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Pretreatment with gangliosides reduces abnormal nociceptive responses associated with a rodent peripheral mononeuropathy.

作者信息

Hayes Ronald L, Mao Jianren, Price Donald D, Germano Antonino, d'Avella Dominico, Fiori Mario, Mayer D J

机构信息

Medical College of Virginia, MCV Station, Richmond, VA 23298 USA Department of Neurosurgery, University of Messina, MessinaItaly Fidia Pharmaceuticals, PadovaItaly.

出版信息

Pain. 1992 Mar;48(3):391-396. doi: 10.1016/0304-3959(92)90089-T.

DOI:10.1016/0304-3959(92)90089-T
PMID:1317543
Abstract

A peripheral mononeuropathy was produced in adult male rats by placing loosely constrictive ligatures around the common sciatic nerve. As reported by others, this procedure reliably results in postoperative behavior indicative of hyperalgesia, allodynia, and potentially, spontaneous pain. In these experiments, thermal hyperalgesia was assessed by measuring foot-withdrawal latencies to radiant heat aimed at the plantar surface of rat hind paws. Behaviors potentially indicative of spontaneous pain were assessed by rating spontaneous hind paw guarding positions. Rats with sciatic nerve ligation were divided into 5 groups (n = 6/group). Three groups received injections (i.p.) of either 10, 20 or 40 mg/kg of cerebral ganglioside mixture, GA. The 4th group was injected with 10 mg/kg of the purified ganglioside GM1, and the 5th group received an equal volume of saline. All injections were given daily for 2 days before surgery, the day of surgery and 9 days after surgery. All animals were behaviorally assessed for 2 days prior to surgery, the day of surgery, as well as 1, 3, 5, 7, and 10 days afterwards. All 5 groups had significantly reduced latencies to hind paw withdrawal on the side ipsilateral to sciatic nerve ligation. However, these hyperalgesic responses were significantly attenuated in rats receiving GA or GM1 pretreatment. These data suggest that this animal model of peripheral neuropathic pain is sensitive to pharmacological manipulations useful for understanding mechanisms of neuropathic pain, including mechanisms related to excitotoxic processes. Such studies could lead to development of clinical approaches to treat this disorder.

摘要

相似文献

1
Pretreatment with gangliosides reduces abnormal nociceptive responses associated with a rodent peripheral mononeuropathy.
Pain. 1992 Mar;48(3):391-396. doi: 10.1016/0304-3959(92)90089-T.
2
Post-injury treatment with GM1 ganglioside reduces nociceptive behaviors and spinal cord metabolic activity in rats with experimental peripheral mononeuropathy.损伤后用单唾液酸四己糖神经节苷脂(GM1)治疗可减轻实验性周围单神经病大鼠的伤害性反应行为和脊髓代谢活性。
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Intrathecal GM1 ganglioside and local nerve anesthesia reduce nociceptive behaviors in rats with experimental peripheral mononeuropathy.鞘内注射GM1神经节苷脂和局部神经麻醉可减轻实验性周围单神经病大鼠的伤害性反应。
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A peripheral mononeuropathy in rat that produces disorders of pain sensation like those seen in man.一种在大鼠中引发的周围性单神经病,可产生类似于人类所见的疼痛感觉障碍。
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Spatial patterns of increased spinal cord membrane-bound protein kinase C and their relation to increases in 14C-2-deoxyglucose metabolic activity in rats with painful peripheral mononeuropathy.疼痛性周围单神经病大鼠脊髓膜结合蛋白激酶C增加的空间模式及其与14C-2-脱氧葡萄糖代谢活性增加的关系。
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Spatial patterns of spinal cord [14C]-2-deoxyglucose metabolic activity in a rat model of painful peripheral mononeuropathy.疼痛性周围单神经病大鼠模型中脊髓[14C]-2-脱氧葡萄糖代谢活性的空间模式
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Differential roles of NMDA and non-NMDA receptor activation in induction and maintenance of thermal hyperalgesia in rats with painful peripheral mononeuropathy.NMDA和非NMDA受体激活在周围性单神经病性疼痛大鼠热痛觉过敏的诱导和维持中的不同作用
Brain Res. 1992 Dec 11;598(1-2):271-8. doi: 10.1016/0006-8993(92)90193-d.

引用本文的文献

1
Activation of protein kinase C in the spinal cord produces mechanical hyperalgesia by activating glutamate receptors, but does not mediate chronic muscle-induced hyperalgesia.脊髓中蛋白激酶C的激活通过激活谷氨酸受体产生机械性痛觉过敏,但不介导慢性肌肉诱导的痛觉过敏。
Mol Pain. 2006 Apr 3;2:13. doi: 10.1186/1744-8069-2-13.
2
The role of excitatory amino acid receptors and intracellular messengers in persistent nociception after tissue injury in rats.兴奋性氨基酸受体和细胞内信使在大鼠组织损伤后持续性伤害感受中的作用。
Mol Neurobiol. 1993 Fall-Winter;7(3-4):229-46. doi: 10.1007/BF02769177.
3
Spinal mediators of hyperalgesia.
痛觉过敏的脊髓介质。
Drugs. 1994;47 Suppl 5:10-20; discussion 46-7. doi: 10.2165/00003495-199400475-00004.