| First Author | Di Angelantonio S | Year | 2011 |
| Journal | Neurobiol Dis | Volume | 41 |
| Issue | 2 | Pages | 528-37 |
| PubMed ID | 21056666 | Mgi Jnum | J:168343 |
| Mgi Id | MGI:4888068 | Doi | 10.1016/j.nbd.2010.10.024 |
| Citation | Di Angelantonio S, et al. (2011) Lack of dystrophin functionally affects alpha3beta2/beta4-nicotinic acethylcholine receptors in sympathetic neurons of dystrophic mdx mice. Neurobiol Dis 41(2):528-37 |
| abstractText | In the sympathetic superior cervical ganglion (SCG), nicotinic acetylcholine receptors (nAChRs) mediate fast synaptic transmission. We previously demonstrated that in SCG neurons of mdx mice, an animal model for Duchenne muscular dystrophy, lack of dystrophin causes a decrease, compared to the wild-type, in post-synaptic nAChRs containing the alpha3 subunit associated with beta2 and/or beta4 (alpha3beta2/beta4-nAChRs), but not in those containing the alpha7 subunit. Here we show, by whole cell patch-clamp recordings from cultured SCG neurons, that both nicotine and acetylcholine-evoked currents through alpha3beta2/beta4-nAChRs are significantly reduced in mdx mice compared to the wild-type, while those through alpha7-nAChR are unaffected. This reduction associates with that of protein levels of alpha3, beta2 and beta4 subunits. Therefore, we suggest that, in mdx mouse SCG neurons, lack of dystrophin, by specifically affecting membrane stabilization of alpha3beta2/beta4-nAChRs, could determine an increase in receptor internalization and degradation, with consequent reduction in the fast intraganglionic cholinergic transmission. |
