In the present communication, we determined the dynamic release of amino acid transmitters from spinal dorsal horn induced by scorpion Buthus martensi Karsch (BmK) venom and a neurotoxin (BmK I). The results found that glutamate and aspartate release could be evoked significantly within the initial 30 min with the applied doses of either 0.05 and 0.01mg BmK venom or 0.01 and 0.002mg BmK I. However, γ-aminobutyric acid (GABA) release could be largely evoked during the second 30 min by the venom, but not by BmK I. The result suggested that nociceptive afferent fibers could be activated to induce excitatory amino acid release from spinal dorsal horn by nociceptive factors such as BmK I, but the delayed release of GABA might be attributed to the modulating role of some antinociceptive components in the venom.

The antihyperalgesia effect of BmK AS, a novel sodium channel-specific polypeptide modulator from Chinese scorpion venom in rats was investigated in this study. PWLs (paw withdrawal latency) were increased to 150628, 203634 and 250617% of the control by administration of BmK AS (10

In this study, the nociceptive responses induced by subcutaneous injection of scorpion BmK venom into the plantar surface of rat hind paw were quantified. The suitable dose of the venom is between 0.01 and 0.05 mg. The venom injection could induce local edema and tonicpain responses, which had lasted more than 1 h. The pain scores reached peak intensity within 20 min, and then decreased slowly. Morphine, as a classic analgesic drug, could inhibit the spontaneous nociceptive response induced by the venom. With Morphine pretreatment, the mean pain scores for the entire 60 min were significantly decreased ( P < .05). BmK I, a main lethal component, was also found to induce nociceptive responses with dose-dependent means. The nociceptive responses induced by BmK I could be partially inhibited by morphine.

The aim of this study was to assess the cell-type and distribution of highly activated neurons in rat spinal cord underlying nociceptive responses induced by scorpion BmK venom using Fos immunohistochemistry. BmK venom was intraplantarly injected into one hind paw of a conscious rat. Fos-like immunoreactive neurons were found to predominantly distribute at L4-5 segments in the rat spinal cord after BmK venom application. c-Fos labeling was most dense in the medial half portion of laminae I_/II, moderately dense in laminae V-VI and less dense in laminae III-IV, VII-X. c-Fos labeling could be detected at 0.5 h, reached the peak at 2 h, decreased steeply from 4 h and then almost disappeared at 24 h. Ten to fifty micrograms of BmK venom was deemed to be a sufficient dosage to evoke c-Fos expression. On the other hand, c-Fos expression induced by BmK venom could be suppressed partially by systemic morphine in a dose-dependent manner. The results suggest that the different extent of activities of neuronal subpopulation in the spinal cord involved in nociceptive transmission manifesting as c-Fos expression, were mainly correlated with mechanisms underlying the generation, maintenance and/or modulation of spontaneous pain and hyperalgesia evoked by BmK venom.

In the present study, the effects of scorpion Buthus martensi Karsch (BmK) venom on plasma extravasation and paw withdrawal latency (PWL) to radiant heat have been investigated in rats. BmK venom (20-200 microg/kg) by subcutaneous injection under the surface of the rat hindpaw causes dose-dependant increased plasma extravasation that could be partially inhibited by intraperitoneal (i.p.) injected morphine (6 mg/kg). Peak plasma extravasation was reached at 10 min and persisted for 60 min at a dose of 200 microg/kg. BmK venom induced cutaneous hyperalgesia as indicated by decreased PWL to radiant heat in the ipsilateral paw following subcutaneous injection of 20 microg/kg BmK venom without effect on PWL of the contralateral hindpaw. Meanwhile, it was found that i.p. morphine injection could inhibit this decreased ipsilateral PWL. The results thus suggest that BmK venom could induce peripheral inflammation in rat by subcutaneous injection, and may prove a valuable animal model for investigating the pathophysiology of a number of inflammatory diseases and identifying potential anti-inflammatory and analgesic drugs.