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Related Experiment Videos

Death commitment point is advanced by axotomy in sympathetic neurons.

G C Fletcher1, L Xue, S K Passingham

  • 1Department of Biochemistry, University of Cambridge, Cambridge, CB2 1QW, United Kingdom.

The Journal of Cell Biology
|August 23, 2000
PubMed
Summary

Axotomized sympathetic neurons commit to cell death before caspase activation, even when caspases are inhibited. Nerve Growth Factor (NGF) cannot rescue these neurons due to mitochondrial loss and uncoupled protein synthesis.

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Molecular Biology

Background:

  • Axotomized neurons exhibit distinct characteristics compared to intact neurons.
  • Nerve Growth Factor (NGF) plays a crucial role in neuronal survival and function.
  • Caspase activation is a key event in programmed cell death (apoptosis).

Purpose of the Study:

  • To investigate the sequence of events leading to cell death in axotomized sympathetic neurons.
  • To determine the role of caspases and NGF in neuronal survival following axotomy.
  • To elucidate the mechanisms underlying NGF-induced rescue failure in axotomized neurons.

Main Methods:

  • Culturing sympathetic neurons and inducing axotomy.
  • Treating neurons with NGF and a pan-caspase inhibitor (BAF).

Related Experiment Videos

  • Assessing neuronal survival, protein synthesis, ATP levels, mitochondrial integrity, and cytochrome c release.

    • Main Results:

    • Axotomized neurons deprived of NGF committed to die before caspase activation, as evidenced by rescue with NGF even when caspases were inhibited.
    • NGF-induced signaling (Akt, ERK) failed to restore protein synthesis, ATP levels, or growth in axotomized neurons.
    • Mitochondria disappeared within 3 days, and cytosolic cytochrome c rapidly killed axotomized neurons, while intact neurons were rescued.
    • NGF rescue failed in axotomized neurons even after BAF treatment, indicating a critical loss of repair capacity.

    Conclusions:

    • Axotomy induces premature death commitment in sympathetic neurons, independent of initial caspase activation.
    • NGF cannot repair axotomized neurons due to uncoupled protein synthesis and severe mitochondrial damage.
    • The sequence of events in neuronal death commitment is flexible and subject to regulation, with axotomy altering this process.