Boosting of Synaptic Potentials and Spine Ca Transients by the Peptide Toxin SNX-482 Requires Alpha-1E-Encoded Voltage-Gated Ca Channels 英文参考文献.docVIP
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Boosting of Synaptic Potentials and Spine Ca Transients by the Peptide Toxin SNX-482 Requires Alpha-1E-Encoded Voltage-Gated Ca Channels 英文参考文献
BoostingofSynapticPotentialsandSpineCaTransients
bythePeptideToxinSNX-482RequiresAlpha-1E-
EncodedVoltage-GatedCaChannels
AndrewJ.Giessel,BernardoL.Sabatini*
DepartmentofNeurobiology,HowardHughesMedicalInstitute,HarvardMedicalSchool,Boston,Massachusetts,UnitedStatesofAmerica
Abstract
The majority of glutamatergic synapses formed onto principal neurons of the mammalian central nervous system are
associatedwithdendriticspines.Spinesaretinyprotuberancesthathousetheproteinsthatmediatetheresponseofthe
postsynapticcelltothepresynapticreleaseofglutamate.Postsynapticsignalsareregulatedbyanionchannelsignaling
cascadethatisactiveinindividualdendriticspinesandinvolvesvoltage-gatedcalcium(Ca)channels,smallconductance
(SK)-typeCa-activatedpotassiumchannels,andNMDA-typeglutamatereceptors.Pharmacologicalstudiesusingthetoxin
SNX-482indicatedthatthevoltage-gatedCachannelsthatsignalwithinspinestoopenSKchannelsbelongtotheclass
CaV2.3,whichisencodedbytheAlpha-1Epore-formingsubunit.Inordertospecificallytestthisconclusion,weexamined
theeffectsofSNX-482onsynapticsignalsinacutehippocampalslicesfromknock-outmicelackingtheAlpha-1Egene.We
find that in these mice, application of SNX-482 has no effect on glutamate-uncaging evoked synaptic potentials and Ca
influx,indicatingthatthatSNX-482indeedactsviatheAlpha-1E-encodedCaV2.3channel.
Citation: Giessel AJ, Sabatini BL (2011) Boosting of Synaptic Potentials and Spine Ca Transients by the Peptide Toxin SNX-482 Requires Alpha-1E-Encoded
Voltage-GatedCaChannels.PLoSONE6(6):e20939.doi:10.1371/journal.pone.0020939
Editor:OlivierJacquesManzoni,InstitutNationaldelaSante′ etdelaRechercheMe′dicale,France
ReceivedMarch9,2011;AcceptedMay13,2011;PublishedJune9,2011
Copyright: ?2011Giessel, Sabatini. This isanopen-access article distributedunder theterms ofthe Creative Commons AttributionLicense, which permits
unrestricteduse,distribution,andreproductioninanymedium,providedtheoriginalauthorandsourcearecredited.
Funding:Thisworkwassupportedbygrantsfromt
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