Changes in expression of voltage-gated potassium channels in dorsal root ganglion neurons following axotomy

Citation
K. Ishikawa et al., Changes in expression of voltage-gated potassium channels in dorsal root ganglion neurons following axotomy, MUSCLE NERV, 22(4), 1999, pp. 502-507
Citations number
42
Categorie Soggetti
da verificare
Journal title
MUSCLE & NERVE
ISSN journal
0148639X → ACNP
Volume
22
Issue
4
Year of publication
1999
Pages
502 - 507
Database
ISI
SICI code
0148-639X(199904)22:4<502:CIEOVP>2.0.ZU;2-7
Abstract
Several families of voltage-gated potassium channels (Kv), including a spec trum of subtypes, are involved in regulating and modifying the integration and transmission of electrical signals in the nervous system. However, the specific patterns of Ky expression in normal or injured dorsal root ganglio n (DRG) neurons have not been studied. Previous studies have examined the e xpression of voltage-gated sodium channels in DRG neurons, and also the sel ective up- and downregulation of several of these channels following axonal injury to the DRG neurons. In the present study, we used immunocytochemica l methods to investigate the expression of Kv channels (Kv1.1, 1.2, 1.3, 1. 4, 1.5, 1.6, and 2.1) in DRG cells cultured from control and axotomized adu lt rats. Kv1.2 and 2.1 immunoreactivity in DRG neurons showed large decreas es following axotomy, whereas Kv1.1 and 1.3 showed smaller decreases. Kv1.4 and 1.6 immunostaining were not altered by axotomy, and Kv1.5 immunoreacti vity was low in both control and axotomized DRG neurons. These results prov ide molecular correlates for the expression of multiple K+ currents in norm al DRG neurons and indicate that, in relation to changes in sodium channel expression, there are decreases in specific potassium channels following ax otomy in these cells. The alterations in K+ and Na+ channel expression foll owing axonal injury may lead to changes in electrical excitability of the D RG neurons, and might contribute to chronic pain syndromes. (C) 1999 John W iley & Sons, Inc.