Metabotropic Glutamate Receptor Activation Enhances the Activities of Two Types of Ca<sup>2+</sup>-Activated K<sup>+</sup>Channels in Rat Hippocampal Astrocytes

Gebremedhin, Debebe; Yamaura, Ken; Zhang, Chenyang; Bylund, Johan; Koehler, Raymond C.; Harder, David R.

doi:10.1523/jneurosci.23-05-01678.2003

Cited by 81 publications

(60 citation statements)

References 48 publications

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“…S4A, Table S1) showed no changes in cortical levels of mRNA for the BK channel poreforming α1-subunit or the neuronal/astrocytic β4 accessory subunit (36,37), suggesting that an increase in perivascular K + concentration rather than changes in BK expression accounts for SAH-induced neurally evoked vasoconstriction. However, these results do not exclude an elevation of BK channel expression specifically in the astrocytic endfoot plasma membrane.…”

Section: Resultsmentioning

confidence: 99%

Inversion of neurovascular coupling by subarachnoid blood depends on large-conductance Ca ²⁺ -activated K ⁺ (BK) channels

Koide

Bonev

Nelson

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

101

108

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The cellular events that cause ischemic neurological damage following aneurysmal subarachnoid hemorrhage (SAH) have remained elusive. We report that subarachnoid blood profoundly impacts communication within the neurovascular unit-neurons, astrocytes, and arterioles-causing inversion of neurovascular coupling. Elevation of astrocytic endfoot Ca 2+ to ∼400 nM by neuronal stimulation or to ∼300 nM by Ca 2+ uncaging dilated parenchymal arterioles in control brain slices but caused vasoconstriction in post-SAH brain slices. Inhibition of K + efflux via astrocytic endfoot large-conductance Ca 2+ -activated K + (BK) channels prevented both neurally evoked vasodilation (control) and vasoconstriction (SAH

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Section: Resultsmentioning

confidence: 99%

Inversion of neurovascular coupling by subarachnoid blood depends on large-conductance Ca ²⁺ -activated K ⁺ (BK) channels

Koide

Bonev

Nelson

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

101

108

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“…Because EETs open VSM K Ca channels (20) and 20-HETE closes K Ca channels (19), 20-HETE might oppose the vasodilator effect of EETs. Alternatively, EETs have also been found to open K Ca channels in astrocytes (21,49). Perhaps increased 20-HETE generated following nNOS inhibition limits VSM hyperpolarization following neuronal activation by closing VSM K Ca channels and thereby limits the effect of K ϩ signaling between astrocyte endfeet and nearby VSM (17).…”

Section: Discussionmentioning

confidence: 99%

Interaction of nitric oxide, 20-HETE, and EETs during functional hyperemia in whisker barrel cortex

Liu

Falck

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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Nitric oxide (NO) modulates vasodilation in cerebral cortex during sensory activation. NO is known to inhibit the synthesis of 20-HETE, which has been implicated in arteriolar constriction during astrocyte activation in brain slices. We tested the hypothesis that the attenuated cerebral blood flow (CBF) response to whisker stimulation seen after NO synthase (NOS) inhibition requires 20-HETE synthesis and that the ability of an epoxyeicosatrienoic acids (EETs) antagonist to reduce the CBF response is blunted after NOS inhibition but restored with simultaneous blockade of 20-HETE synthesis. In anesthetized rats, the increase in CBF during whisker stimulation was attenuated after the blockade of neuronal NOS with 7-nitroindazole. Subsequent administration of the 20-HETE synthesis inhibitor N-hydroxy-NЈ-(4-n-butyl-2-methylphenyl)formamidine (HET0016) restored the CBF response to control levels. After the administration of 7-nitroindazole, the inhibitory effect of an EETs antagonist 14,15-epoxyeicosa-5(Z)-enoic acid (14,15-EEZE) on the CBF response was lost, whereas the simultaneous administration of 7-nitroindazole and HET0016 restored the inhibitory effect of 14,15-EEZE. The administration of HET0016 alone had only a small effect on the evoked CBF response in rats. Furthermore, in neuronal NOS ϩ/ϩ and NOS Ϫ/Ϫ mice, HET0016 administration did not increase the CBF response to whisker stimulation. In neuronal NOS ϩ/ϩ mice, HET0016 also blocked the reduction in the response seen with acute NOS inhibition. These results indicate that 20-HETE synthesis normally does not substantially restrict functional hyperemia. Increased NO production during functional activation may act dynamically to suppress 20-HETE synthesis or downstream signaling and permit EETs-dependent vasodilation. With the chronic loss of neuronal NOS in mice, other mechanisms apparently suppress 20-HETE synthesis or signaling. eicosanoids; epoxyeicosatrienoic acid; functional activation; mouse; rat; vibrissae; 20-hydroxyeicosatetraenoic acid WHEN NEURONS IN A specific brain region increase their activity, local blood flow increases in a temporally and spatially coordinated manner. The physiological mechanisms that underlie this functional coupling are complex and involve adenosine (13,31,39), nitric oxide (NO) (12, 29), arachidonic acid metabolites derived from cyclooxygenase (34) and cytochrome P-450 (CYP) epoxygenase (36) enzymes, Ca 2ϩ -activated K ϩ (K Ca ) channels, and inward-rectifier K ϩ channels (17).Although NO is required for functional hyperemia in cerebellum (50), NO may not be an essential mediator in cerebral cortex. Neuronal NO synthase (nNOS) null mice (nNOS Ϫ/Ϫ ) and endothelial NOS (eNOS) null mice retain normal cerebral blood flow (CBF) responses to whisker stimulation (6,29). Further work demonstrated that NO may act in a permissive fashion in the cerebral cortex to enable vasodilation by other mediators. Inhibition of NOS decreases basal cGMP and increases vascular tone. Restoration of vascular tone after NOS inhibition with either an...

