Related Experiment Video
Updated: Jun 2, 2026

Examination of Anatomical Features of Retinal Ganglion Cells Under N-methyl-D-aspartic Acid (NMDA)-induced Excitotoxicity
Published on: September 19, 2025
Calcium-permeable ion channels involved in glutamate receptor-independent ischemic brain injury
Ming-hua Li1, Koichi Inoue, Hong-fang Si
1Department of Psychology, Washington State University, Vancouver, WA, USA.
Insights
Brain ischemia causes death and disability. This review explores how TRPM7 and acid-sensing channels contribute to neuronal calcium overload, offering new therapeutic targets for brain ischemia.
Area of Science:
- Neuroscience
- Cell Biology
- Pathophysiology
Background:
- Brain ischemia is a major global health issue, leading to significant mortality and long-term disability.
- Current treatments like thrombolysis are limited in efficacy and carry risks such as intracerebral hemorrhage.
- Understanding neuronal injury mechanisms in ischemia is crucial for developing effective therapies.
Purpose of the Study:
- To review the role of specific calcium (Ca2+) channels in neuronal injury during brain ischemia.
- To elucidate the pathways of glutamate-independent Ca2+ toxicity in ischemic conditions.
- To identify potential therapeutic targets for mitigating brain ischemia-induced neuronal damage.
Main Methods:
- Literature review focusing on cellular mechanisms of brain ischemia.
- Analysis of the involvement of TRPM7 channels in Ca2+ homeostasis during ischemia.
- Examination of the function of acid-sensing channels in neuronal Ca2+ overload.
Main Results:
- Intracellular Ca2+ overload is a key factor in neuronal injury following brain ischemia.
- TRPM7 and acid-sensing channels are identified as critical contributors to toxic Ca2+ influx.
- These channels mediate Ca2+ toxicity independently of glutamate excitotoxicity.
Conclusions:
- TRPM7 and acid-sensing channels represent significant pathways for Ca2+ dysregulation in brain ischemia.
- Targeting these channels may offer novel therapeutic strategies for treating brain ischemia.
- Further research into these channels could lead to improved outcomes for patients suffering from stroke.
Abstract:
Brain ischemia is a leading cause of death and long-term disabilities worldwide. Unfortunately, current treatment is limited to thrombolysis, which has limited success and a potential side effect of intracerebral hemorrhage. Searching for new cell injury mechanisms and therapeutic interventions has become a major challenge in the field. It has been recognized for many years that intracellular Ca(2+) overload in neurons is essential for neuronal injury associated with brain ischemia. However, the exact pathway(s) underlying the toxic Ca(2+) loading remained elusive. This review discusses the role of two Ca(2+)-permeable cation channels, TRPM7 and acid-sensing channels, in glutamate-independent Ca(2+) toxicity associated with brain ischemia.
More Related Videos
Related Concept Videos
Ligand-Gated Ion Channel Receptor: Gating Mechanism
Non-gated Ion Channels
Compared to the gated ion channels, the non-gated channels, also known as leakage or passive channels, have no gating mechanism.
Non-gated Ion Channels
Compared to the gated ion channels, the non-gated channels, also known as leakage or passive channels, have no gating mechanism.
The Role of Ion Channels in Neuronal Computation
Sometimes a single EPSP is strong enough to induce an action potential in the postsynaptic neuron. However, multiple presynaptic inputs must often create EPSPs around the same time for the postsynaptic neuron to be sufficiently depolarized to fire an action potential.
Ligand-gated Ion Channels
Three Subfamilies of Ligand-gated Ion Channels
Ligand-gated ion channels fall into three subfamilies. The 'Cys-loop' includes the nicotinic acetylcholine receptors, γ-aminobutyric acid (GABA), glycine, and 5-hydroxytryptamine receptors. The second one is the 'Pore-loop' channels that include the...
Secondary Spinal Cord Injury llI: Pathophysiology

