Skip to main page content
Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
, 2017, 2357653

The Role of MAPK and Dopaminergic Synapse Signaling Pathways in Antidepressant Effect of Electroacupuncture Pretreatment in Chronic Restraint Stress Rats


The Role of MAPK and Dopaminergic Synapse Signaling Pathways in Antidepressant Effect of Electroacupuncture Pretreatment in Chronic Restraint Stress Rats

Xinjing Yang et al. Evid Based Complement Alternat Med.


Acupuncture has demonstrated the function in ameliorating depressive-like behaviors via modulating PKA/CREB signaling pathway. To further confirm the antidepressant mechanism of EA on the mitogen-activated protein kinase (MAPK) and dopaminergic synapse signaling pathways, 4 target proteins were detected based on our previous iTRAQ analysis. Rats were randomly divided into control group, model group, and electroacupuncture (EA) group. Except for the control group, all rats were subjected to 28 days of chronic restraint stress (CRS) protocols to induce depression. In the EA group, EA pretreatment at Baihui (GV20) and Yintang (GV29) was performed daily (1 mA, 2 Hz, discontinuous wave, 20 minutes) prior to restraint. The antidepressant-like effect of EA was measured by body weight and open-field test. The protein levels of DAT, Th, Mapt, and Prkc in the hippocampus were examined by using Western blot. The results showed EA could ameliorate the depression-like behaviors and regulate the expression levels of Prkc and Mapt in CRS rats. The effect of EA on DAT and Th expression was minimal. These findings implied that EA pretreatment could alleviate depression through modulating MAPK signaling pathway. The role of EA on dopaminergic synapse signaling pathways needs to be further explored.


Figure 1
Figure 1
Effects of CRS and EA pretreatment on body weight and locomotor activity in the open-field test before and after treatment (x-  ± SD, n = 15). (a) Body weight (g). (b) and (c) Open-field test. ∗∗p < 0.01 as compared with control group; ##p < 0.01 as compared with model group.
Figure 2
Figure 2
Candidate proteins expression change in three groups. IOD: the integrated optical density; p < 0.05, ∗∗p < 0.01 as compared with control group; #p < 0.05, as compared with model group.
Figure 3
Figure 3
Representative Western blots showing levels of DAT, Th, Prkc, and Mapt in the hippocampus of the following groups (n = 4 per group, repeated 3 times): control, model, and EA.

Similar articles

See all similar articles

Cited by 2 PubMed Central articles


    1. Thompson C., Ostler K., Peveler R. C., Baker N., Kinmonth A. Dimensional perspective on the recognition of depressive symptoms in primary care: the Hampshire depression project 3. British Journal of Psychiatry. 2001;179(4):317–323. doi: 10.1192/bjp.179.4.317. - DOI - PubMed
    1. Carroll L. J., Cassidy J. D., Côté P. Factors associated with the onset of an episode of depressive symptoms in the general population. Journal of Clinical Epidemiology. 2003;56(7):651–658. doi: 10.1016/S0895-4356(03)00118-5. - DOI - PubMed
    1. Moraes M. M. T., Galvão M. C., Cabral D., et al. Propentofylline prevents sickness behavior and depressive-like behavior induced by lipopolysaccharide in rats via neuroinflammatory pathway. PLoS ONE. 2017;12(1) doi: 10.1371/journal.pone.0169446.0169446 - DOI - PMC - PubMed
    1. Kubitz N., Mehra M., Potluri R. C., Garg N., Cossrow N. Characterization of treatment resistant depression episodes in a cohort of patients from a US commercial claims database. PLoS ONE. 2013;8(10) doi: 10.1371/journal.pone.0076882.e76882 - DOI - PMC - PubMed
    1. Fava M. Diagnosis and definition of treatment-resistant depression. Biological Psychiatry. 2003;53(8):649–659. doi: 10.1016/S0006-3223(03)00231-2. - DOI - PubMed

LinkOut - more resources