Neuronal Swelling
Neuronal Swelling - Related Videos
05:53
Mitochondrial Ca2+ Retention Capacity Assay and Ca2+-triggered Mitochondrial Swelling Assay
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Cited by 11 •
2018
This protocol aims to describe a method to examine the Ca2+ retention capacity and Ca2+- triggered mitochondrial swelling of isolated mitochondria of SH-SY5Y cells step-by-step.
07:04
Forskolin-induced Swelling in Intestinal Organoids: An In Vitro Assay for Assessing Drug Response in Cystic Fibrosis Patients
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Cited by 121 •
2017
This protocol describes an assay for measuring CFTR function and CFTR modulator responses in cultured tissue from subjects with cystic fibrosis (CF). Biopsy-derived intestinal organoids swell in a cAMP-driven fashion, a response that is defective (or strongly reduced) in CF organoids and can be restored by exposure to CFTR modulators.
10:26
Rewiring Neuronal Circuits: A New Method for Fast Neurite Extension and Functional Neuronal Connection
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Cited by 8 •
2017
This procedure describes how to rapidly initiate, extend and connect neurites organized in microfluidic chambers using poly-D-lysine-coated beads fixed to micropipettes that guide neurite elongation.
04:13
Studying the Effect of Pesticides on Caenorhabditis elegans Neurons
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2025
This video demonstrates evaluating the neurodegenerative effects of a test chemical on Caenorhabditis elegans with fluorescently tagged neurons. Normal neurons show bright fluorescence of intact soma and processes, while diminished fluorescence, swollen soma, and punctuated processes indicate neurodegeneration.
03:04
Inducing Axonal Varicosities with a Micromechanical Stimulus on Neurons
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2025
This video demonstrates the induction of axonal varicosities by applying micromechanical stimulus on neurons. The system comprises a micropipette attached to a syringe containing buffer via tubing. Using a micromanipulator, the micropipette is positioned above the neurons. Fluid pressure is then applied to induce varicosities in axons.
FAQs
Energy failure impairs the sodium-potassium pump, allowing sodium and other ions to accumulate inside the neuron. Water then enters through osmosis, increasing cellular volume. This links metabolic disruption to swelling: the ionic imbalance is not merely a marker of injury but a direct consequence of failed cellular homeostasis.
Excessive glutamate signaling can increase ion influx, adding to the ionic accumulation produced by impaired pump activity. The resulting osmotic movement draws more water into the neuron and can amplify volume changes. This mechanism helps explain why altered excitatory signaling may worsen cellular injury during nervous system stress.
Increased neuronal volume can impair normal signaling by disturbing the cellular conditions required for neural function. If the underlying ionic imbalance persists, swelling may contribute to cell death. Consequently, volume changes provide a mechanistic connection between disrupted homeostasis, impaired brain function, and progression of nervous system injury.
Measurements of neuronal swelling can indicate the extent of cellular injury and help researchers examine how altered ionic balance affects brain function. They also provide a way to assess injury mechanisms and compare responses to potential neuroprotective treatments. The resulting data connect cellular volume changes with broader outcomes after nervous system damage.
This response is relevant in ischemic stroke, traumatic brain injury, and neurotoxic exposure. Although these conditions differ in cause, each can disrupt cellular homeostasis and produce ionic changes linked to swelling. Studying the response across these settings helps researchers identify shared injury mechanisms while evaluating condition-specific effects on neural function.
Researchers can use swelling measurements to evaluate whether a proposed treatment reduces a cellular change associated with nervous system injury. Comparing swelling under injury conditions with swelling after treatment can help assess neuroprotective effects and clarify whether the intervention influences mechanisms involving ionic balance, glutamate signaling, or both.