Open AccessAntidepressant effect of electroacupuncture regulates signal targeting in the brain and increases brain-derived neurotrophic factor levels
Author(s) -
Dongmei Duan,
Ya Tu,
Ping Liu,
Shuliang Jiao
Publication year - 2016
Publication title -
neural regeneration research/neural regeneration research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.93
H-Index - 38
eISSN - 1876-7958
pISSN - 1673-5374
DOI - 10.4103/1673-5374.193238
Subject(s) - electroacupuncture , creb , brain derived neurotrophic factor , neurotrophic factors , protein kinase a , cyclic adenosine monophosphate , medicine , endocrinology , cyclic amp response element binding protein , adenosine , tropomyosin receptor kinase b , antidepressant , glutamate receptor , hippocampus , pharmacology , kinase , chemistry , biology , microbiology and biotechnology , receptor , acupuncture , biochemistry , transcription factor , alternative medicine , pathology , gene
Electroacupuncture improves depressive behavior faster and with fewer adverse effects than antidepressant medication. However, the antidepressant mechanism of electroacupuncture remains poorly understood. Here, we established a rat model of chronic unpredicted mild stress, and then treated these rats with electroacupuncture at Yintang (EX-HN3) and Baihui (DU20) with sparse waves at 2 Hz and 0.6 mA for 30 minutes, once a day. We found increased horizontal and vertical activity, and decreased immobility time, at 2 and 4 weeks after treatment. Moreover, levels of neurotransmitters (5-hydroxytryptamine, glutamate, and γ-aminobutyric acid) and protein levels of brain-derived neurotrophic factor and brain-derived neurotrophic factor-related proteins (TrkB, protein kinase A, and phosphorylation of cyclic adenosine monophosphate response element binding protein) were increased in the hippocampus. Similarly, protein kinase A and TrkB mRNA levels were increased, and calcium-calmodulin-dependent protein kinase II levels decreased. These findings suggest that electroacupuncture increases phosphorylation of cyclic adenosine monophosphate response element binding protein and brain-derived neurotrophic factor levels by regulating multiple targets in the cyclic adenosine monophosphate response element binding protein signaling pathway, thereby promoting nerve regeneration, and exerting an antidepressive effect.