Chemical or surgical sympathectomy prevents mechanical hyperalgesia induced by intraplantar injection of bee venom in rats.

Sympathetic postganglionic neurons play an important role in pathological pain. This study was designed to investigate the role of sympathetic postganglionic neurons in inflammatory pain induced by bee venom (BV). The effects of chemical (with guanethidine or 6-hydroxydopamine) or surgical sympathectomy on BV-induced spontaneous foot lifting, mechanical hyperalgesia, and edema were observed. The results showed that surgical or chemical sympathectomy significantly attenuated an increase in paw volume (PV) and a decrease in paw withdrawal mechanical threshold (PWMT) induced by BV; however, these interventions had no effect on BV-evoked spontaneous foot lifting. Furthermore, pharmacological blockade of adrenergic receptors via systemic delivery of phentolamine, an alpha-adrenergic receptor antagonist, or prazosin, an alpha1-adrenergic receptor antagonist, produced similar inhibitory effects on BV-induced changes in PV and PWMT, however, yohimbine, an alpha2-adrenergic receptor antagonist, had no such effects. These results suggest that the interaction between sympathetic postganglionic neurons and primary afferent neurons via alpha1-adrenergic receptor play key roles in BV-induced mechanical hyperalgesia and inflammatory swelling but not in spontaneous foot lifting.