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Related Experiment Video

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Calcineurin proteolysis in astrocytes: Implications for impaired synaptic function.

Melanie M Pleiss1, Pradoldej Sompol2, Susan D Kraner2

  • 1Department of Pharmacology and Nutritional Sciences, University of Kentucky College of Medicine, Lexington, KY, USA.

Biochimica Et Biophysica Acta
|May 24, 2016
PubMed
Summary

Proteolytic activation of calcineurin in astrocytes is linked to neural dysfunction in brain injury and disease. This study developed an antibody to detect this activated form, revealing its presence in damaged brain regions and its role in synaptic disruption.

Keywords:
Alzheimer's diseaseAstrocytesCalcineurinMicroinfarctProteolysis

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Pathology

Background:

  • Astrocyte activation is common in neural injury and disease, often linked to calcineurin hyperactivation.
  • Calcineurin hyperactivity frequently results from limited proteolysis, but its status in activated astrocytes is unclear.

Purpose of the Study:

  • To investigate the proteolytic status of calcineurin in activated astrocytes.
  • To develop tools for detecting calcineurin proteolysis in neural pathology.
  • To determine if astrocytic calcineurin hyperactivation impacts synaptic function.

Main Methods:

  • Developed a polyclonal antibody targeting a 45-48kDa calcineurin proteolytic fragment (ΔCN).
  • Applied the ΔCN antibody to postmortem human brain sections for immunohistochemistry.
  • Utilized confocal microscopy to confirm ΔCN expression in astrocytes near pathology.
  • Expressed a ΔCN fragment in rat hippocampal astrocytes via adeno-associated virus.

Main Results:

  • The ΔCN antibody intensely labeled activated astrocytes near amyloid deposits and microinfarcts in human brain tissue.
  • ΔCN expression was also observed in neurons within microinfarct cores.
  • Selective expression of ΔCN in rat astrocytes significantly reduced CA3-CA1 excitatory synaptic strength.

Conclusions:

  • Proteolytic activation of calcineurin occurs in astrocytes associated with neurodegenerative disease and injury.
  • This astrocytic calcineurin hyperactivation is sufficient to disrupt synaptic function.
  • Proteolytic calcineurin activation in astrocytes may be a key mechanism in neural dysfunction.