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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
Summary
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.
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.