ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2012
Pyramidal cells and cytochrome P450 epoxygenase products in the neurovascular coupling response to basal forebrain cholinergic input.
Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 32 citations in OpenAlex.
- Translational difficulties in establishing a pharmacologically induced neurovascular uncoupling model in rats.Scientific reports · 2026Article
- Pericyte pannexin1 controls cerebral capillary diameter and supports memory function.Nature communications · 2025Article
- Fluorescent sensors for intracellular signaling in the brain: imaging neurons, glia, and vascular cells.Neurophotonics · 2025Article
- Review
- Serotonergic regulation of cortical neurovascular coupling and hemodynamics upon awakening from sleep in mice.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024Article
- Toolbox for studying neurovascular couplingNeurophotonics · 2022Review
- Differential pial and penetrating arterial responses examined by optogenetic activation of astrocytes and neurons.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021Article
- Article
- Astrocyte dysfunction and neurovascular impairment in neurological disorders: Correlation or causation?Neurochemistry international · 2019Review
- Article
- Impact of Altered Cholinergic Tones on the Neurovascular Coupling Response to Whisker Stimulation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Astrocytes mediate neurovascular signaling to capillary pericytes but not to arterioles.Nature neuroscience · 2016Article
- Purinergic signaling triggers endfoot high-amplitude Ca2+ signals and causes inversion of neurovascular coupling after subarachnoid hemorrhage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2016Article
- Neuronal networks and mediators of cortical neurovascular coupling responses in normal and altered brain states.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2016Review
- Vascular mTOR-dependent mechanisms linking the control of aging to Alzheimer's disease.Biochimica et biophysica acta · 2016Review
- IGF-1 deficiency impairs neurovascular coupling in mice: implications for cerebromicrovascular aging.Aging cell · 2015Article
- Purinergic glio-endothelial coupling during neuronal activity: role of P2Y1 receptors and eNOS in functional hyperemia in the mouse somatosensory cortex.American journal of physiology. Heart and circulatory physiology · 2015Article
- COX-2-Derived Prostaglandin E2 Produced by Pyramidal Neurons Contributes to Neurovascular Coupling in the Rodent Cerebral Cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Resveratrol treatment rescues neurovascular coupling in aged mice: role of improved cerebromicrovascular endothelial function and downregulation of NADPH oxidase.American journal of physiology. Heart and circulatory physiology · 2014Article
- Neurovascular signaling in the brain and the pathological consequences of hypertension.American journal of physiology. Heart and circulatory physiology · 2014Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Activation of the basal forebrain (BF), the primary source of acetylcholine (ACh) in the cortex, broadly increases cortical cerebral blood flow (CBF), a response downstream to ACh release. Although endothelial nitric oxide and cholinoceptive GABA (γ-aminobutyric acid) interneurons have been implicated, little is known about the role of pyramidal cells in this response and their possible interaction with astrocytes. Using c-Fos immunohistochemistry as a marker of neuronal activation and laser-Doppler flowmetry, we measured changes in CBF evoked by BF stimulation following pharmacological blockade of c-Fos-identified excitatory pathways, astroglial metabolism, or vasoactive mediators. Pyramidal cells including those that express cyclooxygenase-2 (COX-2) displayed c-Fos upregulation. Glutamate acting via NMDA, AMPA, and mGlu receptors was involved in the evoked CBF response, NMDA receptors having the highest contribution (~33%). In contrast, nonselective and selective COX-2 inhibition did not affect the evoked CBF response (+0.4% to 6.9%, ns). The metabolic gliotoxins fluorocitrate and fluoroacetate, the cytochrome P450 epoxygenase inhibitor MS-PPOH and the selective epoxyeicosatrienoic acids (EETs) antagonist 14,15-epoxyeicosa-5(Z)-enoic acid (14,15-EEZE) all blocked the evoked CBF response by ~50%. Together, the data demonstrate that the hyperemic response to BF stimulation is largely mediated by glutamate released from activated pyramidal cells and by vasoactive EETs, likely originating from activated astrocytes.
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