Accounting for the Delay in the Transition from Acute to Chronic Pain: Axonal and Nuclear Mechanisms

被引:43
作者
Ferrari, Luiz F.
Bogen, Oliver
Reichling, David B.
Levine, Jon D.
机构
[1] Univ Calif San Francisco, Dept Med, San Francisco, CA 94143 USA
[2] Univ Calif San Francisco, Dept Oral Surg, San Francisco, CA 94143 USA
[3] Univ Calif San Francisco, Div Neurosci, San Francisco, CA 94143 USA
基金
美国国家卫生研究院;
关键词
PROTEIN-KINASE-C; MONOCYTE CHEMOATTRACTANT PROTEIN-1; ELEMENT-BINDING PROTEIN; DORSAL-ROOT GANGLION; INFLAMMATORY PAIN; TRANSCRIPTIONAL REGULATION; PKC-EPSILON; INTRATHECAL INJECTION; CORDYCEPS-SINENSIS; SIGNALING PATHWAY;
D O I
10.1523/JNEUROSCI.5147-13.2015
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Acute insults produce hyperalgesic priming, a neuroplastic change in nociceptors that markedly prolongs inflammatory mediator-induced hyperalgesia. After an acute initiating insult, there is a 72 h delay to the onset of priming, for which the underlying mechanism is unknown. We hypothesized that the delay is due to the time required for a signal to travel from the peripheral terminal to the cell body followed by a return signal to the peripheral terminal. We report that when an inducer of hyperalgesic priming (monocyte chemotactic protein 1) is administered at the spinal cord of Sprague Dawley rats, priming is detected at the peripheral terminal with a delay significantly shorter than when applied peripherally. Spinally induced priming is detected not only when prostaglandin E-2 (PGE(2)) is presented to the peripheral nociceptor terminals, but also when it is presented intrathecally to the central terminals in the spinal cord. Furthermore, when an inducer of priming is administered in the paw, priming can be detected in spinal cord (as prolonged hyperalgesia induced by intrathecal PGE(2)), but only when the mechanical stimulus is presented to the paw on the side where the priming inducer was administered. Both spinally and peripherally induced priming is prevented by intrathecal oligodeoxynucleotide antisense to the nuclear transcription factor CREB mRNA. Finally, the inhibitor of protein translation reversed hyperalgesic priming only when injected at the site where PGE(2) was administered, suggesting that the signal transmitted from the cell body to the peripheral terminal is not a newly translated protein, but possibly a newly expressed mRNA.
引用
收藏
页码:495 / 507
页数:13
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