Moderate Treadmill Exercise Protects Synaptic Plasticity of the Dentate Gyrus and Related Signaling Cascade in a Rat Model of Alzheimer’s Disease
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- 作者：An T. Dao ; Munder A. Zagaar ; Karim A. Alkadhi
- 关键词：Treadmill exercise ; Alzheimer’s disease ; Basal synaptic transmission ; Early LTP ; Memory ; BDNF
- 刊名：Molecular Neurobiology
- 出版年：2015
- 出版时间：December 2015
- 年：2015
- 卷：52
- 期：3
- 页码：1067-1076
- 全文大小：882 KB
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Munder A. Zagaar (1)
Karim A. Alkadhi (1)
1. Department of PPS, College of Pharmacy, University of Houston, Houston, TX, 77204-5037, USA - 刊物主题：Neurosciences; Neurobiology; Cell Biology; Neurology;
- 出版者：Springer US
- ISSN：1559-1182
文摘
The dentate gyrus (DG) of the hippocampus is known to be more resistant to the effects of various external factors than other hippocampal areas. This study investigated the neuroprotective effects of moderate treadmill exercise on early-phase long-term potentiation (E-LTP) and its molecular signaling pathways in the DG of amyloid β rat model of sporadic Alzheimer’s disease (AD). Animals were preconditioned to run on treadmill for 4 weeks and concurrently received ICV infusion of Aβ1-2 peptides (250 pmol/day) during the third and fourth weeks of exercise training. We utilized in vivo electrophysiological recordings to assess the effect of exercise and/or AD pathology on basal synaptic transmission and E-LTP magnitude of the perforant pathway synapses in urethane-anesthetized rats. Immunoblotting analysis was used to quantify changes in the levels of learning and memory-related key signaling molecules. The AD-impaired basal synaptic transmission and suppression of E-LTP in the DG were prevented by prior moderate treadmill exercise. In addition, exercise normalized the basal levels of memory and E-LTP-related signaling molecules including Ca2+/calmodulin-dependent protein kinase II (CaMKII), calcineurin (PP2B), and brain-derived neurotrophic factor (BDNF). Exercise also prevented the reduction of phosphorylated CaMKII and aberrant increase of PP2B seen after E-LTP induction in amyloid-infused rats. Our data suggests that by restoring the balance of kinase–phosphatase, 4 weeks of moderate treadmill exercise prevents DG synaptic deficits and deleterious alterations in signaling pathways associated with AD. Keywords Treadmill exercise Alzheimer’s disease Basal synaptic transmission Early LTP Memory BDNF