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首页> 外文期刊>Journal of Neuroscience Research >Early postnatal chronic inflammation produces long-term changes in pain behavior and N-methyl-D-aspartate receptor subtype gene expression in the central nervous system of adult mice.
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Early postnatal chronic inflammation produces long-term changes in pain behavior and N-methyl-D-aspartate receptor subtype gene expression in the central nervous system of adult mice.

机译:产后早期的慢性炎症在成年小鼠的中枢神经系统中引起疼痛行为和N-甲基-D-天冬氨酸受体亚型基因表达的长期变化。

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摘要

The objective of this study was to test whether postnatal chronic inflammation resulted in altered reactivity to pain later in life when reexposed to the same inflammatory agent and whether this alteration correlated with brain-region-specific patterns of N-methyl-D-aspartate (NMDA) receptor subtype gene expression. Neonatal mouse pups received a single injection of complete Freund's adjuvant (CFA) or saline into the left hind paw on postnatal day 1 or 14. At 12 weeks of age, both neonatal CFA- and saline-treated animals received a unilateral injection of CFA in the left hind paw. Adult behavioral responsiveness of the left paw to a radiant heat source was determined in mice treated neonatally with saline or CFA before and after receiving CFA as adults. Twenty-four hours later, brains were dissected and NMDA receptor subunit gene expression was determined in four different brain areas by using an RNase protection assay. The results indicated that NMDA receptor subtype gene expression in adult mice exposed to persistent neonatal peripheral inflammation was brain region specific and that NMDA gene expression and pain reactivity differed according to the day of neonatal CFA exposure. Similarly, adult behavioral responsiveness to a noxious radiant heat source differed according to the age of neonatal exposure to CFA. The data suggest a possible molecular basis for the hypothesis that chronic persistent inflammation experienced early during development may permanently alter the future behavior and the sensitivity to pain later in life, especially in response to subsequent or recurrent inflammatory events. (c) 2006 Wiley-Liss, Inc.
机译:这项研究的目的是检验出生后的慢性炎症是否会在暴露于相同的炎症剂后导致以后对疼痛的反应性改变以及这种改变是否与脑区域特定的N-甲基-D-天冬氨酸(NMDA)模式相关)受体亚型基因表达。新生鼠幼崽在出生后的第1天或第14天向左后爪单次注射完全弗氏佐剂(CFA)或生理盐水。在12周大时,新生CFA和生理盐水治疗的动物均单侧注射CFA。左后爪。在成年接受CFA之前和之后,用盐水或CFA新生治疗的小鼠中确定了左爪对辐射热源的成年行为反应性。 24小时后,解剖大脑,并使用RNase保护测定法在四个不同的大脑区域确定NMDA受体亚基的基因表达。结果表明,暴露于持续性新生儿外周炎症的成年小鼠中NMDA受体亚型基因表达具有大脑区域特异性,并且NMDA基因表达和疼痛反应性随新生儿CFA暴露天数的不同而不同。同样,成人对有害辐射热源的行为反应因新生儿接触CFA的年龄而异。数据提示了以下假设的可能的分子基础:在发育早期经历的慢性持续性炎症可能会永久改变未来的行为以及生命后期对疼痛的敏感性,特别是对随后或复发性炎症事件的响应。 (c)2006年Wiley-Liss,Inc.

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