| First Author | Zhao J | Year | 2010 |
| Journal | J Neurosci | Volume | 30 |
| Issue | 32 | Pages | 10860-71 |
| PubMed ID | 20702715 | Mgi Jnum | J:163230 |
| Mgi Id | MGI:4821478 | Doi | 10.1523/JNEUROSCI.1980-10.2010 |
| Citation | Zhao J, et al. (2010) Small RNAs control sodium channel expression, nociceptor excitability, and pain thresholds. J Neurosci 30(32):10860-71 |
| abstractText | 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. |