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“…Increases in neuronal activity in the brain can facilitate the opening of large conductance Ca 2+ -activated K + (BK Ca ) channels on astrocyte endfeet mediated by increases in Ca 2+ (17,18). The opening of BK Ca channels facilitates the efflux of K + from astrocyte endfeet, which can in turn dilate cerebral vessels.…”

Section: A Mechanistic Understanding Of Neurovascular Couplingmentioning

confidence: 99%

Neurovascular Interactions in the Retina: Physiological and Pathological Roles

et al. 2013

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Abstract. Increasing evidence suggests that the complex interactions among multiple cell types including neuronal, glial, and vascular cells, are critical for maintaining adequate cerebral blood flow that is necessary for normal brain function and survival. The disturbance of these interactions contributes to the pathogenesis of central nervous system disorders such as stroke and Alzheimer's disease. The retina is part of the central nervous system, and the properties of vasculature in the retina are similar to those in the brain. The interactions among multiple cell types in the retina also play an important role in the maintenance of tissue homeostasis, and the impairment of interactions can contribute to the onset and/or progression of retinal diseases. In this review, we describe the neurovascular interactions in the retina and alternations of interactions in pathological conditions such as diabetic retinopathy and glaucoma.

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Metabotropic Glutamate Receptor Activation Enhances the Activities of Two Types of Ca²⁺-Activated K⁺Channels in Rat Hippocampal Astrocytes

Cited by 81 publications

References 48 publications

Inversion of neurovascular coupling by subarachnoid blood depends on large-conductance Ca ²⁺ -activated K ⁺ (BK) channels

Inversion of neurovascular coupling by subarachnoid blood depends on large-conductance Ca ²⁺ -activated K ⁺ (BK) channels

Interaction of nitric oxide, 20-HETE, and EETs during functional hyperemia in whisker barrel cortex

Neurovascular Interactions in the Retina: Physiological and Pathological Roles

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Metabotropic Glutamate Receptor Activation Enhances the Activities of Two Types of Ca2+-Activated K+Channels in Rat Hippocampal Astrocytes

Cited by 81 publications

References 48 publications

Inversion of neurovascular coupling by subarachnoid blood depends on large-conductance Ca 2+ -activated K + (BK) channels

Inversion of neurovascular coupling by subarachnoid blood depends on large-conductance Ca 2+ -activated K + (BK) channels

Interaction of nitric oxide, 20-HETE, and EETs during functional hyperemia in whisker barrel cortex

Neurovascular Interactions in the Retina: Physiological and Pathological Roles

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Metabotropic Glutamate Receptor Activation Enhances the Activities of Two Types of Ca²⁺-Activated K⁺Channels in Rat Hippocampal Astrocytes

Inversion of neurovascular coupling by subarachnoid blood depends on large-conductance Ca ²⁺ -activated K ⁺ (BK) channels

Inversion of neurovascular coupling by subarachnoid blood depends on large-conductance Ca ²⁺ -activated K ⁺ (BK) channels