| First Author | Zenker J | Year | 2012 |
| Journal | J Neurosci | Volume | 32 |
| Issue | 22 | Pages | 7493-8 |
| PubMed ID | 22649228 | Mgi Jnum | J:184972 |
| Mgi Id | MGI:5427021 | Doi | 10.1523/JNEUROSCI.0719-12.2012 |
| Citation | Zenker J, et al. (2012) Altered distribution of juxtaparanodal kv1.2 subunits mediates peripheral nerve hyperexcitability in type 2 diabetes mellitus. J Neurosci 32(22):7493-8 |
| abstractText | Peripheral nerve hyperexcitability (PNH) is one of the distal peripheral neuropathy phenotypes often present in patients affected by type 2 diabetes mellitus (T2DM). Through in vivo and ex vivo electrophysiological recordings in db/db mice, a model of T2DM, we observed that, in addition to reduced nerve conduction velocity, db/db mice also develop PNH. By using pharmacological inhibitors, we demonstrated that the PNH is mediated by the decreased activity of K(v)1-channels. In agreement with these data, we observed that the diabetic condition led to a reduced presence of the K(v)1.2-subunits in juxtaparanodal regions of peripheral nerves in db/db mice and in nerve biopsies from T2DM patients. Together, these observations indicate that the T2DM condition leads to potassium channel-mediated PNH, thus identifying them as a potential drug target to treat some of the DPN related symptoms. |
