Anoxia increases potassium conductance in hippocampal nerve cells

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Anoxia increases potassium conductance in hippocampal nerve cells. / HANSEN, A. J.; HOUNSGAARD, J.; JAHNSEN, H.

In: Acta Physiologica Scandinavica, Vol. 115, No. 3, 07.1982, p. 301-310.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

HANSEN, AJ, HOUNSGAARD, J & JAHNSEN, H 1982, 'Anoxia increases potassium conductance in hippocampal nerve cells', Acta Physiologica Scandinavica, vol. 115, no. 3, pp. 301-310. https://doi.org/10.1111/j.1748-1716.1982.tb07082.x

APA

HANSEN, A. J., HOUNSGAARD, J., & JAHNSEN, H. (1982). Anoxia increases potassium conductance in hippocampal nerve cells. Acta Physiologica Scandinavica, 115(3), 301-310. https://doi.org/10.1111/j.1748-1716.1982.tb07082.x

Vancouver

HANSEN AJ, HOUNSGAARD J, JAHNSEN H. Anoxia increases potassium conductance in hippocampal nerve cells. Acta Physiologica Scandinavica. 1982 Jul;115(3):301-310. https://doi.org/10.1111/j.1748-1716.1982.tb07082.x

Author

HANSEN, A. J. ; HOUNSGAARD, J. ; JAHNSEN, H. / Anoxia increases potassium conductance in hippocampal nerve cells. In: Acta Physiologica Scandinavica. 1982 ; Vol. 115, No. 3. pp. 301-310.

Bibtex

@article{88dc2b90a49b4c258c573af990d5a7af,
title = "Anoxia increases potassium conductance in hippocampal nerve cells",
abstract = "The effect of anoxia on nerve cell function was studied by intra‐ and extracellular micro‐electrode recordings from the CA1 and CA3 region in guinea pig hippocampal slices. Hyperpolarization and concomitant reduction of the nerve cell input resistance was observed early during anoxia. During this period the spontaneous activity first disappeared, then the evoked activity gradually disappeared. The hyperpolarization was followed by depolarization and an absence of a measurable input resistance. All the induced changes were reversed when the slice was reoxygenated. Reversal of the electro‐chemical gradient for Cl‐ across the nerve cell membrane did not affect the course of events during anoxia. Aminopyridines blocked the anoxic hyperpolarization and attenuated the decrease of membrane resistance, but had no effect on the later depolarization. Blockers of synaptic transmission, Mn++, Mg++‐ and of Na+‐channels (TTX) were without effect on the nerve cell changes during anoxia. It is suggested that the reduction of nerve cell excitability in anoxia is primarily due to increased K+‐conductance. Thus, the nerve cells are hyper‐polarized and the input resistance reduced, causing higher threshold and reduction of synaptic potentials. The mechanism of the K+‐conductance activation is unknown at present.",
keywords = "Anoxia, hippocampus, K‐conductance, neuronal activity",
author = "HANSEN, {A. J.} and J. HOUNSGAARD and H. JAHNSEN",
year = "1982",
month = jul,
doi = "10.1111/j.1748-1716.1982.tb07082.x",
language = "English",
volume = "115",
pages = "301--310",
journal = "Acta Physiologica Scandinavica",
issn = "0001-6772",
publisher = "Blackwell Science Ltd.",
number = "3",

}

RIS

TY - JOUR

T1 - Anoxia increases potassium conductance in hippocampal nerve cells

AU - HANSEN, A. J.

AU - HOUNSGAARD, J.

AU - JAHNSEN, H.

PY - 1982/7

Y1 - 1982/7

N2 - The effect of anoxia on nerve cell function was studied by intra‐ and extracellular micro‐electrode recordings from the CA1 and CA3 region in guinea pig hippocampal slices. Hyperpolarization and concomitant reduction of the nerve cell input resistance was observed early during anoxia. During this period the spontaneous activity first disappeared, then the evoked activity gradually disappeared. The hyperpolarization was followed by depolarization and an absence of a measurable input resistance. All the induced changes were reversed when the slice was reoxygenated. Reversal of the electro‐chemical gradient for Cl‐ across the nerve cell membrane did not affect the course of events during anoxia. Aminopyridines blocked the anoxic hyperpolarization and attenuated the decrease of membrane resistance, but had no effect on the later depolarization. Blockers of synaptic transmission, Mn++, Mg++‐ and of Na+‐channels (TTX) were without effect on the nerve cell changes during anoxia. It is suggested that the reduction of nerve cell excitability in anoxia is primarily due to increased K+‐conductance. Thus, the nerve cells are hyper‐polarized and the input resistance reduced, causing higher threshold and reduction of synaptic potentials. The mechanism of the K+‐conductance activation is unknown at present.

AB - The effect of anoxia on nerve cell function was studied by intra‐ and extracellular micro‐electrode recordings from the CA1 and CA3 region in guinea pig hippocampal slices. Hyperpolarization and concomitant reduction of the nerve cell input resistance was observed early during anoxia. During this period the spontaneous activity first disappeared, then the evoked activity gradually disappeared. The hyperpolarization was followed by depolarization and an absence of a measurable input resistance. All the induced changes were reversed when the slice was reoxygenated. Reversal of the electro‐chemical gradient for Cl‐ across the nerve cell membrane did not affect the course of events during anoxia. Aminopyridines blocked the anoxic hyperpolarization and attenuated the decrease of membrane resistance, but had no effect on the later depolarization. Blockers of synaptic transmission, Mn++, Mg++‐ and of Na+‐channels (TTX) were without effect on the nerve cell changes during anoxia. It is suggested that the reduction of nerve cell excitability in anoxia is primarily due to increased K+‐conductance. Thus, the nerve cells are hyper‐polarized and the input resistance reduced, causing higher threshold and reduction of synaptic potentials. The mechanism of the K+‐conductance activation is unknown at present.

KW - Anoxia

KW - hippocampus

KW - K‐conductance

KW - neuronal activity

UR - http://www.scopus.com/inward/record.url?scp=0019949843&partnerID=8YFLogxK

U2 - 10.1111/j.1748-1716.1982.tb07082.x

DO - 10.1111/j.1748-1716.1982.tb07082.x

M3 - Journal article

C2 - 6295068

AN - SCOPUS:0019949843

VL - 115

SP - 301

EP - 310

JO - Acta Physiologica Scandinavica

JF - Acta Physiologica Scandinavica

SN - 0001-6772

IS - 3

ER -

ID: 237700391