Immunohistochemical study on the distribution of neuronal voltage-gated calcium channels in the rat cerebellum

Many neuronal processes are regulated by calcium influx through voltage-gated calcium channels (VGCCs), including protein phosphorylation, gene expression, neurotransmitter release, and firing patterns of action potential. In the present study, we have used anti-peptide antibodies directed against a...

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Published in:Brain research Vol. 865; no. 2; pp. 278 - 282
Main Authors: Chung, Yoon Hee, Shin, Chung-min, Park, Kyeong Han, Cha, Choong Ik
Format: Journal Article
Language:English
Published: London Elsevier B.V 26-05-2000
Amsterdam Elsevier
New York, NY
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Summary:Many neuronal processes are regulated by calcium influx through voltage-gated calcium channels (VGCCs), including protein phosphorylation, gene expression, neurotransmitter release, and firing patterns of action potential. In the present study, we have used anti-peptide antibodies directed against a unique sequence in rat α 1A, α 1B, α 1C and α 1D subunits of VGCCs to determine their cellular distribution in normal rat cerebellum. Throughout the molecular layer, immunoreactivity for α 1B and α 1D subunits were found in the cell bodies of basket and stellate cells as well as in the neuropil. In the Purkinje cells, only α 1C-IR was observed in the dendritic branches of Purkinje cells, whereas immunoreactivity for α 1B and α 1D subunits were rarely found in the cell bodies of Purkinje cells. Immunoreactivity for the α 1A, α 1B, and α 1D subunits were strong in the granule cell bodies, whereas α 1C-IR was not prominent in the cell bodies. In the cerebellar nuclei, a distinct band of punctate immunoreactivity for the α 1A, α 1B, α 1C, and α 1D subunits were observed. The overall results of the above localization study showed clearly that the α 1A, α 1B, α 1C and α 1D pore forming subunits of VGCCs have differential distribution in the rat cerebellum. The present studies may provide useful data for such future investigations to understand the role of calcium channels in neurological pathways.
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ISSN:0006-8993
1872-6240
DOI:10.1016/S0006-8993(00)02288-5