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Generation and characterization of mutant mice lacking ryanodine receptor type 3
H Takeshima1, T Ikemoto, M Nishi
1Department of Pharmacology, Faculty of Medicine, University of Tokyo, Bunkyo-ku, Tokyo 113, Japan.
The Journal of Biological Chemistry
|August 16, 1996
Summary
Mice lacking the ryanodine receptor type 3 (RyR-3) showed normal growth but increased locomotor activity. This suggests RyR-3 deficiency impacts central nervous system neurons, impacting Ca2+ signaling.
Area of Science:
- Molecular Biology
- Neuroscience
- Physiology
Background:
- The ryanodine receptor type 3 (RyR-3) is a Ca2+-induced Ca2+ release channel found in various cell types.
- The physiological functions of RyR-3 in vivo remain largely unknown.
Purpose of the Study:
- To investigate the in vivo physiological roles of RyR-3.
- To understand the consequences of RyR-3 deficiency.
Main Methods:
- Gene targeting was used to generate RyR-3 knockout mice.
- Phenotypic analysis included assessment of growth, reproduction, skeletal muscle function, smooth muscle, lymphocytes, and locomotor activity.
Main Results:
- RyR-3 knockout mice exhibited normal growth and reproduction.
- Skeletal muscle Ca2+ sensitivity was altered, but excitation-contraction coupling remained normal.
- No significant disturbances were observed in smooth muscle or lymphocytes.
- Mutant mice displayed a 2-fold increase in locomotor activity.
Conclusions:
- The absence of RyR-3 does not cause gross abnormalities.
- RyR-3 deficiency is linked to abnormalities in certain central nervous system neurons.
- These findings suggest a role for RyR-3-mediated Ca2+ signaling in neuronal function.
