SK2 channels are neuroprotective for ischemia-induced neuronal cell death
In mouse hippocampal CA1 pyramidal neurons, the activity of synaptic small-conductance Ca2+-activated K+ channels type 2 (SK2 channels) provides a negative feedback on N-methyl-d-aspartate receptors (NMDARs), reestablishing Mg2+ block that reduces Ca2+ influx. The well-established role of NMDARs in...
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| Published in | Journal of cerebral blood flow and metabolism Vol. 31; no. 12; pp. 2302 - 2312 |
|---|---|
| Main Authors | , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London, England
SAGE Publications
01.12.2011
Nature Publishing Group Sage Publications Ltd |
| Subjects | |
| Online Access | Get full text |
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| Abstract | In mouse hippocampal CA1 pyramidal neurons, the activity of synaptic small-conductance Ca2+-activated K+ channels type 2 (SK2 channels) provides a negative feedback on N-methyl-d-aspartate receptors (NMDARs), reestablishing Mg2+ block that reduces Ca2+ influx. The well-established role of NMDARs in ischemia-induced excitotoxicity led us to test the neuroprotective effect of modulating SK2 channel activity following cerebral ischemia induced by cardiac arrest and cardiopulmonary resuscitation (CA/CPR). Administration of the SK channel positive modulator, 1-ethyl-benzimidazolinone (1-EBIO), significantly reduced CA1 neuron cell death and improved CA/CPR-induced cognitive outcome. Electrophysiological recordings showed that CA/CPR-induced ischemia caused delayed and sustained reduction of synaptic SK channel activity, and immunoelectron microscopy showed that this is associated with internalization of synaptic SK2 channels, which was prevented by 1-EBIO treatment. These results suggest that increasing SK2 channel activity, or preventing ischemia-induced loss of synaptic SK2 channels, are promising and novel approaches to neuroprotection following cerebral ischemia. |
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| AbstractList | In mouse hippocampal CA1 pyramidal neurons, the activity of synaptic small-conductance Ca
2+
-activated K
+
channels type 2 (SK2 channels) provides a negative feedback on
N
-methyl--aspartate receptors (NMDARs), reestablishing Mg
2+
block that reduces Ca
2+
influx. The well-established role of NMDARs in ischemia-induced excitotoxicity led us to test the neuroprotective effect of modulating SK2 channel activity following cerebral ischemia induced by cardiac arrest and cardiopulmonary resuscitation (CA/CPR). Administration of the SK channel positive modulator, 1-ethyl-benzimidazolinone (1-EBIO), significantly reduced CA1 neuron cell death and improved CA/CPR-induced cognitive outcome. Electrophysiological recordings showed that CA/CPR-induced ischemia caused delayed and sustained reduction of synaptic SK channel activity, and immunoelectron microscopy showed that this is associated with internalization of synaptic SK2 channels, which was prevented by 1-EBIO treatment. These results suggest that increasing SK2 channel activity, or preventing ischemia-induced loss of synaptic SK2 channels, are promising and novel approaches to neuroprotection following cerebral ischemia. In mouse hippocampal CA1 pyramidal neurons, the activity of synaptic small-conductance Ca(2+)-activated K(+) channels type 2 (SK2 channels) provides a negative feedback on N-methyl-D-aspartate receptors (NMDARs), reestablishing Mg(2+) block that reduces Ca(2+) influx. The well-established role of NMDARs in ischemia-induced excitotoxicity led us to test the neuroprotective effect of modulating SK2 channel activity following cerebral ischemia induced by cardiac arrest and cardiopulmonary resuscitation (CA/CPR). Administration of the SK channel positive modulator, 1-ethyl-benzimidazolinone (1-EBIO), significantly reduced CA1 neuron cell death and improved CA/CPR-induced cognitive outcome. Electrophysiological recordings showed that CA/CPR-induced ischemia caused delayed and sustained reduction of synaptic SK channel activity, and immunoelectron microscopy showed that this is associated with internalization of synaptic SK2 channels, which was prevented by 1-EBIO treatment. These results suggest that increasing SK2 channel activity, or preventing ischemia-induced loss of synaptic SK2 channels, are promising and novel approaches to neuroprotection following cerebral ischemia. In mouse hippocampal CA1 pyramidal neurons, the activity of synaptic small-conductance Ca2+-activated K+ channels type 2 (SK2 channels) provides a negative feedback on N-methyl-d-aspartate receptors (NMDARs), reestablishing Mg2+ block that reduces Ca2+ influx. The well-established role of NMDARs in ischemia-induced excitotoxicity