Immunohistochemical study of the distribution of neuronal voltage-gated calcium channels in the nNOS knock-out mouse cerebellum

Neuroscience Letters
Myeung Ju KimChoong Ik Cha

Abstract

Nitric oxide (NO) participates in synaptic plasticity, neuronal development, and apoptosis. The involvement of NO and ionic calcium in synaptic plasticity imply that NO may exert an effect on Ca2+ channels. Therefore, we investigated changes in the expressions of calcium channel subunits (Cav1.2/alpha1C, Cav1.3/alpha(1D), Cav2.1/alpha1A, and Cav2.2/alpha1B) in nNOS knock-out (-/-) (nNOS((-/-))) mouse cerebellum using an immunohistochemical approach. We found that the immunoreactivities of the Cav1.2 and Cav1.3 subunits were reduced in the cell bodies of Purkinje cells in these mice and that the signal of the Cav1.2 subunit in neurons and of the Cav1.3 subunit in the neuropils of nNOS((-/-)) mice cerebellar nuclei were significantly down-regulated. We show, for the first time, that prolonged NO deficiency in the cerebellum may affect calcium channel protein expressions, especially, of the Cav1.2 and Cav1.3 subunits.

References

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Citations

Jun 9, 2012·Human Molecular Genetics·Somisetty V SatheeshHans Gerd Nothwang
Apr 9, 2005·IEEE Transactions on Nanobioscience·Robert J French, Gerald W Zamponi
May 4, 2016·Cellular and Molecular Neurobiology·Daniel C Moreira-LoboFernando A Oliveira
Jun 30, 2018·Alcoholism, Clinical and Experimental Research·Dylan ToddDaniel J Bonthius
Nov 22, 2008·Biochemical Society Transactions·Ilaria PelizzoniFranca Codazzi

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