Immunohistochemical study on the expression of calcium binding proteins (calbindin-D28k, calretinin, and parvalbumin) in the cerebral cortex and in the hippocampal region of nNOS knock-out(-/-) mice.
10.5115/acb.2011.44.2.106
- Author:
Yu Jin CHO
1
;
Jae Chul LEE
;
Bong Gu KANG
;
Jaeyeol AN
;
Hyeon Suk SONG
;
Onju SON
;
Do Hyun NAM
;
Choong Ik CHA
;
Kyeung Min JOO
Author Information
1. Department of Anatomy, College of Medicine, Seoul National University, Seoul, Korea. kmjoo@snu.ac.kr
- Publication Type:Original Article
- Keywords:
Calcium binding proteins;
Cerebral cortex and hippocampal region;
Immunohistochemistry;
Neuronal nitric oxide synthase (nNOS);
nNOS knock-out(-/-) mice
- MeSH:
Animals;
Calcium;
Calcium-Binding Protein, Vitamin D-Dependent;
Calcium-Binding Proteins;
Carrier Proteins;
Cerebral Cortex;
Homeostasis;
Immunohistochemistry;
Mice;
Neurons;
Nitric Oxide;
Nitric Oxide Synthase;
Synaptic Transmission
- From:Anatomy & Cell Biology
2011;44(2):106-115
- CountryRepublic of Korea
- Language:English
-
Abstract:
Nitric oxide (NO) modulates the activities of various channels and receptors to participate in the regulation of neuronal intracellular Ca2+ levels. Ca2+ binding protein (CaBP) expression may also be altered by NO. Accordingly, we examined expression changes in calbindin-D28k, calretinin, and parvalbumin in the cerebral cortex and hippocampal region of neuronal NO synthase knockout(-/-) (nNOS-/-) mice using immunohistochemistry. For the first time, we demonstrate that the expression of CaBPs is specifically altered in the cerebral cortex and hippocampal region of nNOS-/- mice and that their expression changed according to neuronal type. As changes in CaBP expression can influence temporal and spatial intracellular Ca2+ levels, it appears that NO may be involved in various functions, such as modulating neuronal Ca2+ homeostasis, regulating synaptic transmission, and neuroprotection, by influencing the expression of CaBPs. Therefore, these results suggest another mechanism by which NO participates in the regulation of neuronal Ca2+ homeostasis. However, the exact mechanisms of this regulation and its functional significance require further investigation.
