First Author | Rasband MN | Year | 1999 |
Journal | J Neurocytol | Volume | 28 |
Issue | 4-5 | Pages | 319-31 |
PubMed ID | 10739574 | Mgi Jnum | J:121354 |
Mgi Id | MGI:3709831 | Doi | 10.1023/a:1007057512576 |
Citation | Rasband MN, et al. (1999) K+ channel distribution and clustering in developing and hypomyelinated axons of the optic nerve. J Neurocytol 28(4-5):319-31 |
abstractText | The localization of Shaker-type K(+) channels in specialized domains of myelinated central nervous system axons was studied during development of the optic nerve. In adult rats Kv1.1, Kv1.2, Kv1.6, and the cytoplasmic beta-subunit Kvbeta2 were colocalized in juxtaparanodal zones. During development, clustering of K(+) channels lagged behind that for nodal Na(+) channels by about 5 days. In contrast to the PNS, K(+) channels were initially expressed fully segregated from nodes and paranodes, the latter identified by immunofluorescence of Caspr, a component of axoglial junctions. Clusters of K(+) channels were first detected at postnatal day 14 (P14) at a limited number of sites. Expression increased until all juxtaparanodes had immunoreactivity by P40. Developmental studies in hypomyelinating Shiverer mice revealed dramatically disrupted axoglial junctions, aberrant Na(+) channel clusters, and little or no detectable clustering of K(+) channels at all ages. These results suggest that in the optic nerve, compact myelin and normal axoglial junctions are essential for proper K(+) channel clustering and localization. |