Electroacupuncture Ameliorates Learning and Memory via Activation of the CREB Signaling Pathway in the Hippocampus to Attenuate Apoptosis after Cerebral Hypoperfusion
Author(s) -
Xiaohua Han,
Xiuxiu Zhao,
Min Lu,
Fang Liu,
Feng Guo,
Jinghui Zhang,
Xiaolin Huang
Publication year - 2013
Publication title -
evidence-based complementary and alternative medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.552
H-Index - 90
eISSN - 1741-4288
pISSN - 1741-427X
DOI - 10.1155/2013/156489
Subject(s) - creb , morris water navigation task , hippocampus , electroacupuncture , hippocampal formation , apoptosis , neuroscience , signal transduction , memory impairment , medicine , pharmacology , chemistry , psychology , endocrinology , cognition , acupuncture , pathology , transcription factor , biochemistry , alternative medicine , gene
Studies have shown that electroacupuncture (EA) ameliorates learning and memory after ischemic injury. However, there have been few studies elucidating the mechanisms of EA on learning and memory in cerebral hypoperfusion. In this study, we explored the cAMP response element-binding protein (CREB) signaling pathway-mediated antiapoptotic action involved in EA-induced improvement of learning and memory. EA at GV20 and GV14 acupoints was applied in cerebral hypoperfusion rats. A Morris water maze task was performed, and the immunoreactivities of pCREB, Bcl-2, and Bax in the hippocampal CA1 area were evaluated by the Western blotting technique. Our findings indicated that (1) EA ameliorated spatial learning and memory impairment in cerebral hypoperfusion rats; (2) EA increased the immunoreactivities of pCREB and Bcl-2 and decreased the immunoreactivity of Bax; (3) intracerebroventricular administration of H89 (the inhibitor of protein kinase A) blocked EA-induced, pCREB-mediated antiapoptotic action and improved learning and memory. These results suggest that EA can ameliorate learning and memory via activation of the CREB signaling pathway in the hippocampus to attenuate apoptosis after cerebral hypoperfusion.
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