Impaired K+ homeostasis and altered electrophysiological properties of post-traumatic hippocampal gila

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Abstract

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 posttraumatic hippocampus, there has been relatively little understanding of changes in ionic homeostasis, failure of which can result in neuronal hyperexcitability and abnormal synchronization. Because gila play a crucial role in the homeostasis of the brain microenvironment, we investigated the effects of TBI on rat hippocampal gila. 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 posttraumatic 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 gila 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.

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D’Ambrosio, R., Maris, D. O., Grady, M. S., Winn, H. R., & Janigro, D. (1999). Impaired K+ homeostasis and altered electrophysiological properties of post-traumatic hippocampal gila. Journal of Neuroscience, 19(18), 8152–8162. https://doi.org/10.1523/jneurosci.19-18-08152.1999

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