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Spreading depression in human neocortical slices.

A Gorji1, D Scheller, H Straub

  • 1Institut für Physiologie, Universität Münster, Robert-Koch-Strasse 27a, Münster 48149, Germany. gorgial@uni-muenster.de

Brain Research
|June 30, 2001
PubMed
Summary

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Cortical spreading depression (CSD) in human brain tissue was investigated. Modulating calcium (Ca2+) dynamics increased CSD susceptibility, suggesting the glutamatergic pathway

Area of Science:

  • Neuroscience
  • Neurophysiology
  • Epileptology

Background:

  • Cortical spreading depression (CSD) is linked to neurological conditions like epilepsy, migraine aura, and brain injury.
  • Previous research on human neocortical slices is limited, necessitating comprehensive studies on CSD in humans.

Purpose of the Study:

  • To investigate the occurrence and characteristics of CSD in human neocortical tissue.
  • To explore the role of calcium (Ca2+) dynamics and glutamatergic pathways in human CSD.

Main Methods:

  • Utilized human neocortical slices obtained from epilepsy surgery.
  • Induced CSD using KCl injection and by modulating T-type Ca2+ currents with amiloride or NiCl2.
  • Recorded DC-fluctuations and measured extracellular potassium levels; blocked CSD with NMDA receptor antagonist.

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Main Results:

  • KCl injection triggered single CSD propagating at 3.1 mm/min.
  • Repetitive CSD occurred spontaneously with T-type Ca2+ channel blockers, increasing extracellular potassium to 50 mM.
  • CSD was consistently blocked by the NMDA receptor antagonist 2-amino-5-phosphonovaleric acid.

Conclusions:

  • Modulation of Ca2+ dynamics enhances human neocortical slice susceptibility to CSD.
  • The glutamatergic pathway plays a significant role in the CSD phenomenon in humans.
  • This study provides novel insights into human CSD mechanisms relevant to neurological disorders.