DEVELOPMENTAL REGULATION OF NA-CELLS OF MOUSE HIPPOCAMPAL BRAIN-SLICES( AND K+ CONDUCTANCES IN GLIAL)

Citation
K. Kressin et al., DEVELOPMENTAL REGULATION OF NA-CELLS OF MOUSE HIPPOCAMPAL BRAIN-SLICES( AND K+ CONDUCTANCES IN GLIAL), Glia, 15(2), 1995, pp. 173-187
Citations number
64
Categorie Soggetti
Neurosciences
Journal title
GliaACNP
ISSN journal
08941491
Volume
15
Issue
2
Year of publication
1995
Pages
173 - 187
Database
ISI
SICI code
0894-1491(1995)15:2<173:DRONOM>2.0.ZU;2-S
Abstract
The relative contribution of voltage activated Na+ and K+ currents to the whole cell current pattern of hippocampal glial cells was analyzed and compared during different stages of postnatal maturation. The pat ch-clamp technique was applied to identified cells in thin brain slice s obtained from animals between postnatal day 5 and 35 (p5-35). We foc used on a subpopulation of glial cells in the CAI stratum radiatum whi ch most probably represents a pool of immature astrocytes, termed ''co mplex'' cells. These cells could not be labelled by O1/O4 antibodies, but some of the older cells were positively stained for glial fibrilla ry acidic protein (GFAP). In the early postnatal days, the current pat tern of the ''complex'' cells was dominated by two types of K+ outward currents: a delayed rectifier and a transient component. In addition, all cells expressed significant tetrodotoxin (TTX)-sensitive Na+ curr ents. During maturation, the contribution of delayed rectifier and A-t ype currents significantly decreased. Furthermore, almost all cells af ter p20 lacked Na+ currents. This down-regulation of voltage gated Na and K+ outward currents was accompanied by a substantial increase in passive and inward rectifier K+ conductances. We found increasing evid ence of electrical coupling between the ''complex'' cells with continu ed development. It is concluded that these developmental changes in th e electrophysiological properties of ''complex'' glial cells could be jointly responsible for the well known impaired Kf homeostasis in the early postnatal hippocampus. (C) 1995 Wiley-Liss, Inc.