Cav2.1通道信号在谷氨酸相关脑损伤中的作用

Tae Yeon Kim, K. Niimi, Eiki Takahashi
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引用次数: 0

摘要

电压门控Ca2+通道(VGCCs)在神经递质释放、轴突生长、膜兴奋性和突触可塑性等细胞内过程中起关键作用。三个主要的突触前Cav2通道,包括Cav2.1通道,参与Ca2+依赖性兴奋性毒性的机制。谷氨酸是受Cav2.1通道调节的兴奋性神经递质之一。谷氨酸相关兴奋性毒性是一种与癫痫发作、外伤性脑损伤和脑缺血相关的病理过程。本文就Cav2.1通道的激活与这些不同类型脑损伤的关系作一综述。
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Role of Cav2.1 Channel Signaling in Glutamate-Related Brain Injury
Voltage-gated Ca2+ channels (VGCCs) play a pivotal role in intracellular processes such as neurotransmitter release, axonal outgrowth, membrane excitability, and synaptic plasticity. Three major presynaptic Cav2 channels, including the Cav2.1 channel, are involved in the mechanism underlying Ca2+-dependent excitotoxicity. Glutamate is among the excitatory neurotransmitters regulated by the Cav2.1 channel. Glutamate-related excitotoxicity is a pathological process associated with seizures, traumatic brain injury, and cerebral ischemia. This review emphasizes the relationship between activation of the Cav2.1 channel and these various types of brain injury.
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