Related Experiment Video
Updated: Oct 21, 2026

Modeling Neuronal Death and Degeneration in Mouse Primary Cerebellar Granule Neurons
Published on: November 6, 2017
ASIC1a as an integrating node in ischemic neurotoxicity: crosstalk with NMDAR and TRPM signaling
Ke Lai1, Lu-Yang Wang2,3
1Department of Otorhinolaryngology, Shanghai Sixth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200032, China. ilaike@sjtu.edu.cn.
Abstract:
Ischemic stroke triggers acidosis, glutamate excitotoxicity and oxidative stress, which converge to disturb ionic homeostasis through several cation channels, including acid-sensing ion channel 1a (ASIC1a), N-methyl-D-aspartate receptors (NMDARs) and transient receptor potential melastatin (TRPM) channels. Emerging evidence suggests that ASIC1a functions as a context-dependent integrating node: protons directly gate ASIC1a, glutamate and bilirubin-associated signaling can modulate ASIC1a-dependent injury pathways. ASIC1a directly couples with NMDAR-dependent signaling and indirectly engages TRPM-associated pathways. Here, we discuss the mechanistic basis, therapeutic potential and unresolved questions regarding ASIC1a-associated signaling in ischemic brain injury.
Related Concept Videos
Ligand-Gated Ion Channel Receptor: Gating Mechanism
Integration of Synaptic Events
Secondary Spinal Cord Injury llI: Pathophysiology
Neurochemical Transmission: Sites of Drug Action
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.
Excitatory and Inhibitory Effects of Neurotransmitters
