Astrocyte Inositol Triphosphate Receptor Type 2 and Cytosolic Phospholipase A2 Alpha Regulate Arteriole Responses in Mouse Neocortical Brain Slices 英文参考文献.docVIP
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Astrocyte Inositol Triphosphate Receptor Type 2 and Cytosolic Phospholipase A2 Alpha Regulate Arteriole Responses in Mouse Neocortical Brain Slices 英文参考文献
AstrocyteInositolTriphosphateReceptorType2and
CytosolicPhospholipaseA2AlphaRegulateArteriole
ResponsesinMouseNeocorticalBrainSlices
LihuaHe1,DavidJ.Linden2,AdamSapirstein1*
1Department of Anesthesiology and Critical Care Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America,
2DepartmentofNeuroscience,TheJohnsHopkinsUniversitySchoolofMedicine,Baltimore,Maryland,UnitedStatesofAmerica
Abstract
Functionalhyperemiaofthecerebralvascularsystemmatchesregionalbloodflowtothemetabolicdemandsofthebrain.
One current model of neurovascular control holds that glutamate released by neurons activates group I metabotropic
glutamate receptors (mGluRs) on astrocytes, resulting in the production of diffusible messengers that act to regulate
smooth muscle cells surrounding cerebral arterioles. The acute mouse brain slice is an experimental system in which
changesinarteriolediametercanpreciselymeasuredwithlightmicroscopy.Stimulationofthebrainslicetriggersspecific
cellularresponsesthatcanbecorrelatedtochangesinarteriolediameter.Hereweusedinositoltrisphosphatereceptortype
2(IP3R2)andcytosolicphospholipaseA2alpha(cPLA2a)deficientmicetodetermineifastrocytemGluRactivationcoupled
2+
toIP3R2-mediatedCa releaseandsubsequentcPLA2aactivationisrequiredforarterioleregulation.Wemeasuredchanges
inastrocytecytosolicfreeCa andarteriolediametersinresponsetomGluRagonistorelectricalfieldstimulationinacute
2+
2+
neocorticalmousebrainslicesmaintainedin95%or20%O2.AstrocyteCa andarterioleresponsestomGluRactivation
2+
wereabsentinIP3R22/2slices.AstrocyteCa responsestomGluRactivationwereunchangedbydeletionofcPLA2abut
arteriole responses to either mGluR agonist or electrical stimulation were ablated. The valence of changes in arteriole
diameter (dilation/constriction) was dependent upon both stimulus and O2 concentration. Neuron-derived NO and
activationofthegroupImGluRsarerequiredforresponsestoelectricalstimulation.ThesefindingsindicatethatanmGlu
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