Medical Research

Electroacupuncture at St36 prevents stress induced increases in neuropeptide Y in rats

Kristen Sparrow • March 03, 2012

This study confirms the value of electroacupuncture at St36 in reducing one of the sympathetic pathways involved in the stress response and adds some additional evidence. This effect was discussed in different contexts here and here. In the first post electroacupuncture at St36 was used for migraine prophylaxis and was found to decrease the stress response (decrease LFR/HFR.) In the second post, electroacupuncture was used to decrease blood pressure.
Exp Biol Med (Maywood). 2012 Jan 1;237(1):18-23. Epub 2011 Dec 7.

Acupuncture at ST36 prevents chronic stress-induced increases in neuropeptide Y in rat.
Eshkevari L, Egan R, Phillips D, Tilan J, Carney E, Azzam N, Amri H, Mulroney SE.
Department of Nursing, School of Nursing and Health Studies, Georgetown University Medical Center, Washington, DC 20007, USA.

Chronic stress, as seen in post-traumatic stress disorder, can exacerbate existing diseases. Electroacupuncture (EA) has been proposed to treat chronic stress, although information on its efficacy or mechanism(s) of action is limited. While many factors contribute to the chronic stress response, the sympathetic peptide, neuropeptide Y (NPY), has been shown to be elevated in chronic stress and is hypothesized to contribute to the physiological stress response. Our objective was to determine if EA at acupuncture point stomach 36 (ST(36)) is effective in mitigating cold stress-induced increase in NPY in rats. Both pretreatment and concomitant treatment with EA ST(36) effectively suppressed peripheral and central NPY after 14 d of cold stress (P < 0.05). The effect was specific, as NPY in Sham-EA rats was not different than observed in stress-only rats. Additionally, the effect of EA ST(36) was long-lasting, as NPY levels remained suppressed despite early cessation of EA ST(36), while exposure to cold stress was continued. In the paraventricular nucleus (PVN), it was notable that changes in NPY mirrored plasma NPY levels, and that the significant elevation in PVN Y1 receptor observed with stress was also prevented with EA ST(36). The findings indicate that EA ST(36) is effective in preventing one of the sympathetic pathways stimulated during chronic stress, and thus may be a useful adjunct therapy in stress-related disorders.