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Open Access Research article

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

Jack Yu-Shih Lin12, Yu-Che Cheng3, Julia Yi-Ru Chen4, Chih-Cheng Chien3, Shih-Chang Lin3, Yeong-Ray Wen5, Tsung-Shan Tsou26 and Qing-Dong Ling23*

Author Affiliations

1 Municipal Wan-Fang Hospital and Shung-Ho Hospital, Taipei Medical University, Taipei, Taiwan

2 Graduate Institute of Systems Biology and Bioinformatics, National Central University, Chungli, Taiwan

3 Cathay Medical Research Institute, Cathay General Hospital, Jian-Cheng Road, Sijhih City Taipei, Taiwan

4 School of Medicine, Taipei Medical University, Taipei, Taiwan

5 Department of Anesthesiology, Shin-Kong Wu Ho-Su Memorial Hospital, Wen Chang Road, Taipei, Taiwan

6 Graduate Institute of Statistics, National Central University, Chungli, Taiwan

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BMC Neuroscience 2010, 11:139  doi:10.1186/1471-2202-11-139

Published: 25 October 2010

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.