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The Journal of Neuroscience, September 15, 1999, 19(18):8152-8162
Impaired K+ Homeostasis and Altered
Electrophysiological Properties of Post-Traumatic Hippocampal Glia
Raimondo
D'Ambrosio,
Donald O.
Maris,
M. Sean
Grady,
H.
Richard
Winn, and
Damir
Janigro
Department of Neurological Surgery, University of Washington,
School of Medicine, Harborview Medical Center, Seattle, Washington
98104
Traumatic brain injury (TBI) can be associated with memory
impairment, cognitive deficits, or seizures, all of which can reflect altered hippocampal function. Whereas previous studies have focused on
the involvement of neuronal loss in post-traumatic hippocampus, there
has been relatively little understanding of changes in ionic homeostasis, failure of which can result in neuronal hyperexcitability and abnormal synchronization. Because glia play a crucial role in the
homeostasis of the brain microenvironment, we investigated the effects
of TBI on rat hippocampal glia. Using a fluid percussion injury (FPI)
model and patch-clamp recordings from hippocampal slices, we have found
impaired glial physiology 2 d after FPI. Electrophysiologically,
we observed reduction in transient outward and inward
K+ currents. To assess the functional consequences
of these glial changes, field potentials and extracellular
K+ activity were recorded in area CA3 during
antidromic stimulation. An abnormal extracellular K+
accumulation was observed in the post-traumatic hippocampal slices, accompanied by the appearance of CA3 afterdischarges. After
pharmacological blockade of excitatory synapses and of
K+ inward currents, uninjured slices showed the same
altered K+ accumulation in the absence of abnormal
neuronal activity. We suggest that TBI causes loss of
K+ conductance in hippocampal glia that results in
the failure of glial K+ homeostasis, which in turn
promotes abnormal neuronal function. These findings provide a new
potential mechanistic link between traumatic brain injury and
subsequent development of disorders such as memory loss, cognitive
decline, seizures, and epilepsy.
Key words:
glial neuronal interactions; ion homeostasis; patch
clamp; potassium selective microelectrodes; epilepsy; traumatic brain
injury
Copyright © 1999 Society for Neuroscience 0270-6474/99/19188152-11$05.00/0
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