Nmda Injury Model
Nmda Injury Model - Related Videos
01:59
Modeling Neuronal Injury in Mouse Primary Cerebellar Granule Neurons
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2025
This video demonstrates the generation of a neuronal injury model in mouse primary cerebellar granule neurons. It outlines the steps involved in inducing neuronal injury using NMDA, an excitatory neurotransmitter receptor agonist, and glycine, a co-agonist. NMDA and glycine bind to specific neuronal receptors, causing their overstimulation and resulting in a massive intracellular calcium influx, which leads to neuronal cell damage and death.
06:33
The Organotypic Hippocampal Slice Culture Model for Examining Neuronal Injury
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Cited by 9 •
2010
The organoptypic hippocampal slice culture model is an in vitro model used to examine neuronal injury in a variety of paradigms. In this article, we describe the methods for generating slice cultures and quantifying neuronal injury.
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.
07:11
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.
04:19
A Mouse Model of Single and Repetitive Mild Traumatic Brain Injury
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Cited by 16 •
2017
Athletes absorb several hundred mild traumatic brain injuries (mTBI)/concussions every year; however, the consequence of these on the brain is poorly understood. Therefore, an animal model of single and repetitive mTBI that consistently replicates clinically relevant symptoms provides the means to advance the study of mTBI and concussion.
FAQs
Excessive receptor stimulation opens calcium-permeable ion channels, so calcium enters neurons persistently rather than producing a limited signaling event. The resulting calcium load disrupts cellular signaling and increases metabolic stress. These linked changes provide a mechanistic bridge between NMDA receptor activation and neuronal death, allowing investigators to examine how excitotoxic injury progresses at the cellular level.
Sustained calcium influx matters because it links prolonged NMDA receptor activity to multiple forms of cellular stress. Elevated intracellular calcium can disrupt signaling systems and increase the metabolic burden placed on neurons, creating conditions that may progress toward cell death. Studying this sequence helps researchers distinguish receptor activation from the damaging downstream processes that follow it.
A controlled NMDA exposure gives investigators a defined way to compare how strongly neuronal injury develops across experimental conditions. Researchers can examine differences in the extent of damage and evaluate whether particular pathways or compounds alter the response. This makes the model useful for connecting the intensity of receptor-driven stress with measurable changes in neuronal survival or injury progression.
The experimental system applies NMDA under controlled conditions to either cultured neurons or brain tissue. Researchers then examine the resulting cellular injury and use the observations to compare injury severity or responses to an intervention. Because the exposure is experimentally controlled, the model supports focused analysis of excitotoxic mechanisms without requiring the complexity of an entire disease condition.
Neuroprotective compounds can be studied by comparing neuronal injury after controlled NMDA exposure with the response observed when a candidate compound or pathway is examined. The central outcome is whether the intervention changes the extent or progression of damage. This approach helps identify cellular mechanisms that may reduce excitotoxic injury and prioritizes pathways for further neuroscience research.
The model reproduces cellular injury driven by excessive NMDA receptor activation, a mechanism relevant to several forms of neurological damage. Researchers can therefore use it to investigate pathways and potential protective responses associated with ischemic injury, traumatic brain damage, and neurodegenerative disease. It provides a controlled cellular context for studying shared excitotoxic features across these conditions.