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

Jack Y. Lin, Yu Che Cheng, Julia Y. Chen, Chih Cheng Chien, Shih Chang Lin, Yeong Ray Wen, Tsung Shan Tsou, Qing Dong Ling

研究成果: 雜誌貢獻文章

2 引文 (Scopus)

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.
原文英語
文章編號139
期刊BMC Neuroscience
11
DOIs
出版狀態已發佈 - 十月 25 2010
對外發佈Yes

指紋

Hyperalgesia
Gene Expression
Pain
Extracellular Signal-Regulated MAP Kinases
Inflammation
Neuronal Plasticity
preproenkephalin
Spinal Cord
Hypersensitivity
Hot Temperature
Neurons
Injections

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience
  • Neuroscience(all)

引用此文

Increased spinal prodynorphin gene expression in reinflammation-associated hyperalgesia after neonatal inflammatory insult. / Lin, Jack Y.; Cheng, Yu Che; Chen, Julia Y.; Chien, Chih Cheng; Lin, Shih Chang; Wen, Yeong Ray; Tsou, Tsung Shan; Ling, Qing Dong.

於: BMC Neuroscience, 卷 11, 139, 25.10.2010.

研究成果: 雜誌貢獻文章

Lin, Jack Y. ; Cheng, Yu Che ; Chen, Julia Y. ; Chien, Chih Cheng ; Lin, Shih Chang ; Wen, Yeong Ray ; Tsou, Tsung Shan ; Ling, Qing Dong. / Increased spinal prodynorphin gene expression in reinflammation-associated hyperalgesia after neonatal inflammatory insult. 於: BMC Neuroscience. 2010 ; 卷 11.
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abstract = "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.",
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AU - Wen, Yeong Ray

AU - Tsou, Tsung Shan

AU - Ling, Qing Dong

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