The bee venom (BV) model is a valid inflammatory pain model in animals and has been extended to human studies using its principle protein, mellitin. After subcutaneous (s.c.) injection of BV, long-lasting spontaneous nociception followed by thermal hyperalgesia, static allodynia, and local inflammatory response (edema) can be observed in rats. We hypothesize that (1) neurogenic components may contribute to the BV-induced inflammatory response and (2) static and dynamic mechanical allodynia may exist simultaneously in the BV model. Using different approaches including sciatic nerve transection (SCT), L4–L6 dorsal rhizotomy (DRT) and local treatment of the sciatic nerve with capsaicin, we found that SCT, DRT, and local capsaicin onto the sciatic nerve produced a significant inhibition of the BV-induced increase in volume of the injected paw, with a stronger effect of the SCT and the local capsaicin treatments than that of the DRT treatment. Static and dynamic mechanical allodynia in the BV test was assessed by measuring the paw withdrawal mechanical threshold and the paw withdrawal latency before and after the BV injection, respectively. Local capsaicin onto the sciatic nerve produced a significant inhibition of the BV-induced decrease in the paw withdrawal mechanical threshold, but not the paw withdrawal latency, of the injected paw. These findings suggest that neurogenic components, via dorsal root reflex and axon reflex mechanisms, are probably involved in the maintenance and the development of the BV-induced inflammation. In addition, the capsaicin-sensitive primary afferents may play differential roles in the development of the BV-induced static and dynamic mechanical allodynia.