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Glucose modulation of spreading depression susceptibility
Ulrike Hoffmann1, Inna Sukhotinsky, Katharina Eikermann-Haerter
1Neurovascular Research Laboratory, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA.
Summary
High blood sugar levels make brain tissue more resistant to spreading depolarization (SD), a wave linked to migraines and brain injury. Low blood sugar, however, prolongs SD events.
Area of Science:
- Neuroscience
- Physiology
- Biochemistry
Background:
- Spreading depolarization (SD) is a significant wave of neural activity linked to conditions like migraine aura and brain injury.
- While pharmacological interventions for SD are studied, the impact of systemic physiological factors, particularly blood glucose levels, remains less understood.
- Understanding these modulations is crucial for identifying potential therapeutic targets for neurological disorders.
Purpose of the Study:
- To systematically investigate how varying blood glucose levels (hyperglycemia and hypoglycemia) affect susceptibility to spreading depolarization in a rat model.
- To determine if glycemic state influences key parameters of SD, including threshold, frequency, duration, amplitude, and propagation speed.
Main Methods:
- Anesthetized rats were subjected to controlled physiological monitoring.
- Hyperglycemia (approx. 400 mg/dL) and hypoglycemia (approx. 40 mg/dL) were induced via dextrose or insulin infusion, respectively.
- Spreading depolarizations were evoked using cortical electrical stimulation to assess threshold and topical KCl application to measure frequency.
Main Results:
- Hyperglycemia significantly increased the electrical threshold for evoking SD and decreased the frequency of KCl-induced SDs.
- Hypoglycemia notably prolonged the duration of individual and cumulative SD events but did not affect the electrical threshold, frequency, amplitude, or propagation speed.
- These findings indicate that elevated blood glucose confers resistance to SD initiation and propagation.
Conclusions:
- Cerebral glucose availability plays a critical role in modulating the brain's susceptibility to spreading depolarization.
- Hyperglycemia enhances resistance to SD, suggesting a protective effect in conditions where SD is detrimental.
- Hypoglycemia, conversely, exacerbates SD events, highlighting the importance of maintaining euglycemia in neurological emergencies.
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