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Seizures elevate gliovascular unit Ca2+ and cause sustained vasoconstriction.
Cam Ha T Tran1,2,3, Antis G George1,4, G Campbell Teskey1,4
1Hotchkiss Brain Institute and.
JCI Insight
|October 2, 2020
Summary
Seizures cause brain blood vessel constriction and hypoxia, impairing memory. Preventing this vasoconstriction may offer a new treatment for epilepsy patients experiencing post-seizure impairments.
Area of Science:
- Neuroscience
- Vascular Biology
- Cellular Physiology
Background:
- Seizures can lead to severe hypoperfusion and hypoxia, causing postictal memory and behavioral deficits.
- In vivo visualization of postictal microvascular and cellular calcium (Ca2+) changes has been lacking, obscuring underlying mechanisms.
Purpose of the Study:
- To visualize in vivo the microvascular and cellular Ca2+ dynamics in the brain during and after seizures.
- To elucidate the cellular mechanisms contributing to seizure-induced hypoperfusion and hypoxia.
Main Methods:
- Utilized 2-photon microvascular and Ca2+ imaging in awake mice during induced seizures.
- Administered ibuprofen pretreatment to assess the role of cyclooxygenase 2 (COX-2).
Main Results:
- Seizures induced robust vasoconstriction of cortical penetrating arterioles, correlating with prolonged postictal hypoxia.
- Postictal vasoconstriction was prevented by ibuprofen, indicating dependence on cyclooxygenase 2.
- Elevated astrocyte endfoot Ca2+ was observed during seizures, while vascular smooth muscle cells showed increased Ca2+ during and up to 75 minutes after seizures.
Conclusions:
- Demonstrated enduring postictal vasoconstriction and specific cellular Ca2+ activities within the neurovascular unit linked to seizure-induced hypoperfusion/hypoxia.
- Suggests that preventing seizure-induced hypoperfusion/hypoxia could be a novel therapeutic strategy for epilepsy-related impairments.
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