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Anatomy & Cell Biology ; : 64-71, 2010.
Artigo em Inglês | WPRIM | ID: wpr-43656

RESUMO

Nitric Oxide (NO) actively participates in the regulation of neuronal intracellular Ca2+ levels by modulating the activity of various channels and receptors. To test the possibility that modulation of Ca2+ buffer protein expression level by NO participates in this regulatory effect, we examined expression of calbindin-D28k, calretinin, and parvalbumin in the cerebellum of neuronal NO synthase knock-out (nNOS(-/-)) mice using immunohistochemistry. We observed that in the cerebellar cortex of the nNOS(-/-) mice, expression of calbindin-D28k and parvalbumin were significantly increased while expression of calretinin was significantly decreased. These results suggest another mechanism by which NO can participate in the regulation of Ca2+ homeostasis.


Assuntos
Animais , Camundongos , Cálcio , Proteína G de Ligação ao Cálcio S100 , Proteínas de Ligação ao Cálcio , Córtex Cerebelar , Cerebelo , Homeostase , Imuno-Histoquímica , Neurônios , Óxido Nítrico , Óxido Nítrico Sintase
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