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 journal › Journal article › Research › peer-review
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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