简介：Thehumanbrainisknowntobeinfluencedbyenvironmentalstimuli(Feeneyetal.,1982;Kaplan,1988).Therefore,researchonthebrainactivationpatternbyexternalstimulihasbeenanimportanttopicinneuroscience(Kaplan,1988).Chewinggumhasbeenknowntohaveapositiveeffectoncognition,includingalertness,attention,cognitiveprocessingspeed,

简介：Nestin+neuronshavebeenshowntoexpresscholineacetyltransferase(ChAT)inthemedialseptum-diagonalbandofBrocainadultrats.Thisstudyexploredtheprojectionofnestin+neuronstotheolfactorybulbandthetimecourseofnestin+neuronsinthemedialseptum-diagonalbandofBrocainadultratsduringinjuryrecoveryafterolfactorynervetransection.Thisstudyobservedthatallnestin+neuronsweredouble-labeledwithChATinthemedialseptum-diagonalbandofBroca.Approximately53.6%ofnestin+neuronswereprojectedtotheolfactorybulbandco-labeledwithfastblue.Alargenumberofnestin+neuronswerenotpresentineachregionofthemedialseptum-diagonalbandofBroca.Nestin+neuronsinthemedialseptumandverticallimbofthediagonalbandofBrocashowedobviouscompensatoryfunction.Thenumberofnestin+neuronsdecreasedtoaminimumlaterthannestin–/ChAT+neuronsinthemedialseptum-diagonalbandofBroca.Theresultssuggestthatnestin+cholinergicneuronsmayhaveacloserconnectiontoolfactorybulbneurons.Nestin+cholinergicneuronsmayhaveastrongertolerancetoinjurythanNestin–/ChAT+neurons.Thedifferencebetweennestin+andnestin–/ChAT+neuronsduringtherecoveryprocessrequiresfurtherinvestigations.

简介：BACKGROUND:Ithasbeenshownthatginsenoside,theeffectivecomponentofginseng,canenhanceexpressionofcholineacetyltransferase,aswellasbrain-derivedneurotrophicfactor(BDNF)anditsreceptortyrosinekinaseB(TrkB),incholinergicneuronsofthebasalforebrain.OBJECTIVE:ToqualitativelyandquantitativelyverifytheinfluenceofginsenosideonexpressionofBDNFanditsreceptor,TrkB,inthemedialseptumofagedrats,andtoprovideamolecularbasisforclinicalapplication.DESIGN,TIMEANDSETTING:Acontraststudy,whichwasperformedintheDepartmentofAnatomy,ChinaMedicalUniversity,andtheDepartmentofAnatomy,ShenyangMedicalCollegebetweenDecember2005andMay2007.MATERIALS:Thirty-five,healthy,female,SpragueDawleyratswereselectedforthisstudy.Ginsenoside(81%purity)wasprovidedbyJilinJi’anWantaiChineseMedicineFactory;anti-BDNFantibody,anti-TrkBantibody,andtheirkitswereprovidedbyWuhanBosterCompany.METHODS:Atotalof35ratsweredividedintothreegroups:young(fourmonthsold),aging(26monthsold),andginsenoside.Ratsintheginsenosidegroupwereadministeredginsenoside(25mg/kg/d)between17monthsand26months.MAINOUTCOMEMEASURES:ImmunohistochemistryandinsituhybridizationwereusedtomeasureexpressionofBDNFandTrkBinthemedialseptumofagedrats,andthedetectedresultswereexpressedasgrayvalues.RESULTS:①Qualitativedetection:usingmicroscopy,degenerativeneuronswerevisibleinthemedialseptumintheaginggroup.However,neuronalmorphologyintheginsenosidegroupwassimilartoneuronsintheyounggroup.②Quantitativedetection:themeangrayvalueofBDNF-positiveandTrkB-positiveproductsintheaginggroupweresignificantlyhigherthanintheyounggroup(t=3.346,4.169,P<0.01);however,themeangrayvalueintheginsenosidegroupwassignificantlylowerthanintheaginggroup(t=2.432,2.651,P<0.01).CONCLUSION:GinsenosidecanincreaseexpressionofBDNFandTrkBinth