Acupuncture at ST36 prevents chronic stress-induced increases in neuropeptide Y in rat

  1. Susan E Mulroney2

+ Author Affiliations


  1. 1Department of Nursing, School of Nursing and Health Studies

  2. 2Department of Pharmacology & Physiology

  3. 3Department of Human Science, School of Nursing and Health Studies

  4. 4Department of Neuroscience

  5. 5Department of Biochemistry and Cell and Molecular Biology, Georgetown University Medical Center, Washington, DC 20007, USA
  1. Corresponding author: Ladan Eshkevari, School of Nursing and Health Studies, 421 St Mary’s Hall, 4000 Reservoir Road, NW, Washington, DC 20007, USA. Email: eshkevl@georgetown.edu

Abstract

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 (ST36) is effective in mitigating cold stress-induced increase in NPY in rats. Both pretreatment and concomitant treatment with
EA ST36 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 ST36 was long-lasting, as NPY levels remained suppressed despite early cessation of EA ST36, 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 ST36. The findings indicate that EA ST36 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.

  • Received June 23, 2011.
  • Accepted September 2, 2011.