to the lesion compared to the contralateral striatum or to t he striatum of normal rats. This increase was mostly evident at 3 weeks pos tlesion and tended to decrease toward normal levels at 6, 10, and 18 weeks postlesion. In unlesioned animals, L-DOPA administration did not induce cha nges in the expression of calretinin. In unilaterally lesioned animals, L-D OPA reversed the increase in the number of calretinin-positive cells induce d by the lesion. However, chronic L-DOPA administration was less effective than acute L-DOPA in reversing the effect of the lesion. The present data s uggests that striatal calretinin neurons are sensitive to dopamine depletio n. Increased expression of calretinin in striatal cells may be consequent t o enhanced striatal excitatory input. (C) 2000 Academic Press.