4.6 Article

Exercise prevents the impairment of learning and memory in prenatally phthalate-exposed male rats by improving the expression of plasticity-related proteins

期刊

BEHAVIOURAL BRAIN RESEARCH
卷 413, 期 -, 页码 -

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ELSEVIER
DOI: 10.1016/j.bbr.2021.113444

关键词

Di-(2-ethylhexyl)-phthalate; Brain-derived neurotrophic factor; N-methyl-D-aspartic acid receptor; Activity-regulated cytoskeleton associated protein; Exercise

资金

  1. Ministry of Science and Technology of Taiwan [MOST 1032410H037011]

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Regular exercise has been shown to enhance neuroplasticity and improve functional outcomes after brain injuries. This study investigated the impact of prenatal DEHP exposure on hippocampal Arc expression and the protective role of exercise in male rats exposed to DEHP. The results demonstrated that DEHP exposure led to impaired spatial learning and memory, along with down-regulation of BDNF, NMDAR, Arc, and synaptophysin. However, aerobic exercise during childhood-adolescence prevented these impairments by restoring the expression of key proteins related to neuroplasticity.
Regular exercise has been identified to facilitate neuroplasticity that maximize functional outcome after brain injuries. Brain-derived neurotrophic factor (BDNF) has emerged as a key facilitator of neuroplasticity after exercise. The activity-regulated cytoskeleton associated protein (Arc) is induced by BDNF and N-methyl-D-aspartic acid receptor (NMDAR), contributing to functional modification of neuroplasticity in the hippocampus. Meanwhile, early-life exposure to neuroendocrine disruptor di-(2-ethylhexyl)-phthalate (DEHP) is a risk factor for behavioral deficits, but the mechanisms responsible for DEHP-induced neurotoxicity are not well understood. The purpose of this study is to investigate whether hippocampal Arc expression is impaired by DEHP exposure and to examine the protective role of exercise in the prenatally DEHP-exposed male rats. Sprague Dawley dams were fed with vehicle or DEHP during gestation. The male offspring were trained to treadmill running for 5 weeks followed by examination of behavioral and biochemical outcomes. The results showed that DEHP-exposed rats exhibited impairment of spatial learning and memory as well as down-regulations of BDNF, NMDAR, Arc, and synaptophysin. Importantly, aerobic exercise during childhood-adolescence prevented the impairment of learning and memory by recovering the expressions of BDNF, NMDAR, Arc, and synaptophysin. These findings suggest that exercise may provide beneficial effects on ameliorating the impairment of neuroplasticity in the prenatally DEHP-exposed male rats at late adolescence.

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