Electroacupuncture (EA) is used to treat a variety of inflammatory diseases; however, the neurophysiological mechanisms underlying EA's anti-inflammatory effect remain unclear. Accumulating evidence suggests that the sympathetic nervous system regulates immunologic and inflammatory responses and thus we hypothesized that this system could be involved in EA's anti-inflammatory effect (EA-AI). The goal of the present study was to evaluate whether the sympathetic nervous system plays a critical role in EA-AI using a mouse air pouch inflammation model. We found that bilateral low-frequency (1 Hz) EA applied to the Zusanli acupoint significantly suppressed the number of zymosan-induced leukocytes migrating into the air pouch. Furthermore, double-labeling immunohistochemical experiments showed that EA stimulation increased Fos expression in choline acetyltransferase (ChAT)-positive sympathetic pre-ganglionic neurons in the intermediolateral region of thoracic spinal cord segments. Chemical sympathetic denervation by intraperitoneal injection of 6-hydroxydopamine (which spares sympathetic adrenal medullary innervation) significantly inhibited EA-AI. In contrast, adrenalectomy did not alter EA-AI. Finally, systemic propranolol administration significantly inhibited EA's anti-inflammatory effect, suggesting that β-adrenoceptors are involved. Collectively, these results suggest that EA produces an anti-inflammatory effect in this mouse air pouch model by activating the sympathetic nervous system leading to the release of catecholamines from post-ganglionic nerve terminals, which act on β-adrenoceptors on immune cells to inhibit their migration.
Bibliographical noteFunding Information:
This work was supported by the SRC program of KOSEF (R11-2005-014). In addition, this study was supported by a Research Fund from the Research Institute for Veterinary Science (RIVS) in the College of Veterinary Medicine, Seoul National University.
- Air pouch
- Sympathetic pre-ganglionic neuron