ERK MAP kinase activation in superficial spinal cord neurons induces prodynorphin and NK-1 upregulation and contributes to persistent inflammatory pain hypersensitivity.

作者: Ru-Rong Ji , Katia Befort , Gary J. Brenner , Clifford J. Woolf

DOI: 10.1523/JNEUROSCI.22-02-00478.2002

关键词:

摘要: Activation of ERK (extracellular signal-regulated kinase) MAP (mitogen-activated protein) kinase in dorsal horn neurons the spinal cord by peripheral noxious stimulation contributes to short-term pain hypersensitivity. We investigated activation inflammation and its involvement regulating gene expression contributing inflammatory Injection complete Freund's adjuvant (CFA) into a hindpaw produced persistent sustained superficial layers (laminae I-IIo) horn. CFA also induced an upregulation prodynorphin neurokinin-1 (NK-1) neurons, which was suppressed intrathecal delivery MEK (MAP inhibitor U0126. CFA-induced phospho-ERK primarily colocalized with NK-1 neurons. Although injection U0126 did not affect basal sensitivity, it attenuate both establishment maintenance heat mechanical pathway subset nociceptive contributes, therefore, hypersensitivity, possibly via transcriptional regulation genes, such as NK-1.

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