Lesion-induced changes of electrophysiological properties in astrocytes ofthe rat dentate gyrus

Citation
W. Schroder et al., Lesion-induced changes of electrophysiological properties in astrocytes ofthe rat dentate gyrus, GLIA, 28(2), 1999, pp. 166-174
Citations number
50
Categorie Soggetti
Neurosciences & Behavoir
Journal title
GLIA
ISSN journal
08941491 → ACNP
Volume
28
Issue
2
Year of publication
1999
Pages
166 - 174
Database
ISI
SICI code
0894-1491(199911)28:2<166:LCOEPI>2.0.ZU;2-7
Abstract
Reorganization of the adult dentate gyrus following unilateral entorhinal c ortex lesion (ECL) is a well-established model for studying mechanisms of t rauma-induced neuronal plasticity, The lesion induces deafferentiation of t he outer molecular layer, which is accompanied by a strong astroglial react ion. This glial response is thought to contribute to subsequent, repair pro cesses, but the underlying mechanisms are poorly understood. In this study we addressed the question whether denervation leads to modifications in the electrophysiological properties of astrocytes, assuming that such changes might be involved in the remodeling of neural circuitry. Patch-clamp record ings were obtained from astrocytes in the dentate gyrus of adult rats that underwent ECL and compared to corresponding data from control animals. We o bserved a significant reduction of inward rectifier K+ current densities, a positive shift of resting potentials, and an increase in input resistance in astrocytes of the denervated molecular layer. Current densities were red uced between 6 and 19 days postlesion (dpl), reaching a minimum at 10 dpl. Voltage-gated outward K+ currents were not affected by the lesion. Inward r ectifier K+ currents increase with maturation in astrocytes, Thus, our resu lts provide evidence that, following ECL, mature astrocytes dedifferentiate d and readapted an immature current pattern. Presumably, these changes lead to stronger and prolonged depolarization of glial cells and neurons in res ponse to activity-dependent K+ release, which in turn might enhance the syn thesis of neurotrophic factors and contribute to a permissive environment f or neuronal reorganization. (C) 1999 Wiley-Liss, Inc.