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Impaired glial buffering hampers antidromic conduction of CA1 neurons during hypoxia

Authors
Park, Youn-KwanKim, Seok-Joon
Issue Date
14-7월-2009
Publisher
ELSEVIER SCIENCE BV
Keywords
Conduction block; Current source density; Extracellular potassium; Evoked potential; Hippocampal slice; Ion selective recording
Citation
BRAIN RESEARCH, v.1280, pp.90 - 97
Indexed
SCIE
SCOPUS
Journal Title
BRAIN RESEARCH
Volume
1280
Start Page
90
End Page
97
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/119676
DOI
10.1016/j.brainres.2009.05.013
ISSN
0006-8993
Abstract
Increased potassium conductance during hypoxia causes membrane hyperpolarization and a resultant increase in extracellular potassium concentration ([K+](o)). In addition, glial buffering of [K+](o) is the key mechanism for clearing excess K+ and is important for neuronal function and survival. Here, we studied the effect of glial buffering of [K+](o) on neural impulse conduction during hypoxia using a potassium-selective electrode and evoked potential recording in rat hippocampal slices. The increase in [K+](o) during hypoxia was modest and there were no significant differences between the layers. The [K+](o) during hypoxia was significantly elevated by addition of barium (1 mM), especially in the stratum pyramidale and stratum oriens. Although synaptic transmission was depressed during hypoxia, the presynaptic volley and antidromic population spike mostly remained unchanged. With the addition of barium, antidromic conduction was more profoundly affected than the presynaptic volley. When presynaptic inhibition was precluded by including a selective A1 adenosine receptor blocker to restore synaptic transmission, blockade of the antidromic conduction became more evident compared with the blockade of other recorded field potentials. These findings are compatible with regional differences in the increase of [K+](o) and suggest that glial buffering of high [K+](o) is important in antidromic conduction during hypoxia. (C) 2009 Published by Elsevier B.V.
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