The expression of the calcium binding protein calretinin in the rat striatum: effects of dopamine depletion and L-DOPA treatment.
The activity of the striatum is regulated by glutamate and dopamine neurotransmission. Consequent to striatal dopamine depletion the corticostriatal excitatory 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 administration. Immunohistochemical methods were used to assess calretinin in the striatum of rats with unilateral lesions of the nigrostriatal system. In these animals we observed a loss of the patchy distribution of calretinin fibers. Moreover, after dopaminergic depletion we detected two new, not previously described, calretinin cell types, the presence of which could be related to morphological changes induced by loss of a dopaminergic input. We also found an increase in the number of calretinin-labeled cells in the striatum ipsilateral to the lesion compared to the contralateral striatum or to the striatum of normal rats. This increase was mostly evident at 3 weeks postlesion and tended to decrease toward normal levels at 6, 10, and 18 weeks postlesion. In unlesioned animals, l-DOPA administration did not induce changes in the expression of calretinin. In unilaterally lesioned animals, l-DOPA reversed the increase in the number of calretinin-positive cells induced 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 suggests that striatal calretinin neurons are sensitive to dopamine depletion. Increased expression of calretinin in striatal cells may be consequent to enhanced striatal excitatory input.
Mura
A
A
Behavioral Neurobiology Laboratory, Swiss Federal Institute of Technology, Schorenstrasse 16, Zurich, Schwerzenbach, CH-8603, Switzerland. mura@toxi.biolethz.ch
Feldon
J
J
Mintz
M
M
D000818:Animals; D064032:Calbindin 2; D002135:Calcium-Binding Proteins / Q000096:biosynthesis; D002452:Cell Count / Q000187:drug effects; D003342:Corpus Striatum / Q000166:cytology / Q000378:metabolism*; D004195:Disease Models, Animal; D004298:Dopamine / Q000172:deficiency / Q000378:metabolism*; D004334:Drug Administration Schedule; D007150:Immunohistochemistry; D007274:Injections, Intraperitoneal; D007980:Levodopa / Q000008:administration & dosage*; D008297:Male; D008474:Medial Forebrain Bundle / Q000187:drug effects / Q000473:pathology; D008845:Microinjections; D019581:Neuropil / Q000378:metabolism / Q000473:pathology; D016627:Oxidopamine; D010302:Parkinson Disease, Secondary / Q000139:chemically induced / Q000188:drug therapy / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D064030:S100 Calcium Binding Protein G / Q000096:biosynthesis* / Q000187:drug effects; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism
C576512:Calb2 protein, rat; D064032:Calbindin 2; D002135:Calcium-Binding Proteins; D064030:S100 Calcium Binding Protein G; D007980:Levodopa; D016627:Oxidopamine; D014446:Tyrosine 3-Monooxygenase; D004298:Dopamine