Graduate Institute of Systems Biology and Bioinformatics, National Central University, Chungli, Taiwan.
BMC Neurosci. 2010 Oct 25;11:139. doi: 10.1186/1471-2202-11-139.
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.
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.
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.
新生儿炎症引起的神经可塑性是神经元活动依赖性变化的综合结果。我们在新生后足底外周炎症的大鼠模型中研究了神经元对有害刺激的敏感性，并评估了成年后外周再炎症时生理和分子水平上疼痛行为的变化。
与正常大鼠相比，在 P1 天接受左后足底炎症注射的大鼠，在 6-8 周龄时接受再炎症刺激后，热刺激引起的足底回缩潜伏期（PWL）降低。在脊髓同侧的背根神经节中观察到前速激肽原（proDYN）基因的表达增加。外周炎症性疼痛过敏的参与通过再炎症后细胞外信号调节激酶（ERK）的磷酸化（pERK）活性增加得到证明。
我们的结果表明，新生儿期的外周炎症可以在随后对该区域的感觉刺激过程中永久改变疼痛处理途径。阐明发育中疼痛回路的机制将为理解早期疼痛行为和随后对疼痛的适应提供新的见解。
