Role of nociceptor αCaMKII in transition from acute to chronic pain (hyperalgesic priming) in male and female rats.
作者： L. F. Ferrari , O. Bogen , J. D. Levine
DOI: 10.1523/JNEUROSCI.1785-13.2013
关键词:
摘要: We have previously shown that activation of protein kinase Ce (PKCe) in male rats induces a chronic, long-lasting change nociceptors such subsequent exposure to proinflammatory mediators produces markedly prolonged mechanical hyperalgesia. This neuroplastic change, hyperalgesic priming, is dependent on cytoplasmic polyadenylation element-binding (CPEB), downstream PKCe, and consequent translation mRNAs the peripheral terminal nociceptor. Since α calmodulin-dependent II (αCaMKII), molecule implicated neuroplasticity, target CPEB can also affect function, we investigated its role transition from acute chronic pain. Priming induced by direct PKCe be prevented inhibition αCaMKII. In addition, αCaMKII which was not pretreatment with antisense, suggesting induction priming. Activation ryanodine receptors (RyRs), lead αCaMKII, calcium- αCaMKII-dependent manner. Similarly, RyR calcium buffer priming PKCe. Unlike female as well rats. Our results demonstrate contribution phenomenon
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