论文部分内容阅读
近 2 0年来 ,疼痛感觉研究的重要发现之一是 :外周组织损伤能调节背根神经节和中枢神经某些早期基因 (immediateearlygene)和参与伤害性信息整合的神经肽 ,包括内源性阿片肽的表达 ;这些变化可明显地和长时间地提高脊髓中枢神经元的兴奋性 ,使之处于一种高度敏感化状态 ,对外周传入的非伤害性信息产生异常的疼痛性感觉 ,即痛觉过敏。大鼠脚掌注射completeFreundsadjuvant (CFA)在引起局部组织炎症和痛觉过敏的同时 ,脊髓背角强啡肽mRNA表达增强 ,强啡肽合成增多。发育、老年变化和种属差异可明显地调节动物在整体水平和分子水平上对外周组织损伤的反应。防止对伤害性信息的传递起易化作用的改变如上述脊髓强啡肽能神经元活动增强 ,有利于防止外周组织损伤如手术损伤引起的痛觉过敏。
In the recent 20 years, one of the important discoveries in the study of pain sensation is that peripheral tissue damage can regulate some immediateearlygene of dorsal root ganglion and central nervous system and neuropeptides involved in the integration of nociceptive information, including endogenous opioid peptides These changes can significantly and prolong the excitability of the spinal cord central neurons, making it in a highly sensitive state, the introduction of peripheral non-invasive information to produce abnormal pain sensation, that hyperalgesia . CompleteFreundsadjuvant (CFA) injection into the soles of rats induced local tissue inflammation and hyperalgesia, while dorsal horn dynorphin mRNA expression increased, dynorphin synthesis increased. Developmental, age-related changes, and species differences significantly modulate the animal’s response to peripheral tissue damage at both the global and the molecular level. To prevent the transmission of harmful information to ease the changes as above spinal cord dynorphin neurons increased activity is conducive to preventing peripheral tissue damage such as surgical hyperalgesia caused by injury.