Establishment of bee venom-induced contralateral heat hyperalgesia in the rat is dependent upon central temporal summation of afferent input from the site of injury

Prolonged analgesic effect of PLGA-encapsulated bee venom on formalin-induced pain in rats

“…BV acupuncture has been known to exert a remarkable effect in relieving pain and inflammation in various acute or chronic diseases (Chen et al, 2001;Hartman et al, 1991;Kim et al, 2005;Kwon et al, 2001a,b;Son et al, 2007). On the other hand, the BV injection also induces a systemic or local allergic response, accompanying fever, tonic pain and edema, itching, etc.…”

“…On the other hand, it has been reported that animals show most types of nociception and hypersensitivity following subcutaneous treatment of BV (Lariviere and Melzack, 1996). The BV test, a well-established experimental animal model mimicking honeybee sting-induced natural tissue injury, is produced by subcutaneous injection of a given dose of honeybee venom into one hind paw (Chen et al, 2001).…”

Differential Roles of Spinal Protein Kinases C and A in Development of Primary Heat and Mechanical Hypersensitivity Induced by Subcutaneous Bee Venom Chemical Injury in the Rat

“…However, in the central processes of the BV-induced PSN and MIH hypersensitivity, which are primarily dependent upon the ongoing primary afferent input and its central temporal summation [15,30], DAG-PKC and cAMP-PKA are likely to be coactivated. The proposed roles of spinal PKC and PKA in the central processes of the BVinduced different types of nociception and hypersensitivity are shown in a schematic drawing (fig.…”

“…Regarding the central neural mechanisms of the BV-induced MIH hypersensitivity, we have demonstrated that: (1) the BV-induced MIH hypersensitivity is a consequence of central sensitization because after transection of the sciatic nerve 2 h after BV injection into the ipsilateral hind paw pad, the well-established MIH hypersensitivity was not blocked [21]; (2) the establishment of the MIH hypersensitivity-dependent central sensitization requires a time window for central summation of the ongoing primary afferent impulses in the spinal cord and the time window is likely to be determined by the intensity of injury, e.g. the more intense the peripheral injury is the more easily the central neurons are sensitized [30]; (3) activation of the descending nociceptive facilitatory pathway of the rostral medial medulla spinal cord is involved in the production of MIH hypersensitivity, since chemical destruction of the bilateral rostral medial medulla can eliminate the BV-induced PSN and MIH hypersensitivity but without any influence on primary heat and mechanical hypersensitivity [13]; (4) spinal NMDA and non-NMDA as well as NK1/2 receptors are likely to be activated in the central processes of MIH hypersensitivity because intrathecal application of the antagonists against these receptors could significantly block the induction and maintenance of MIH hypersensitivity as well as PSN [11,21,22].…”

Mu-Opioid Receptor in the Nucleus Submedius: Involvement in Opioid-Induced Inhibition of Mirror-Image Allodynia in a Rat Model of Neuropathic Pain

“…In these models, the underlying mechanisms of peripheral and central increased sensitivity have been well investigated [4,5]. In addition to ongoing inputs from primary afferents of the injured side, central sensitization may contribute to mirror-image hypersensitivity [6], and may be closely related to a central change mediated by spinal commissural interneurons [7]. Furthermore, the brainstem's descending facilitatory system from the rostral medial medulla (RMM) has been found to contribute to secondary hypersensitivity, as well as mirror-image pain, but not primary hypersensitivity [4,5].…”