The Stress Reducing Effects of Acupuncture in a Rat Model of Chronic Stress

Abstract

There is a growing body of evidence that links chronic stress to the development of numerous disease processes including cardiovascular disease, cancer and obesity. Electro-acupuncture (EA) is a useful adjunct therapy in the treatment of many disorders including stress and anxiety. Although, EA is utilized worldwide as an anxiolytic and a stress reliever, its general mechanism of action, especially with regards to chronic stress pathways, has not yet been elucidated. Hence, the overarching hypothesis for this project was that EA allays the stress response, and that it does so by affecting the two classical stress pathways: the hypothalamic-pituitary-adrenal axis (HPA) and the sympathetic nervous system (SNS). We therefore investigated the possible role of EA in lowering both central and peripheral stress hormones associated with these pathways in a chronic-stress rat model. The HPA hormones investigated in our chronic stress paradigm were brain corticotrophin relasing hormone (CRH), plasma adenocorticotropin hormone (ACTH), and serum corticosterone (CORT). The SNS response markers of interest were adrenal tyrosine hydroxylase (TH), an important enzyme in the synthesis of norepinephrine (NE), plasma neuropeptide Y (NPY) and (NE). In our chronic stress paradigm stress-induced elevations in plasma neurohormones associated with the HPA and SNS were suppressed upon treatment with EA. Although NE levels were unchanged in our model of chronic stress, EA was effective at reducing adrenal mRNA expression levels of NPY and tyrosine hydroxylase (TH). These findings were confirmed by the significant decrease of mRNA expression and immunoreactivity of corticotropin releasing hormone (CRH) and NPY, in the paraventricular nucleus (PVN). In some of the protocols EA was also able to modulate NPY receptors Y1 and Y2 in the brain PVN. Behavioral testing further confirmed the central effects of EA in allaying stress-induced depression and anxiety in our stress paradigm. Findings from blocking the HPA and SNS by RU-486 and propranolol, respectively, indicated that althought the SNS was modulated by EA, the HPA may be the main pathway responsible for the chronic-stress allaying effects of EA.