| First Author | Ding H | Year | 2012 |
| Journal | Endocrine | Volume | 42 |
| Issue | 1 | Pages | 118-24 |
| PubMed ID | 22371119 | Mgi Jnum | J:327444 |
| Mgi Id | MGI:6882003 | Doi | 10.1007/s12020-012-9637-8 |
| Citation | Ding H, et al. (2012) Alterations of gene expression of sodium channels in dorsal root ganglion neurons of estrogen receptor knockout (ERKO) mice induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Endocrine 42(1):118-24 |
| abstractText | Estrogen receptors (ERalpha and ERbeta) mediate the neuroprotection of estrogens against MPTP-induced striatal dopamine (DA) depletion. Pain is an important and distressing symptom in Parkinson's disease (PD). Voltage-gated sodium channels in sensory neurons are involved in the development of neuropathic pain. In this study, MPTP caused changes in nociception and alterations of gene expression of voltage-gated sodium channels in dorsal root ganglion (DRG) neurons in ER knockout (ERKO) mice were investigated. We found that administration of MPTP (11 mg/kg) to WT mice led to an extensive depletion of DA and its two metabolites, alphaERKO mice were observed to be more susceptible to MPTP toxicity than betaERKO or WT mice. In addition, we found that the mRNA levels of TTX-S and TTX-R sodium channel subtypes were differentially affected in MPTP-treated WT animals. The MPTP-induced up-regulation of Nav1.1 and Nav1.9, down-regulation of Nav1.6 in DRG neurons may be through ERbeta, up-regulation of Nav1.7 and down-regulation of Nav1.8 are dependent on both ERalpha and ERbeta. Therefore, the MPTP-induced alterations of gene expression of sodium channels in DRG neurons could be an important mechanism to affect excitability and nociceptive thresholds, and the ERs appear to play a role in nociception in PD. |
