Neuronal Death Assessment
Neuronal Death Assessment - 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.
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.
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...
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
Caspase activation indicates engagement of the molecular machinery associated with apoptosis, while DNA fragmentation provides a second readout of the same type of cellular loss. Examining both markers helps researchers determine whether reduced neuronal viability reflects an apoptotic pathway rather than relying on a single indicator. This distinction is useful when analyzing nervous system injury, disease, or infection-related damage.
Loss of plasma membrane integrity is a marker of necrotic neuronal death and provides information that apoptosis-associated measurements cannot supply alone. Including this readout helps distinguish membrane-disrupting cell loss from death characterized by caspase activation or DNA fragmentation. In infection and inflammatory studies, that distinction can clarify how damaging signals affect neurons.
A viability measurement indicates whether neurons remain alive, but it does not by itself identify the pathway responsible for their loss. Pairing viability assays with apoptosis and necrosis markers links the overall outcome to a mechanism. This combined strategy can reveal whether pathogens, inflammatory mediators, or immune-cell activity produce neuronal damage through different forms of cell death.
A practical workflow begins by measuring neuronal viability, followed by evaluation of caspase activation and DNA fragmentation for apoptotic changes and plasma membrane integrity for necrotic changes. Interpreting these readouts together connects the extent of neuronal loss with its likely pathway. The approach allows investigators to compare damage produced by pathogens, inflammatory mediators, or immune-cell activity.
The assessment can separate neuronal damage associated with a pathogen from effects linked to inflammatory mediators or immune-cell activity by comparing viability and death-pathway markers. Such comparisons help identify whether nervous system injury reflects direct or immune-associated damaging processes, as supported by the experimental design. This information contributes to understanding disease mechanisms in immunology and infection research.
Researchers can compare treatment conditions by examining whether neuronal viability is preserved or reduced and by determining which death markers change. A treatment that maintains viability while limiting apoptosis- or necrosis-associated signals may show protective effects, whereas worsening outcomes may indicate neurotoxicity. These measurements support evaluation of interventions intended to preserve neuronal function.