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

Fingerprint

Neuroglia
Neurons
Potassium
Barium
Synaptic Transmission
Adenosine A1 Receptors
Neural Conduction
Evoked Potentials
Hypoxia
Electrodes
Membranes
Population

Keywords

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

ASJC Scopus subject areas

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

Cite this

Impaired glial buffering hampers antidromic conduction of CA1 neurons during hypoxia. / Park, Youn-Kwan; Kim, Seok Joon.

In: Brain Research, Vol. 1280, 14.07.2009, p. 90-97.

Research output: Contribution to journalArticle

@article{1fb9a110225b417eae754008298d320a,
title = "Impaired glial buffering hampers antidromic conduction of CA1 neurons during hypoxia",
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.",
keywords = "Conduction block, Current source density, Evoked potential, Extracellular potassium, Hippocampal slice, Ion selective recording",
author = "Youn-Kwan Park and Kim, {Seok Joon}",
year = "2009",
month = "7",
day = "14",
doi = "10.1016/j.brainres.2009.05.013",
language = "English",
volume = "1280",
pages = "90--97",
journal = "Brain Research",
issn = "0006-8993",
publisher = "Elsevier",

}

TY - JOUR

T1 - Impaired glial buffering hampers antidromic conduction of CA1 neurons during hypoxia

AU - Park, Youn-Kwan

AU - Kim, Seok Joon

PY - 2009/7/14

Y1 - 2009/7/14

N2 - 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.

AB - 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.

KW - Conduction block

KW - Current source density

KW - Evoked potential

KW - Extracellular potassium

KW - Hippocampal slice

KW - Ion selective recording

UR - http://www.scopus.com/inward/record.url?scp=67649440677&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=67649440677&partnerID=8YFLogxK

U2 - 10.1016/j.brainres.2009.05.013

DO - 10.1016/j.brainres.2009.05.013

M3 - Article

VL - 1280

SP - 90

EP - 97

JO - Brain Research

JF - Brain Research

SN - 0006-8993

ER -