Journal
JOURNAL OF NEUROSCIENCE
Volume 30, Issue 32, Pages 10860-10871Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.1980-10.2010
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Funding
- Medical Research Council
- Biotechnology and Biological Sciences Research Council
- Wellcome Trust
- Korean Ministry of Education, Science, and Technology [R31-2008-000-10103-0]
- National Research Foundation of Korea
- University of Granada
- Biotechnology and Biological Sciences Research Council [BB/F000227/1] Funding Source: researchfish
- Medical Research Council [MC_U120027516, G0901905] Funding Source: researchfish
- BBSRC [BB/F000227/1] Funding Source: UKRI
- MRC [G0901905, MC_U120027516] Funding Source: UKRI
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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.
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