1. Treadmill exercise inhibits hippocampal apoptosis through enhancing N -methyl-D-aspartate receptor expression in the MK-801-induced schizophrenic mice
- Author
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Tae-Woon Kim, Chang-Ju Kim, Sang-Bin Baek, Jin Woo Chung, and Jinhee Seo
- Subjects
medicine.medical_specialty ,biology ,business.industry ,Receptor expression ,Cytochrome c ,Glutamate receptor ,Hippocampus ,Physical Therapy, Sports Therapy and Rehabilitation ,Hippocampal formation ,Endocrinology ,nervous system ,Apoptosis ,Internal medicine ,medicine ,biology.protein ,NMDA receptor ,Orthopedics and Sports Medicine ,Receptor ,business - Abstract
Schizophrenia is a severe mental disorder characterized by abnormal mental functioning and disruptive behaviors. Abnormal expression of N-methyl-D-aspartate (NMDA) receptor, one of the glutamate receptor subtypes, has also been suggested to contribute to the symptoms of schizophrenia. The effect of treadmill exercise on schizophrenia-induced apoptosis in relation with NMDA receptor has not been evaluated. In the present study, we investigated the effect of treadmill exercise on neuronal apoptosis in the hippocampus using MK-801-induced schizophrenic mice. MK-801 was intraperitoneally injected once a day for 2 weeks. The mice in the exercise groups were forced to run on a treadmill exercise for 60 min, once a day for 2 weeks. In the present results, repeated injection of the NMDA receptor antagonist MK-801 reduced expression of NMDA receptor in hippocampal CA2-3 regions. MK-801 injection increased casapse-3 expression and enhanced cytochrome c release in the hippocampus. The ratio of Bax to Bcl-2 was higher in the MK-801-induced schizophrenia mice than the normal mice. In contrast, treadmill exercise enhanced NMDA receptor expression, suppressed caspae-3 activation and cytochrome c release, and inhibited the ratio of Bax to Bcl-2. Based on present finding, we concluded that NMDA receptor hypofunctioning induced neuronal apoptosis in MK-801-induced schizophrenic mice. Treadmill exercise suppressed neuronal apoptosis through enhancing NMDA receptor expression in schizophrenic mice.
- Published
- 2014