Immunohistochemical study of the distribution of neuronal voltage-gated calcium channels in the nNOS knock-out mouse cerebellum.
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.
Kim
Myeung Ju
MJ
Department of Anatomy, Cheju National University College of Medicine, 1 Ara 1-Dong, Jeju-Si, Jeju-Do 690-756, South Korea.
Chung
Yoon Hee
YH
Joo
Kyeung Min
KM
Oh
Goo Taeg
GT
Kim
Jaewoo
J
Lee
Bonghee
B
Cha
Choong Ik
CI
D000818:Animals; D015220:Calcium Channels / Q000378:metabolism*; D002531:Cerebellum / Q000166:cytology* / Q000378:metabolism; D005786:Gene Expression Regulation / Q000235:genetics*; D007150:Immunohistochemistry / Q000379:methods; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009474:Neurons / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000172:deficiency / Q000235:genetics*; D052248:Nitric Oxide Synthase Type I; D021122:Protein Subunits / Q000378:metabolism
D015220:Calcium Channels; D021122:Protein Subunits; D019001:Nitric Oxide Synthase; D052248:Nitric Oxide Synthase Type I; C496321:Nos1 protein, mouse