DIFFERENTIAL ACTIVATION OF SPINAL-CORD DYNORPHIN AND ENKEPHALIN NEURONS DURING HYPERALGESIA - EVIDENCE USING CDNA HYBRIDIZATION
DIFFERENTIAL ACTIVATION OF SPINAL-CORD DYNORPHIN AND ENKEPHALIN NEURONS DURING HYPERALGESIA - EVIDENCE USING CDNA HYBRIDIZATION
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DOI：
10.1016/0006-8993(88)90078-9
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发表时间：
1988-07-12
期刊：
影响因子：
2.9
通讯作者：
NARANJO, JR
中科院分区：
文献类型：
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作者：
IADAROLA, MJ;DOUGLASS, J;NARANJO, JR
后肢单侧实验性炎症对机械刺激和辐射热刺激均产生痛觉过敏，且发作迅速。在此期间，强啡肽生物合成的参数升高到比enkaphalin系统的那些更大的程度。强啡肽A（1-8）的含量增加发生在接受来自受影响肢体的感觉输入的脊髓节段中。这伴随着编码强啡肽蛋白前体的mRNA水平的快速（24小时内）和显著增加。前强啡肽原mRNA的最大升高（6至8倍）在诱导炎症后的第2天和第5天之间观察到。与mRNA的增加相比，强啡肽A（1-8）肽的增加明显延迟且不成比例;在炎症第5天观察到肽的最大增加（3倍）。背侧脊髓前脑啡肽原mRNA升高程度较低（50-80%）。然而，前脑啡肽原mRNA的增加显然不足以产生脑啡肽原衍生肽met 5-脑啡肽-Arg 6-Gly 7-Leu 8的可测量的增加，其水平在14天的炎症期内没有显示出显著的变化。这些数据表明，阿片类神经元，特别是那些含有强啡肽，在脊髓水平，在外周炎性疼痛状态的感觉传入输入的调制的积极参与。
A unilateral experimental inflammation of the hindlimb produces hyperalgesia to both mechanical and radiant thermal stimuli that is rapid in onset. During this period, parameters of dynorphin biosynthesis are elevated to a much greater degree than those of the enkaphalin system. An increase in the content of the peptide dynorphin A(1-8) occurs in the spinal cord segments that receive sensory input from the affected limb. This is accompanied by a rapid (within 24 h) and pronounced increase in the levels of mRNA coding for the dynorphin protein precursor. Maximum elevations (6- to 8-fold) of preprodynorphin mRNA are observed between days 2 and 5 subsequent to the induction of inflammation. Compared to the increase in mRNA, the increase in dynorphin A(1-8) peptide was appreciably delayed and proportionately less; maximal increases in peptide (3-fold) were seen at day 5 of inflammation. Dorsal spinal cord preproenkephalin mRNA is elevated to a lesser degree (50-80%). However, the increase in preproenkephalin mRNA is apparently not enough to yield a measureable increase in the proenkephalin-derived peptide met5-enkephalin-Arg6-Gly7-Leu8, the levels of which showed no significant change during the 14-day inflammatory period. These data suggest the active participation of opioid neurons, especially those containing dynorphin, at the spinal level, in the modulation of sensory afferent input during peripheral inflammatory pain states.