Impaired glial buffering hampers antidromic conduction of CA1 neurons during hypoxia

Youn Kwan Park, Seok Joon Kim

Research output: Contribution to journalArticle

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.

Original languageEnglish
Pages (from-to)90-97
Number of pages8
JournalBrain Research
Volume1280
DOIs
Publication statusPublished - 2009 Jul 14

Keywords

  • Conduction block
  • Current source density
  • Evoked potential
  • Extracellular potassium
  • Hippocampal slice
  • Ion selective recording

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology

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