Apoptotic Neuronal Death
Apoptotic Neuronal Death - Related Videos
01:30
TUNEL Assay for Detecting Apoptotic Cell Death in a Brain Slice
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2025
To detect apoptotic cell death using the TUNEL assay, treat the brain slice with the enzyme proteinase-K.
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...
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.
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.
10:36
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.
FAQs
Apoptotic neuronal death is often analyzed as a sequence that begins upstream of caspase activation. Intrinsic stress can impair mitochondria and promote cytochrome c release, linking organelle dysfunction to initiator caspases. These then activate executioner caspases, which fragment cellular components in an orderly manner. Mapping this sequence helps separate initiating stress signals from the later dismantling phase.
Energy dependence distinguishes this regulated pathway from a passive loss of cellular integrity. Because the process requires cellular energy and proceeds through coordinated molecular steps, researchers can examine whether mitochondrial disruption and caspase activation reflect an organized death program. The relative absence of inflammation, compared with necrosis, also helps interpret how dying neurons may affect surrounding neural tissue.
During development, selective neuronal elimination helps shape functional neural circuits rather than simply reducing cell number. If apoptosis is insufficient, inappropriate neurons may remain; if it is excessive, developing populations may be depleted. This balance gives neuroscience research a framework for relating regulated cell loss to circuit formation and to developmental disorders when normal tissue maintenance is disrupted.
Reliable interpretation depends on combining molecular markers with the order of signaling events. Evidence for mitochondrial disruption, cytochrome c release, and caspase activation can place a neuron along the pathway, while the pattern of cellular fragmentation supports the downstream outcome. Considering these features together is more informative than treating any single signal as a complete account of neuronal death.
In disease-focused neuroscience, the pathway provides a mechanism for investigating why particular neuronal populations are lost after stress, injury, or during neurodegenerative processes. Comparing the extent and sequence of apoptotic signaling across these contexts can connect cellular events with tissue-level loss. The same framework also supports study of developmental disorders involving abnormal neuronal elimination.
Cytochrome c release, initiator caspases, and executioner caspases represent distinct points for investigating intervention. Researchers can ask whether a candidate strategy preserves mitochondrial function, limits downstream caspase activation, or changes the final cellular dismantling pattern. These measurements help test neuroprotective ideas mechanistically rather than relying only on whether fewer neurons appear to be lost.