“Remark”>(charge transfer on the cell surface), excessive release of the excitatory neurotransmitter glutamate, and sodium in neurons(Na ) and potassium (K) ions are out of balance.
Excessive release of glutamate will activate n-methylaspartate(NMDA) receptors on brain cells, which is essential for maintenance The intracellular Na/K balance of the cell pump has an adverse effect. Excitatory toxicity, these receptors overactivate excessive glutamate, NMDA and other toxic substances, leading to further ion imbalance of neurons and accumulation of metabolites, especially calcium chelation, which further contributes to the toxic microenvironment.
The toxic microenvironment leads to a variety of secondary cellular effects, causing further damage. An example of secondary damage is the activation of brain immune cells, such as microglia and astrocytes. For laboratory mice hitting the cerebral cortex under controlled conditions, this is a severe brain trauma model, the result of which is to induce the release of the amino acid D-serine. D-serine binds to NMDA receptors, causing damage to the synapses, which are the junctions for communication between brain cells.
In this animal model, blocking the release of D-serine plays a protective role. It is believed that long-term persistent adverse cell reactions and reduced axonal transport are another mechanism that causes damage. Through the brain sugar gland (glymphatic) system and other means to reduce the removal of metabolites, and aggravate the toxicity and toxins of the microenvironment.[such as hyperphosphorylated tau protein (pTau)] accumulation. In chronic traumatic encephalopathy and other neurodegenerative diseases, nerve fiber nodules formed by pTau, especially those formed around small blood vessels in the brain, are found to cause cell death.
In recent years, there has been a great accumulation of knowledge about brain injury molecules and cell mechanisms, most of which are based on experimental research. However, these studies all use quite serious injury models, which are very different from injuries that usually occur in sports. Another important constraint on our understanding of clinical phenomena is that the mechanism of human brain injury cannot be directly observed in vivo.