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Spreading depression and central nervous system pharmacology.
K H Reid1, R Marrannes, A Wauquier
1Department of Physiology, School of Medicine, University of Louisville, Kentucky 40292.
Journal of Pharmacological Methods
|March 1, 1988
Summary
Spreading depression, a brain response, is linked to migraine auras. This study found that high extracellular potassium levels (8-12 mM) trigger spreading depression in rats, not minor injuries.
Area of Science:
- Neuroscience
- Physiology
Background:
- Spreading depression (SD) is a wave of neuronal and glial depolarization in the brain.
- It is hypothesized to be the mechanism behind the aura phase of classic migraine headaches.
Purpose of the Study:
- To investigate the properties and mechanisms of stimulus-induced spreading depression in rat parietal neocortex.
- To determine the threshold for extracellular potassium concentration ([K+]) that triggers spreading depression.
- To assess whether minor cortical injury can induce spreading depression.
Main Methods:
- Stimulus-induced spreading depression using a cup electrode in alfentanil-anesthetized rats.
- Recording extracellular [K+] and potential changes in the parietal neocortex.
- Applying pressure and causing minor dural damage to the cortex.
Main Results:
- Spreading depression was observed when extracellular [K+] exceeded 8-12 mM in the upper 100-200 microns of the cortex.
- Extracellular [K+] could increase post-stimulus without after-discharge.
- Minor cortical injury, unlike pressure, rarely induced spreading depression.
Conclusions:
- High extracellular potassium is a key factor in inducing spreading depression.
- Minor neurovascular injury is unlikely to be the source of migraine-associated spreading depression.
- Further research into SD mechanisms and pharmacology is warranted.