| First Author | Molliver DC | Year | 2005 |
| Journal | Pain | Volume | 113 |
| Issue | 3 | Pages | 277-84 |
| PubMed ID | 15661434 | Mgi Jnum | J:144157 |
| Mgi Id | MGI:3830180 | Doi | 10.1016/j.pain.2004.10.025 |
| Citation | Molliver DC, et al. (2005) Overexpression of NGF or GDNF alters transcriptional plasticity evoked by inflammation. Pain 113(3):277-84 |
| abstractText | Transcriptional changes evoked in nociceptive sensory neurons by inflammatory injury play a substantial role in the generation of and recovery from painful hypersensitivity. Transgenic mice overexpressing nerve growth factor (NGF) or glial cell line-derived neurotrophic factor (GDNF) in the skin possess a greatly increased number of nociceptors. Surprisingly, NGF-overexpressers display reduced hypersensitivity and recovered more rapidly in response to inflammation, suggesting a compensatory suppression of nociceptive transmission in these mice. To determine whether these transgenic mice show changes in inflammation-evoked transcriptional plasticity, we examined the expression of a panel of genes implicated in nociceptive signaling in response to injection of complete Freund's adjuvant into the hindpaw. Relative mRNA levels were quantified 1, 4 and 15 days after injection using real-time PCR. In wild type mice CFA injection elicited a reproducible pattern of altered gene expression that returned to baseline over a 2-week period. In mice overexpressing NGF or GDNF the expression patterns for several genes were substantially altered; these changes in injury-evoked patterns of gene expression suggest the existence of endogenous regulatory mechanisms that can compensate for increased nociceptive input by modulating the expression of a limited subset of genes. |
