Neuronal Death Induction
Neuronal Death Induction - Related Videos
04:25
Neuronal Death Assay to Evaluate Cell Death in Ex Vivo Epilepsy Model
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2025
This video demonstrates the technique of assessing neuronal death in rhinal cortex-hippocampus organotypic slices. Neuronal death occurs via evolving epileptic seizures — resembling in vivo epilepsy — and is detected through dual-staining of the dead cells using propidium iodide and immunofluorescence.
10:36
Modeling Neuronal Death and Degeneration in Mouse Primary Cerebellar Granule Neurons
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Cited by 2 •
2017
This protocol describes a simple method for isolating and culturing primary mouse cerebral granule neurons (CGNs) from 6-7 day old pups, efficient transduction of CGNs for loss and gain of function studies, and modelling NMDA-induced neuronal excitotoxicity, low-potassium-induced cell death, DNA-damage, and oxidative stress using the same culture model.
01:59
Modeling Reactive Oxygen Species-Induced Neuronal Death in Mouse Cerebellar Granule Neurons
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2025
This video outlines the generation of a neuronal injury model using reactive oxygen species (ROS) in mouse primary cerebellar granule neurons. It details the process of inducing oxidative stress by adding high concentrations of hydrogen peroxide. ROS exposure causes DNA strand breaks and genomic instability. Additionally, the oxidation of cellular proteins impairs their functions, while lipid peroxidation compromises membrane integrity. This cascade leads to cytochrome c release and caspase...
03:50
An Ex Vivo Technique to Induce Neuronal Death via Oligodendrocyte-Specific CD8+ T Cells
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2025
This video demonstrates an ex vivo technique to induce brain cell death mediated through cytotoxic CD8+ T cells. Upon obtaining brain slices, activated oligodendrocyte-directed CD8+ T cells are transferred onto the slices to target the myelin sheath and oligodendrocytes. Post-incubation, the damage to myelin and neuronal death can be assessed histologically in the regions of interest.
10:44
Sex Stratified Neuronal Cultures to Study Ischemic Cell Death Pathways
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Cited by 7 •
2013
Primary disassociated embryonic hippocampal neuronal cultures are useful for investigating the signaling mechanisms involved in neuron death. Sexing the embryos before the isolation and dissociation of the hippocampus allows the preparation of separate male and female cultures, which enables the researcher to identify and investigate sex-specific cell signaling.
FAQs
Different injury triggers converge on several damaging events. Excitotoxic glutamate can promote calcium overload, while oxidative stress can impair mitochondria; trophic-factor withdrawal and neurotoxins may also activate intracellular death pathways. These changes can lead to caspase activation and culminate in apoptotic or necrotic loss, allowing researchers to relate an initiating insult to specific molecular responses.
Separating apoptotic and necrotic outcomes helps clarify how neurons respond to experimental injury. Caspase activation is associated with apoptotic pathway analysis, whereas broader injury models may produce necrotic loss. This distinction matters because researchers can compare molecular mechanisms rather than treating every reduction in neuron number as the same biological process.
The chosen stressor determines which aspect of neuronal injury the model emphasizes. Excitotoxic glutamate highlights calcium-related damage, oxidative stress focuses attention on redox injury and mitochondrial dysfunction, and trophic-factor withdrawal examines loss of survival support. Comparing these triggers helps investigators distinguish shared mechanisms from pathway-specific effects in nervous tissue.
Researchers first apply a controlled injury stimulus, such as excitotoxic glutamate, oxidative stress, a neurotoxin, or trophic-factor withdrawal. They then compare affected neurons with an appropriate untreated or contrasting condition, assessing cell survival, structural changes, and functional outcomes. This sequence links the imposed stress to measurable consequences and supports evaluation of candidate protective responses.
These models are useful when researchers need a controlled way to examine nervous-tissue damage relevant to neurodegenerative disease, stroke, trauma, or developmental processes. By selecting an injury trigger and measuring its consequences, investigators can study how neurons fail under distinct conditions and identify mechanisms that may be shared across different forms of neurological injury.
A candidate compound can be assessed by comparing neuronal survival, structural changes, and functional outcomes after a controlled injury, with and without the intervention. Improvement across these measures supports a protective effect, while pathway-related observations can indicate whether the compound influences calcium overload, mitochondrial dysfunction, caspase activation, or another injury-associated process.