Different pathomechanisms, for example, immune-mediated inflammation, oxidative stress and excitotoxicity, are involved in the immunopathology of MS.
多发性硬化症的免疫病理学的不同病理机制包括免疫介导炎症、氧化应激、兴奋毒等。
Excitotoxicity
英语例句库
原声例句
Osmosis-遗传
Cell death might be related to excitotoxicity – which is excessive signaling of these neurons, which leads to high intracellular calcium.
神经元细胞死亡可能与兴奋性毒性有关，即这些神经元细胞接受过度信号传递，引起细胞内钙离子浓度升高。
电台实验室
MONICA MURPHY: Well, excitotoxicity— and this is tricky stuff, and it's controversial.
莫妮卡·墨菲：嗯，兴奋性毒性——这是一个棘手的问题，而且是有争议的。
英语百科
Excitotoxicity
![Low Ca2+ buffering and excitotoxicity under physiological stress and pathophysiological conditions in motor neuron (MNs). Low Ca2+ buffering in amyotrophic lateral sclerosis (ALS) vulnerable hypoglossal MNs exposes mitochondria to higher Ca2+ loads compared to highly buffered cells. Under normal physiological conditions, the neurotransmitter opens glutamate, NMDA and AMPA receptor channels, and voltage dependent Ca2+ channels (VDCC) with high glutamate release, which is taken up again by EAAT1 and EAAT2. This results in a small rise in intracellular calcium that can be buffered in the cell. In ALS, a disorder in the glutamate receptor channels leads to high calcium conductivity, resulting in high Ca2+ loads and increased risk for mitochondrial damage. This triggers the mitochondrial production of reactive oxygen species (ROS), which then inhibit glial EAAT2 function. This leads to further increases in the glutamate concentration at the synapse and further rises in postsynaptic calcium levels, contributing to the selective vulnerability of MNs in ALS. Jaiswal et al., 2009.[1]](/uploads/202501/12/Low_Ca2+_buffering_and_excitotoxicity_under_physiological_stress_and_pathophysiological_conditions_in_motor_neuron_(MNs)4030.jpg)
Excitotoxicity is the pathological process by which nerve cells are damaged or killed by excessive stimulation by neurotransmitters such as glutamate and similar substances. This occurs when receptors for the excitatory neurotransmitter glutamate (glutamate receptors) such as the NMDA receptor and AMPA receptor are overactivated by glutamatergic storm. Excitotoxins like NMDA and kainic acid which bind to these receptors, as well as pathologically high levels of glutamate, can cause excitotoxicity by allowing high levels of calcium ions (Ca) to enter the cell. Ca influx into cells activates a number of enzymes, including phospholipases, endonucleases, and proteases such as calpain. These enzymes go on to damage cell structures such as components of the cytoskeleton, membrane, and DNA.
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