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Related Experiment Videos

Apolipoprotein E expression by neurons surviving excitotoxic stress.

U Boschert1, E Merlo-Pich, G Higgins

  • 1Geneva Biomedical Research Institute, 14 Chemin des Aulx, Geneva, 1228, Switzerland.

Neurobiology of Disease
|December 22, 1999
PubMed
Summary

Apolipoprotein E (apoE) mRNA is upregulated in rat neurons following brain injury, suggesting a potential neuroprotective role. This unexpected finding challenges previous assumptions about apoE expression in the adult brain.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cell Biology

Background:

  • Apolipoprotein E (apoE) mRNA is traditionally considered to be expressed by non-neuronal cells in the adult brain.
  • Following brain damage, apoE protein has been observed in neurons, raising questions about its expression patterns under pathological conditions.

Purpose of the Study:

  • To investigate the expression of apolipoprotein E (apoE) mRNA in neurons following induced neurodegeneration.
  • To determine if neuronal apoE expression is a response to brain injury and its potential role in neuroprotection.

Main Methods:

  • Systemic administration of kainic acid (KA) to rats to induce hippocampal neurodegeneration.
  • In situ hybridization to detect apoE mRNA levels in neurons.
  • Immunohistochemistry using neuronal (MAP2) and glial (GFAP, OX42) markers to confirm cell identity.

Related Experiment Videos

  • Analysis of c-fos expression as a marker for neuronal stress.

    • Main Results:

    • A moderate increase in apoE levels was observed in astrocytes.
    • A significant and unexpected upregulation of apoE mRNA was detected in CA1 and CA3 pyramidal neurons.
    • These apoE-expressing cells exhibited neuronal morphology and markers (MAP2), and were negative for astrocytic (GFAP) and microglial (OX42) markers.
    • Co-localization with c-fos indicated that apoE expression occurred in stressed neurons.

    Conclusions:

    • Neuronal expression of apoE mRNA is induced following excitotoxic brain injury.
    • The upregulation of apoE in neurons, particularly in the absence of programmed cell death signs, suggests a potential endogenous neuroprotective or rescue mechanism.
    • These findings challenge the established view of apoE expression in the adult brain and highlight its potential role in neuronal repair.