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High‐intensity treadmill running impairs cognitive behavior and hippocampal synaptic plasticity of rats via activation of inflammatory response
Author(s) -
Sun Lina,
Li Xiaolong,
Wang Fei,
Zhang Jun,
Wang Dandan,
Yuan Li,
Wu Meina,
Wang Zhaojun,
Qi Jinshun
Publication year - 2017
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.23996
Subject(s) - hippocampal formation , long term potentiation , hippocampus , synaptic plasticity , microglia , barnes maze , p38 mitogen activated protein kinases , neuroscience , morris water navigation task , medicine , open field , mapk/erk pathway , neuroplasticity , ltp induction , psychology , inflammation , endocrinology , chemistry , phosphorylation , spatial learning , biochemistry , receptor
Although appropriate exercise is beneficial for enhancing brain functions, high‐intensity exercise (HIE)‐induced cognitive dysfunction is causing more and more concerns nowadays. In the present study, we observed the effects of high‐intensity treadmill running on the spatial learning of the adult Sprague Dawley male rats in Y‐maze ( n = 16 per group), and investigated its possible electrophysiological and molecular mechanisms by examining in vivo hippocampal long‐term potentiation (LTP), central inflammatory responses, and JNK/p38/ERK signal pathway. The Y‐maze active avoidance test showed that high‐intensity treadmill running impaired spatial learning ability of rats, with increased error times and prolonged training time in recognizing safety condition. Associated with the cognitive dysfunction, the induction and maintenance of hippocampal LTP were also impaired by the HIE. Furthermore, accompanied by elevated levels of inflammatory factors IL‐1β, TNF‐α, and iNOS, overactivation of microglia and astrocytes was also found in the CA1 region of hippocampus in the excessive exercise group, indicating an inflammatory response induced by HIE. In addition, Western blot assay showed that the phosphorylation of JNK/p38/ERK proteins was enhanced in the exercise group. These results suggest that exercise stress–induced neuronal inflammatory responses in the hippocampus are associated with HIE‐induced cognitive deficits, which may be involved in the upregulation of the JNK/p38/ERK pathway. © 2016 Wiley Periodicals, Inc.