Seizures elevate gliovascular unit Ca2+ and cause sustained vasoconstriction
Seizures can result in a severe hypoperfusion/hypoxic attack that causes postictal memory and behavioral impairments. However, neither postictal changes to microvasculature nor Ca2+ changes in key cell types controlling blood perfusion have been visualized in vivo, leaving essential components of th...
| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
| Published: |
American Society for Clinical investigation
2020-10-01
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| Series: | JCI Insight |
| Subjects: | |
| Online Access: | https://doi.org/10.1172/jci.insight.136469 |
| _version_ | 1818956071663828992 |
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| author | Cam Ha T. Tran Antis G. George G. Campbell Teskey Grant R. Gordon |
| author_facet | Cam Ha T. Tran Antis G. George G. Campbell Teskey Grant R. Gordon |
| author_sort | Cam Ha T. Tran |
| collection | DOAJ |
| description | Seizures can result in a severe hypoperfusion/hypoxic attack that causes postictal memory and behavioral impairments. However, neither postictal changes to microvasculature nor Ca2+ changes in key cell types controlling blood perfusion have been visualized in vivo, leaving essential components of the underlying cellular mechanisms unclear. Here, we use 2-photon microvascular and Ca2+ imaging in awake mice to show that seizures result in a robust vasoconstriction of cortical penetrating arterioles, which temporally mirrors the prolonged postictal hypoxia. The vascular effect was dependent on cyclooxygenase 2, as pretreatment with ibuprofen prevented postictal vasoconstriction. Moreover, seizures caused a rapid elevation in astrocyte endfoot Ca2+ that was confined to the seizure period, and vascular smooth muscle cells displayed a significant increase in Ca2+ both during and following seizures, lasting up to 75 minutes. Our data show enduring postictal vasoconstriction and temporal activities of 2 cell types within the neurovascular unit that are associated with seizure-induced hypoperfusion/hypoxia. These findings support prevention of this event may be a novel and tractable treatment strategy in patients with epilepsy who experience extended postseizure impairments. |
| first_indexed | 2024-12-20T10:48:08Z |
| format | Article |
| id | doaj.art-1887ad402b024477bcbfdef289570e19 |
| institution | Directory Open Access Journal |
| issn | 2379-3708 |
| language | English |
| last_indexed | 2024-12-20T10:48:08Z |
| publishDate | 2020-10-01 |
| publisher | American Society for Clinical investigation |
| record_format | Article |
| series | JCI Insight |
| spelling | doaj.art-1887ad402b024477bcbfdef289570e192022-12-21T19:43:20ZengAmerican Society for Clinical investigationJCI Insight2379-37082020-10-01519Seizures elevate gliovascular unit Ca2+ and cause sustained vasoconstrictionCam Ha T. TranAntis G. GeorgeG. Campbell TeskeyGrant R. GordonSeizures can result in a severe hypoperfusion/hypoxic attack that causes postictal memory and behavioral impairments. However, neither postictal changes to microvasculature nor Ca2+ changes in key cell types controlling blood perfusion have been visualized in vivo, leaving essential components of the underlying cellular mechanisms unclear. Here, we use 2-photon microvascular and Ca2+ imaging in awake mice to show that seizures result in a robust vasoconstriction of cortical penetrating arterioles, which temporally mirrors the prolonged postictal hypoxia. The vascular effect was dependent on cyclooxygenase 2, as pretreatment with ibuprofen prevented postictal vasoconstriction. Moreover, seizures caused a rapid elevation in astrocyte endfoot Ca2+ that was confined to the seizure period, and vascular smooth muscle cells displayed a significant increase in Ca2+ both during and following seizures, lasting up to 75 minutes. Our data show enduring postictal vasoconstriction and temporal activities of 2 cell types within the neurovascular unit that are associated with seizure-induced hypoperfusion/hypoxia. These findings support prevention of this event may be a novel and tractable treatment strategy in patients with epilepsy who experience extended postseizure impairments.https://doi.org/10.1172/jci.insight.136469Neuroscience |
| spellingShingle | Cam Ha T. Tran Antis G. George G. Campbell Teskey Grant R. Gordon Seizures elevate gliovascular unit Ca2+ and cause sustained vasoconstriction JCI Insight Neuroscience |
| title | Seizures elevate gliovascular unit Ca2+ and cause sustained vasoconstriction |
| title_full | Seizures elevate gliovascular unit Ca2+ and cause sustained vasoconstriction |
| title_fullStr | Seizures elevate gliovascular unit Ca2+ and cause sustained vasoconstriction |
| title_full_unstemmed | Seizures elevate gliovascular unit Ca2+ and cause sustained vasoconstriction |
| title_short | Seizures elevate gliovascular unit Ca2+ and cause sustained vasoconstriction |
| title_sort | seizures elevate gliovascular unit ca2 and cause sustained vasoconstriction |
| topic | Neuroscience |
| url | https://doi.org/10.1172/jci.insight.136469 |
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