excitotoksisuuteen

Excitotoxicity is a neurotoxic process where nerve cells are damaged or killed by excessive stimulation by neurotransmitters, particularly glutamate. Glutamate is the primary excitatory neurotransmitter in the central nervous system, and its receptors, such as NMDA and AMPA receptors, play crucial roles in synaptic plasticity, learning, and memory. However, under pathological conditions, such as stroke, traumatic brain injury, or neurodegenerative diseases, there can be an excessive release of glutamate into the synaptic cleft.

This surge in glutamate leads to prolonged activation of glutamate receptors. This overactivation causes an influx of calcium ions into the postsynaptic neuron. While calcium is essential for normal neuronal function, excessive intracellular calcium can trigger a cascade of detrimental events. These include the activation of proteases, lipases, and endonucleases, which can degrade cellular components. Furthermore, the overstimulation can lead to mitochondrial dysfunction, an increase in reactive oxygen species, and ultimately cell death through apoptosis or necrosis.

The concept of excitotoxicity was first proposed in the 1960s and has since been a major focus of research in neuroscience and neurology. Understanding the mechanisms of excitotoxicity has led to the development of therapeutic strategies aimed at blocking glutamate receptors or reducing glutamate levels. However, the complexity of glutamate signaling and the critical role of glutamate in normal brain function have made developing effective and safe treatments challenging. Despite these challenges, research continues to explore potential excitotoxicity-targeting therapies for a range of neurological disorders.