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 language | English |
|---|---|
| Pages (from-to) | 90-97 |
| Number of pages | 8 |
| Journal | Brain Research |
| Volume | 1280 |
| DOIs | |
| Publication status | Published - 2009 Jul 14 |
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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 journal › Article
}
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
C2 - 19445906
AN - SCOPUS:67649440677
VL - 1280
SP - 90
EP - 97
JO - Brain Research
JF - Brain Research
SN - 0006-8993
ER -