Increased spinal prodynorphin gene expression in reinflammation-associated hyperalgesia after neonatal inflammatory insult

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题名:	Increased spinal prodynorphin gene expression in reinflammation-associated hyperalgesia after neonatal inflammatory insult
作者:	Lin,JYS;Cheng,YC;Chen,JYR;Chien,CC;Lin,SC;Wen,YR;Tsou,TS;Ling,QD
贡献者:	系統生物與生物資訊研究所
关键词:	LONG-LASTING ALLODYNIA;NERVE-INJURED RATS;PERIPHERAL INFLAMMATION;CORD NEURONS;DORSAL-HORN;PAIN HYPERSENSITIVITY;NEUROPATHIC PAIN;DYNORPHIN-A;ADULT RATS;PLASTICITY
日期:	2010
上传时间:	2012-03-27 18:20:33 (UTC+8)
出版者:	國立中央大學
摘要:	Background: Neuroplasticity induced by neonatal inflammation is the consequence of a combination of activity-dependent changes in neurons. We investigated neuronal sensitivity to a noxious stimulus in a rat model of neonatal hind-paw peripheral inflammation and assessed changes in pain behaviour at the physiological and molecular levels after peripheral reinflammation in adulthood. Results: A decrease in paw withdrawal latency (PWL) after a heat stimulus was documented in rats that received inflammatory injections in their left hind paws on postnatal day one (P1) and a reinflammation stimulus at postnatal 6-8 weeks of age, compared with normal rats. An increase in the expression of the prodynorphin (proDYN) gene was noted after reinflammation in the spinal cord ipsilateral to the afferents of the neonatally treated hind paw. The involvement of the activation of extracellular signal-regulated kinases (ERK) in peripheral inflammatory pain hypersensitivity was evidenced evident by the increase in phospho-ERK (pERK) activity after reinflammation. Conclusions: Our results indicate that peripheral inflammation in neonates can permanently alter the pain processing pathway during the subsequent sensory stimulation of the region. Elucidation of the mechanism underlying the developing pain circuitry will provide new insights into the understanding of the early pain behaviours and the subsequent adaptation to pain.
關聯:	BMC NEUROSCIENCE
显示于类别:	[系統生物與生物資訊研究所] 期刊論文

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