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 Ca 2+ channels. Therefore, we investigated changes in the expressions of calcium channel subunits (Ca v1.2/α 1C, Ca v1.3/ α 1D, Ca v2.1/α 1A, and Ca v2.2/α 1B) in nNOS knock-out (-/-) (nNOS (-/-)) mouse cerebellum using an immunohistochemical approach. We found that the immunoreactivities of the Ca v1.2 and Ca v1.3 subunits were reduced in the cell bodies of Purkinje cells in these mice and that the signal of the Ca v1.2 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 Ca v1.2 and Ca v1.3 subunits.
- Calcium channel subunit
- Neuronal NO synthase (nNOS) knock-out (-/-) mice
- Nitric oxide (NO)