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Alteration of calmodulin distribution does not accompany dopaminergic supersensitization of the mouse striatum
Author(s) -
May P. C.,
Osterburg H. H.,
Mandel R. J.,
Morgan D. G.,
Randall P. K.,
Finch C. E.
Publication year - 1987
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.490170307
Subject(s) - calmodulin , striatum , dopaminergic , dopamine , endocrinology , chemistry , dopamine receptor , medicine , radioimmunoassay , biology , neuroscience , biochemistry , enzyme
Membrane‐bound calmodulin increases following dopaminergic supersensitization of the rat striatum. To assess the generality of this relationship, mice were treated with two different supersensitization paradigms. Calmodulin levels and subcellular distribution were determined by radioimmunoassay. Chronic haloperidol treatment increased striatal D 2 dopamine receptor density by 25% but had no effect on membrane‐bound calmodulin levels. Similarly, 6‐hydroxy‐dopamine (6‐OHDA) lesions depleted striatal dopamine content > 95% without affecting membrane‐bound calmodulin. In contrast, soluble calmodulin levels decreased by 15% in the 6‐OHDA‐lesioned striatum, suggesting that soluble calmodulin is enriched in presynaptic dopaminergic terminals. We conclude that dopaminergic supersensitization can occur in the mouse striatum in the absence of any change in calmodulin distribution.