ArticleScientific reports2016
Contribution of prostanoid signaling to the evolution of spreading depolarization and the associated cerebral blood flow response.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- Systematic review of the pharmacological agents that have been tested against spreading depolarizations.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2018Pooled it
- PGE2 Potentiates Orai1-Mediated Calcium Entry Contributing to Peripheral Sensitization.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Neuroaxonal and cellular damage/protection by prostanoid receptor ligands, fatty acid derivatives and associated enzyme inhibitors.Neural regeneration research · 2023Review
- Astrocyte CaInternational journal of molecular sciences · 2021Article
- The role of Toll-like receptor signaling pathways in cerebrovascular disorders: the impact of spreading depolarization.Journal of neuroinflammation · 2020Review
- The impact of dihydropyridine derivatives on the cerebral blood flow response to somatosensory stimulation and spreading depolarization.British journal of pharmacology · 2019Article
- Spectral and Multifractal Signature of Cortical Spreading Depolarisation in Aged Rats.Frontiers in physiology · 2018Article
- Age-related impairment of metabovascular coupling during cortical spreading depolarizations.American journal of physiology. Heart and circulatory physiology · 2017Article
- Spreading depolarization remarkably exacerbates ischemia-induced tissue acidosis in the young and aged rat brain.Scientific reports · 2017Article
- Functional vascular contributions to cognitive impairment and dementia: mechanisms and consequences of cerebral autoregulatory dysfunction, endothelial impairment, and neurovascular uncoupling in aging.American journal of physiology. Heart and circulatory physiology · 2017Review
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The significance of prostanoid signaling in neurovascular coupling during somatosensory stimulation is increasingly more appreciated, yet its involvement in mediating the cerebral blood flow (CBF) response to spreading depolarization (SD) has remained inconclusive. Selective cyclooxygenase (COX) enzyme inhibitors (NS-398, SC-560) or an antagonist (L161,982) of the EP4 type prostaglandin E2 receptor were applied topically to a cranial window over the parietal cortex of isoflurane-anesthetized Sprague-Dawley rats (n = 60). Global forebrain ischemia was induced by occlusion of both common carotid arteries in half of the animals. SDs were triggered by the topical application of 1M KCl. SD occurrence was confirmed by the acquisition of DC potential, and CBF variations were recorded by laser-Doppler flowmetry. EP4 receptor antagonism significantly decreased peak hyperemia and augmented post-SD oligemia in the intact but not in the ischemic cortex. COX-1 inhibition and EP4 receptor blockade markedly delayed repolarization after SD in the ischemic but not in the intact brain. COX-2 inhibition achieved no significant effect on any of the end points taken. The data suggest, that activation of EP4 receptors initiates vasodilation in response to SD in the intact brain, and - together with COX-1 derived prostanoids - shortens SD duration in the acute phase of ischemia.
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