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- 저자 : Bethry, Audrey (검색결과 1 건)
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Small RNAs control sodium channel expression, nociceptor excitability, and pain thresholds.
Zhao, Jing,Lee, Man-Cheung,Momin, Ali,Cendan, Cruz-Miguel,Shepherd, Samuel T,Baker, Mark D,Asante, Curtis,Bee, Lucy,Bethry, Audrey,Perkins, James R,Nassar, Mohammed A,Abrahamsen, Bjarke,Dickenson, Ant The Society 2010 The Journal of neuroscience Vol.30 No.32
<P>To examine the role of small RNAs in peripheral pain pathways, we deleted the enzyme Dicer in mouse postmitotic damage-sensing neurons. We used a Nav1.8-Cre mouse to target those nociceptors important for inflammatory pain. The conditional null mice were healthy with a normal number of sensory neurons and normal acute pain thresholds. Behavioral studies showed that inflammatory pain was attenuated or abolished. Inflammatory mediators failed to enhance excitability of Nav1.8+ sensory neurons from null mutant mice. Acute noxious input into the dorsal horn of the spinal cord was apparently normal, but the increased input associated with inflammatory pain measured using c-Fos staining was diminished. Microarray and quantitative real-time reverse-transcription PCR (qRT-PCR) analysis showed that Dicer deletion lead to the upregulation of many broadly expressed mRNA transcripts in dorsal root ganglia. By contrast, nociceptor-associated mRNA transcripts (e.g., Nav1.8, P2xr3, and Runx-1) were downregulated, resulting in lower levels of protein and functional expression. qRT-PCR analysis also showed lowered levels of expression of nociceptor-specific pre-mRNA transcripts. MicroRNA microarray and deep sequencing identified known and novel nociceptor microRNAs in mouse Nav1.8+ sensory neurons that may regulate nociceptor gene expression.</P>
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