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Preparation of Synaptic Plasma Membrane and Postsynaptic Density Proteins Using a Discontinuous Sucrose Gradient
Published on: September 3, 2014
Astrocyte swelling leads to membrane unfolding, not membrane insertion
Tina Pangrsic1, Maja Potokar, Philip G Haydon
1Laboratory of Neuroendocrinology-Molecular Cell Physiology, Institute of Pathophysiology, Medical Faculty, University of Ljubljana, Ljubljana, Slovenia.
Journal of Neurochemistry
|October 13, 2006
Summary
Hypotonic conditions cause astrocyte swelling through a mechanism independent of exocytosis. This study reveals that cell membrane unfolding, not regulated exocytosis, accounts for the observed changes in astrocyte size under hypotonic stress.
Area of Science:
- Neuroscience
- Cell Biology
- Biophysics
Background:
- Astrocytes release chemical transmitters, but the mechanisms are not fully understood.
- Hypotonic conditions are known to stimulate the release of glutamate and ATP from astrocytes.
- The precise mechanism by which hypotonicity induces this release remains unclear.
Purpose of the Study:
- To investigate whether hypotonicity activates regulated exocytosis in astrocytes.
- To elucidate the mechanism of astrocyte swelling under hypotonic conditions.
Main Methods:
- Whole-cell patch-clamp technique to monitor membrane capacitance in cultured astrocytes.
- Simultaneous measurement of cell size, membrane conductance, and surface area.
- Application of hypotonic medium (210 mOsm for 200 s).
Main Results:
- Hypotonic medium induced significant astrocyte swelling (average 40% increase in cross-sectional area).
- No corresponding change in membrane surface area was detected.
- Membrane capacitance measurements, sensitive to 0.5% surface area changes, showed no increase.
Conclusions:
- Astrocyte swelling under hypotonic conditions occurs independently of regulated exocytosis.
- The observed swelling is likely mediated by an exocytosis-independent mechanism, possibly involving plasma membrane unfolding.
- This finding clarifies a key aspect of astrocyte response to osmotic stress.
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