led us to test the neuroprotective effect of modulating SK2 channel activity following cerebral ischemia induced by cardiac arrest and cardiopulmonary resuscitation (CA/CPR). Administration of the SK channel positive modulator, 1-ethyl-benzimidazolinone (1-EBIO), significantly reduced CA1 neuron cell death and improved CA/CPR-induced cognitive outcome. Electrophysiological recordings showed that CA/CPR-induced ischemia caused delayed and sustained reduction of synaptic SK channel activity, and immunoelectron microscopy showed that this is associated with internalization of synaptic SK2 channels, which was prevented by 1-EBIO treatment. These results suggest that increasing SK2 channel activity, or preventing ischemia-induced loss of synaptic SK2 channels, are promising and novel approaches to neuroprotection following cerebral ischemia. In mouse hippocampal CA1 pyramidal neurons, the activity of synaptic small-conductance Ca super(2+)-activated K super(+) channels type 2 (SK2 channels) provides a negative feedback on N-methyl-D-aspartate receptors (NMDARs), reestablishing Mg super(2+) block that reduces Ca super(2+) influx. The well-established role of NMDARs in ischemia-induced excitotoxicity led us to test the neuroprotective effect of modulating SK2 channel activity following cerebral ischemia induced by cardiac arrest and cardiopulmonary resuscitation (CA/CPR). Administration of the SK channel positive modulator, 1-ethyl-benzimidazolinone (1-EBIO), significantly reduced CA1 neuron cell death and improved CA/CPR-induced cognitive outcome. Electrophysiological recordings showed that CA/CPR-induced ischemia caused delayed and sustained reduction of synaptic SK channel activity, and immunoelectron microscopy showed that this is associated with internalization of synaptic SK2 channels, which was prevented by 1-EBIO treatment. These results suggest that increasing SK2 channel activity, or preventing ischemia-induced loss of synaptic SK2 channels, are promising and novel approaches to neuroprotection following cerebral ischemia. |
| Author | Nakano, Takaaki Kuroiwa, Masayuki Palmateer, Julie Bond, Chris T Watanabe, Masahiko Maylie, James Herson, Paco S Nakayama, Shin Ballesteros, Carmen Luján, Rafael Adelman, John P Allen, Duane Kosaka, Yasuharu |
| Author_xml | – sequence: 1 givenname: Duane surname: Allen fullname: Allen, Duane – sequence: 2 givenname: Shin surname: Nakayama fullname: Nakayama, Shin – sequence: 3 givenname: Masayuki surname: Kuroiwa fullname: Kuroiwa, Masayuki – sequence: 4 givenname: Takaaki surname: Nakano fullname: Nakano, Takaaki – sequence: 5 givenname: Julie surname: Palmateer fullname: Palmateer, Julie – sequence: 6 givenname: Yasuharu surname: Kosaka fullname: Kosaka, Yasuharu – sequence: 7 givenname: Carmen surname: Ballesteros fullname: Ballesteros, Carmen – sequence: 8 givenname: Masahiko surname: Watanabe fullname: Watanabe, Masahiko – sequence: 9 givenname: Chris T surname: Bond fullname: Bond, Chris T – sequence: 10 givenname: Rafael surname: Luján fullname: Luján, Rafael – sequence: 11 givenname: James surname: Maylie fullname: Maylie, James – sequence: 12 givenname: John P surname: Adelman fullname: Adelman, John P – sequence: 13 givenname: Paco S surname: Herson fullname: Herson, Paco S email: hersonp@ohsu.edu |
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| Keywords | global ischemia electrophysiology hippocampus excitotoxicity cardiac arrest potassium channels Cardiocirculatory arrest Nervous system diseases Toxicity Electrophysiology Cardiovascular disease Inorganic element Cerebral disorder Ischemia Cell death Excitotoxicity Central nervous system disease Potassium Hippocampus Cerebrovascular disease |
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| Snippet | In mouse hippocampal CA1 pyramidal neurons, the activity of synaptic small-conductance Ca2+-activated K+ channels type 2 (SK2 channels) provides a negative... In mouse hippocampal CA1 pyramidal neurons, the activity of synaptic small-conductance Ca(2+)-activated K(+) channels type 2 (SK2 channels) provides a negative... In mouse hippocampal CA1 pyramidal neurons, the activity of synaptic small-conductance Ca 2+ -activated K + channels type 2 (SK2 channels) provides a negative... In mouse hippocampal CA1 pyramidal neurons, the activity of synaptic small-conductance Ca super(2+)-activated K super(+) channels type 2 (SK2 channels)... In mouse hippocampal CA1 pyramidal neurons, the activity of synaptic small-conductance Ca 2+ -activated K + channels type 2 (SK2 channels) provides a negative... |
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| Title | SK2 channels are neuroprotective for ischemia-induced neuronal cell death |
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