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The enemy at the gates. Ca2+ entry through TRPM7 channels and anoxic neuronal death
Pierluigi Nicotera1, Daniele Bano
1MRC Toxicology Unit, University of Leicester, Lancaster Road, LE1 9HN Leicester, UK.
Abstract:
In brain ischemia, gating of postsynaptic glutamate receptors is thought to initiate Ca2+ overload leading to excitotoxic neuronal death. In this issue, Aarts and colleagues describe a novel mechanism, whereby gating of TRPM7, a Ca2+-permeable nonselective cation channel, mediates Ca2+ overload and demise of anoxic neurons.
Insights
Gating of the TRPM7 channel, a calcium-permeable channel, causes calcium overload and neuronal death during brain ischemia. This study reveals a new mechanism for excitotoxic neuronal death in anoxic neurons.
Area of Science:
- Neuroscience
- Cell Biology
- Physiology
Background:
- Brain ischemia leads to excitotoxic neuronal death.
- Postsynaptic glutamate receptor gating is a known cause of calcium overload.
Discussion:
- Aarts and colleagues identified TRPM7 channel gating as a novel mechanism for neuronal demise.
- TRPM7 is a calcium-permeable nonselective cation channel.
Key Insights:
- TRPM7 channel gating mediates calcium overload in anoxic neurons.
- This pathway contributes to excitotoxic neuronal death.
Outlook:
- Targeting TRPM7 may offer new therapeutic strategies for brain ischemia.
- Further research into TRPM7 function in neuronal health and disease is warranted.
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