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Brain metabolism dictates the polarity of astrocyte control over arterioles (2008)

G. R. Gordon ; H. B. Choi ; R. L. Rungta ; [et al.]

Nature Publishing Group (NPG)

In: Nature. 456(7223): 745-9. doi: 10.1038/nature07525.

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Publication Date: 2008-10-31

Description: Calcium signalling in astrocytes couples changes in neural activity to alterations in cerebral blood flow by eliciting vasoconstriction or vasodilation of arterioles. However, the mechanism for how these opposite astrocyte influences provide appropriate changes in vessel tone within an environment that has dynamic metabolic requirements remains unclear. Here we show that the ability of astrocytes to induce vasodilations over vasoconstrictions relies on the metabolic state of the rat brain tissue. When oxygen availability is lowered and astrocyte calcium concentration is elevated, astrocyte glycolysis and lactate release are maximized. External lactate attenuates transporter-mediated uptake from the extracellular space of prostaglandin E(2), leading to accumulation and subsequent vasodilation. In conditions of low oxygen concentration extracellular adenosine also increases, which blocks astrocyte-mediated constriction, facilitating dilation. These data reveal the role of metabolic substrates in regulating brain blood flow and provide a mechanism for differential astrocyte control over cerebrovascular diameter during different states of brain activation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4097022/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉 〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4097022/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gordon, Grant R J -- Choi, Hyun B -- Rungta, Ravi L -- Ellis-Davies, Graham C R -- MacVicar, Brian A -- R01 GM053395/GM/NIGMS NIH HHS/ -- R01 GM053395-13/GM/NIGMS NIH HHS/ -- England -- Nature. 2008 Dec 11;456(7223):745-9. doi: 10.1038/nature07525. Epub 2008 Oct 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Brain Research Centre, Department of Psychiatry, University of British Columbia, British Columbia T2N 2B5, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18971930" target="_blank"〉PubMed〈/a〉

Keywords: Adenosine/metabolism/pharmacology ; Animals ; Arterioles/drug effects/*metabolism ; Astrocytes/*metabolism ; Brain/*blood supply/*metabolism ; Dinoprostone/metabolism ; Glycolysis ; Lactic Acid/metabolism ; Male ; Organic Anion Transporters/metabolism ; Oxygen/metabolism ; Pressure ; Prostaglandin-Endoperoxide Synthases/metabolism ; Rats ; Rats, Sprague-Dawley ; Vasoconstriction/drug effects/*physiology ; Vasodilation/drug effects/*physiology ; Vasodilator Agents/pharmacology

Print ISSN: 0028-0836

Electronic ISSN: 1476-4687

Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics

Published by Nature Publishing Group (NPG)

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Activation of pannexin-1 hemichannels augments aberrant bursting in the hippocampus (2008)

R. J. Thompson ; M. F. Jackson ; M. E. Olah ; [et al.]

American Association for the Advancement of Science (AAAS)

In: Science. 322(5907): 1555-9. doi: 10.1126/science.1165209.

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Publication Date: 2008-12-06

Description: Pannexin-1 (Px1) is expressed at postsynaptic sites in pyramidal neurons, suggesting that these hemichannels contribute to dendritic signals associated with synaptic function. We found that, in pyramidal neurons, N-methyl-d-aspartate receptor (NMDAR) activation induced a secondary prolonged current and dye flux that were blocked with a specific inhibitory peptide against Px1 hemichannels; knockdown of Px1 by RNA interference blocked the current in cultured neurons. Enhancing endogenous NMDAR activation in brain slices by removing external magnesium ions (Mg2+) triggered epileptiform activity, which had decreased spike amplitude and prolonged interburst interval during application of the Px1 hemichannel blocking peptide. We conclude that Px1 hemichannel opening is triggered by NMDAR stimulation and can contribute to epileptiform seizure activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thompson, Roger J -- Jackson, Michael F -- Olah, Michelle E -- Rungta, Ravi L -- Hines, Dustin J -- Beazely, Michael A -- MacDonald, John F -- MacVicar, Brian A -- New York, N.Y. -- Science. 2008 Dec 5;322(5907):1555-9. doi: 10.1126/science.1165209.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry and Brain Research Centre, University of British Columbia, 2211 Wesbrook Mall, Vancouver, BC V6T 2B5, Canada. rj.thompson@ucalgary.ca〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19056988" target="_blank"〉PubMed〈/a〉

Keywords: Action Potentials ; Adenosine Triphosphate/metabolism ; Animals ; Calcium/metabolism ; Cells, Cultured ; Connexins/genetics/*physiology ; Dendrites/physiology ; Electrical Synapses/physiology ; Epilepsy/physiopathology ; Hippocampus/*physiology/physiopathology ; In Vitro Techniques ; Mice ; Nerve Tissue Proteins/genetics/*physiology ; Patch-Clamp Techniques ; Pyramidal Cells/*physiology ; RNA Interference ; Rats ; Rats, Wistar ; Receptors, N-Methyl-D-Aspartate/*metabolism ; Synaptic Transmission

Print ISSN: 0036-8075

Electronic ISSN: 1095-9203

Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics