2010Anatomy & Cell BiologyOpen access

Immunohistochemical study on the expression of calcium binding proteins (calbindin-D28k, calretinin, and parvalbumin) in the cerebellum of the nNOS knock-out(-/-) mice

Jae Chul Lee, Yoon Hee Chung, Yu Jin Cho, Jandi Kim, Nahee Kim, Choong Ik, Kyeung Min Joo

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Abstract

Nitric Oxide (NO) actively participates in the regulation of neuronal intracellular Ca(2+) levels by modulating the activity of various channels and receptors. To test the possibility that modulation of Ca(2+) 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 Ca(2+) homeostasis.

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Nitric Oxide (NO) actively participates in the regulation of neuronal intracellular Ca(2+) levels by modulating the activity of various channels and receptors. To test the possibility that modulation of Ca(2+) 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 Ca(2+) homeostasis.

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Available abstract

Nitric Oxide (NO) actively participates in the regulation of neuronal intracellular Ca(2+) levels by modulating the activity of various channels and receptors. To test the possibility that modulation of Ca(2+) 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 Ca(2+) homeostasis.

Key concepts: Calretinin, Parvalbumin, Calbindin, Calcium-binding protein, Cerebellum, Immunohistochemistry, Cell biology, Chemistry

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Immunohistochemical study on the expression of calcium binding proteins (calbindin-D28k, calretinin, and parvalbumin) in the cerebellum of the nNOS knock-out(-/-) mice — Research Paper | ScholarLens