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Visualizing Astrocyte Morphology Using Lucifer Yellow Iontophoresis

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Physical memory of astrocytes.

Tasnim Shireen¹, Frederick Sachs², Susan Z Hua³

¹Department of Mechanical and Aerospace Engineering, University at Buffalo, Buffalo, NY 14260, USA.

|September 9, 2022

Summary

This summary is machine-generated.

Traumatic brain injury (TBI) can cause a cellular "memory" of mechanical stress. Astrocytes exhibit potentiation of calcium responses after repeated mechanical stimuli, indicating a long-term physical memory.

Keywords:

Intracellular Ca(2+)Long-term effect Mechanosensitive ion channel (MSC)Nonlinear cell response Shear forces Traumatic brain injury (TBI)

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Isolation and Culture of Mouse Cortical Astrocytes

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Published on: January 19, 2013

Area of Science:

Neuroscience
Cell Biology
Biophysics

Background:

Traumatic brain injury (TBI) is a significant risk factor for neurodegenerative diseases.
Cellular responses to mechanical stress can manifest long after the initial injury.
The physical basis for cellular memory of mechanical events remains unclear.

Purpose of the Study:

To investigate the properties of cellular memory in response to mechanical stimuli.
To explore the mechanisms underlying long-term cellular responses to repetitive impacts.

Main Methods:

Utilized a microfluidic chip to apply controlled fluid shear stress pulses to adult rat astrocytes.
Monitored intracellular calcium (Ca2+) transients in response to repeated stimuli.
Investigated the role of calcium influx and cytoskeletal deformation in memory formation.

Main Results:

Repeated mechanical stimuli, spaced 6-24 hours apart, led to potentiated Ca2+ responses lasting over 24 hours.
The potentiation was more dependent on the number of stimuli than the rest period between them.
Inhibiting Ca2+ influx during initial stimulation did not prevent subsequent potentiation, implicating mechanical deformation.

Conclusions:

Astrocytes possess a long-term physical memory of mechanical stress.
Plastic deformation of the cytoskeleton is a potential mechanism for this cellular memory.
Understanding this memory mechanism is crucial for addressing TBI-induced neurodegeneration.