Immunohistochemical study of the distribution of neuronal voltage-gated calcium channels in the nNOS knock-out mouse cerebellum
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- Immunohistochemical study of the distribution of neuronal voltage-gated calcium channels in the nNOS knock-out mouse cerebellum
- M J Kim; Y H Chung; K M Joo; Goo Taeg Oh; J Kim; B Lee; C I Cha
- Bibliographic Citation
- Neuroscience Letters, vol. 369, no. 1, pp. 39-43
- Publication Year
- 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/α1C, Cav1.3/ α1D, Cav2.1/α1A, and Ca v2.2/α1B) 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 Ca v1.3 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.
- Calcium channel subunitCerebellumImmunohistochemistryNeuronal NO synthase (nNOS) knock-out (-/-) miceNitric oxide (NO)
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