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Volume 17, Number 19,
Issue of October 1, 1997
pp. 7316-7329
Copyright ©1997 Society for Neuroscience
Electrophysiological Changes That Accompany Reactive Gliosis
In Vitro
Received May 21, 1997; revised July 18, 1997; accepted July 22, 1997.
Stacey Nee MacFarlane and
Harald Sontheimer
Department of Neurobiology, University of Alabama, Birmingham,
Birmingham, Alabama 35294
An in vitro injury model was used to examine the
electrophysiological changes that accompany reactive gliosis.
Mechanical scarring of confluent spinal cord astrocytes led to a
threefold increase in the proliferation of scar-associated astrocytes,
as judged by bromodeoxyuridine (BrdU) labeling. Whole-cell patch-clamp recordings demonstrated that current profiles differed absolutely between nonproliferating (BrdU ) and proliferating
(BrdU+) astrocytes. The predominant current type
expressed in BrdU cells was an inwardly rectifying
K+ current (KIR; 1.3 pS/pF).
BrdU cells also expressed transient outward
K+ currents, accounting for less than one-third of
total K+ conductance (G). In
contrast, proliferating BrdU+ astrocytes exhibited a
dramatic, approximately threefold reduction in KIR (0.45 pS/pF) but showed a twofold increase in the conductance of both
transient (KA) (0.67-1.32 pS/pF) and sustained
(KD) (0.42-1.10 pS/pF) outwardly rectifying
K+ currents, with a
GKIR:GKD ratio of
0.4. Relative expression of GKIR:GKD led to
more negative resting potentials in nonproliferating ( 60 mV) versus
proliferating astrocytes (53 mV; p = 0.015). Although 45% of the nonproliferating astrocytes expressed
Na+ currents (0.47 pS/pF), the majority of
proliferating cells expressed prominent Na+ currents
(0.94 pS/pF). Injury-induced electrophysiological changes are rapid and
transient, appearing within 4 hr postinjury and, with the exception of
KIR, returning to control conductances within 24 hr.
These differences between proliferating and nonproliferating astrocytes
are reminiscent of electrophysiological changes observed during
gliogenesis, suggesting that astrocytes undergoing secondary, injury-induced proliferation recapitulate the properties of immature glial cells. The switch in predominance from KIR to
KD appears to be essential for proliferation and scar
repair, because both processes were inhibited by blockade of
KD.
Key words:
gliosis;
BrdU;
patch clamp;
potassium currents;
proliferation;
sodium currents
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