Nmda Excitotoxicity
Nmda Excitotoxicity - Related Videos
07:11
Examination of Anatomical Features of Retinal Ganglion Cells Under N-methyl-D-aspartic Acid (NMDA)-induced Excitotoxicity
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2025
Here, we describe the use of a genetically directed alkaline phosphatase (AP) labeling method to investigate the anatomical features and phenotypes of mouse retinas under NMDA-induced excitotoxicity. In conjunction with several retinal ganglion cell (RGC) subtype-specific reporter lines, we uncover novel phenotypes in dying RGCs throughout the degenerative process.
12:45
Stereotaxic Surgery for Excitotoxic Lesion of Specific Brain Areas in the Adult Rat
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Cited by 22 •
2012
Targeted ablation of specific brain region(s) by infusion of an excitotoxin using stereotaxic coordinates is described. This technique could also be adapted for infusion of other chemicals into the rat brain.
06:42
Application of a NMDA Receptor Conductance in Rat Midbrain Dopaminergic Neurons Using the Dynamic Clamp Technique
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Cited by 5 •
2010
In this video, we demonstrate how to apply a conductance into a dopaminergic neuron recorded in the whole cell configuration in rat brain slices. This technique is called the dynamic clamp.
07:00
Excitotoxic Stimulation of Brain Microslices as an In vitro Model of Stroke
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Cited by 3 •
2014
We have developed a brain slice model which can be used to examine molecular mechanisms involved in excitotoxicity-mediated brain injury. This technique generates viable mature brain tissue and reduces animal numbers required for experimentation, whilst keeping the neuronal circuitry, cellular interactions, and postsynaptic compartments partly intact.
01:30
Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists
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2024
Cognitive enhancers, also known as "smart drugs," are substances used to enhance memory, mental alertness, and concentration. These can be natural or synthetic and improve cognition in conditions like Alzheimer's disease (AD) and other neurodegenerative diseases. Some common examples include caffeine, amphetamines, methylphenidate, modafinil, arecoline, donepezil, vortioxetine, and piracetam. These enhancers work on the principle of synaptic plasticity and altered circuit function. They...
FAQs
Persistent glutamate signaling removes the receptor’s magnesium block, allowing calcium ions to enter the neuron in excess. This changes a normally regulated signaling event into a damaging calcium load. The resulting imbalance is central to NMDA excitotoxicity because it connects prolonged receptor activation with mitochondrial disruption, oxidative stress, and loss of cellular integrity.
Calcium overload links excessive receptor activity to several intracellular disturbances rather than representing an isolated change in ion concentration. Elevated calcium activates pathways that disrupt mitochondria and increase oxidative stress, which can progressively impair neuronal integrity. Studying this transition helps neuroscience researchers examine how calcium homeostasis fails during harmful glutamate signaling.
Normal NMDA receptor activity contributes to regulated synaptic communication, whereas excitotoxic signaling reflects persistent glutamate stimulation and excessive calcium entry. The distinction depends on the balance and duration of receptor activity, not simply on whether the receptor is present. This comparison is important when designing strategies that reduce harmful signaling without eliminating normal communication between neurons.
Mitochondria are a major intracellular target after excessive NMDA receptor activation. Calcium entry is associated with mitochondrial disruption, while the same damaging cascade increases oxidative stress and weakens cellular integrity. Focusing on these linked effects allows researchers to study excitotoxic injury as a connected process involving receptor regulation, calcium balance, energy-related organelle dysfunction, and oxidative damage.
Research commonly frames NMDA excitotoxicity around three connected questions: how NMDA receptors are regulated, how neurons maintain calcium homeostasis, and how harmful signaling might be limited. These areas provide a framework for examining neuronal injury and evaluating potential therapeutic directions. The goal is to reduce damaging receptor activity while preserving the synaptic communication required for normal brain function.
The mechanism is used to help explain neuronal loss associated with ischemic stroke, traumatic brain injury, epilepsy, and some neurodegenerative diseases. These conditions differ clinically, but NMDA excitotoxicity provides a shared neuroscience context for investigating excessive glutamate signaling, calcium imbalance, mitochondrial disruption, and oxidative stress. Its relevance therefore extends across acute injuries and longer-term disease processes.