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Excitotoxicity in the enteric nervous system

A L Kirchgessner1, M T Liu, F Alcantara

  • 1Department of Anatomy and Cell Biology, Columbia University College of Physicians and Surgeons, New York, New York 10032, USA.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|November 14, 1997
PubMed
Summary
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Excessive glutamate exposure causes neurotoxicity in enteric neurons, leading to cell death. This excitotoxicity in the enteric nervous system (ENS) may contribute to intestinal damage.

Area of Science:

  • Neuroscience
  • Gastroenterology
  • Cell Biology

Background:

  • Glutamate is a key excitatory neurotransmitter in the central nervous system (CNS) and the enteric nervous system (ENS).
  • The role of glutamate in ENS neurotoxicity was previously unexplored.

Purpose of the Study:

  • To investigate the hypothesis that excessive glutamate exposure induces neurotoxicity in enteric neurons.
  • To characterize the mechanisms and receptors involved in glutamate-induced excitotoxicity in the ENS.

Main Methods:

  • Stimulation of enteric ganglia with glutamate and NMDA (N-methyl-D-aspartate).
  • Assessment of neurotoxicity using light microscopy for necrosis and apoptosis.
  • Pharmacological blockade using NMDA antagonists.
  • Immunohistochemistry to identify glutamate receptor subunits (NMDA, AMPA, kainate) in enteric neurons.

Related Experiment Videos

  • Mitochondrial function assessment using rhodamine 123 staining.

    • Main Results:

    • Prolonged glutamate stimulation caused necrosis and apoptosis in enteric neurons, with both acute and delayed cell death.
    • NMDA mimicked glutamate neurotoxicity, and this effect was blocked by an NMDA antagonist.
    • Excitotoxicity was more severe in cultured enteric ganglia than in intact bowel preparations, suggesting reduced glutamate uptake.
    • Enteric neurons expressed NMDA, AMPA, and kainate receptor subunits, with receptors clustered on neurites.
    • Kainic acid induced neuronal swelling, neurite blebbing enriched in mitochondria, and loss of mitochondrial membrane potential.

    Conclusions:

    • This study provides the first evidence of excitotoxicity in the ENS.
    • Overactivation of enteric glutamate receptors contributes to neuronal damage.
    • Enteric excitotoxicity may play a role in intestinal injury associated with conditions like anoxia, ischemia, and dietary excitotoxins.