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NRG-1 regulates the proliferation of neural stem cells in adult hippocampus

NRG-1 regulates the proliferation of neural stem cells in ad...

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中国神经科学学会第九届全国学术会议暨第五次会员代表大会

作者： Xiong CAO~1,Hong-Hai HU~1,Liang-Pin LI~1,Qian WANG~1,Ying-Ying FANG~1,Lin MEI~3,Tian-Ming GAO~1,Xin-Hong ZHU~(1,2,*) 1 Department of Neurobiology,2 School of Chinese Traditional Medicine,Southern Medical University,Guangzhou 510515,China 3 Institute of Molecular Medicine and Genetics and Department of Neurology,Georgia's Health Sciences University,Augusta,GA 30912.

Schizophrenia is a severe and disabling mental disorder,cognitive deficits as one of the core symptoms continue to be poorly understood and current antipsychotics are only modestly effective treatments for the cognitive ***-1 and ErbB4 genes,which encode neuregulin-1(NRG-1) and ErbB4 respectively,are two susceptible genes for *** studies suggest that neurogenesis dysfunction in adult hippocampus may contribute to pathogenesis of cognitive deficits caused by schizophrenia,and the underlying molecular mechanisms are largely ***,we investigated the potential role of NRG-1 on the proliferation of neural stem cells in adult *** showed that ErbB4,the NRG-1 receptor,was primarily expressed on the GFP-positive cells in the adult dentate gyrus of the nestin-GFP transgenic *** of exogenous NRG-1(2 nM) leaded to a rapid aggregation of BrdU-positive cells in vivo and in vitro,whereas AG1478,an ErbB4 antagonist and neutralizing peptide ecto-ErbB4 blocked the effect of NRG-1,in vivo and in *** addition,application of ErbB4 shRNA or kinase-dead ErbB4 inhibited the effect of NRG-1 on the proliferation of the neural stem cells in ***,we found that mTOR inhibitor,rapamycin,and mTOR shRNA could block the effect of NRG-1 on the proliferation of cultured neural stem ***,LY94002 and wartmanin,PI3 kinase inhibitors,blocked the effect of NRG-1,suggesting that PI3K-mTOR signaling mediated the NRG-1 's ***,our data show that NRG-1 regulates the proliferation of neural stem cells in adult hippocampus,possibly via PI3K-mTOR pathway,which may lead to a new perspective on cognitive dysfunction in schizophrenia.

关键词： NRG-1 ErbB4 schizophrenia adult neurogenesis

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mTOR signaling play a key role in Tau phosphorylation in SAMP8 mice

mTOR signaling play a key role in Tau phosphorylation in SAM...

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中国神经科学学会第九届全国学术会议暨第五次会员代表大会

作者： Yuan GENG~(1,2),Qin-Ying MA~(1,2),Jing QIANG~(1,2),Ping GU~(1,2),Yan-Yong WANG~(1,2),Ming-Wei WANG~(*,1,2) 1 Department of Neurology,the Frist Hospital of Hebei Medical University,Shijiazhuang 050031,China 2 Brain Aging and Cognitive Neuroscience Laboratory of Hebei,Shijiazhuang 050031,China

Objective The mammalian target of rapamycin(mTOR) kinase is an inhibitor of macroautophagy, which is a conserved intracellular system designed for the degradation of long-lived proteins and organelles in *** evidence suggested that chronic increase in mTOR function occurring during aging may promote the development of Tau *** senescence accelerated mouse prone 8(SAMP8) is a mice strain widely used as a rodent model of aging and senile *** present study aimed to explore whether mTOR signaling pathway has effect in the neurodegenerative changes of SAMP8 mice and whether rapamycin administration could alleviate the neurodegenerative *** The primary neurons were obtained from the hippocampus of newborn SAMP8 and SAMRl mice,and at the seventh day of culture,0.5 or 1.0μM rapamycin was added into the culture medium,and at the tenth day,neurons were observed after immunofluorenscence *** levels of phosphorylated p70S6K,phosphorylated mTOR,Tau[pS199]and Tau[pS396]were detected with Western blot. Results In SAMP8 hippocampal neurons,the levels of phosphorylated p70S6K at Thr389 and mTOR(pSer2448) were significantly higher than in the control *** activity signaling was upregulated in the neurons of SAMP8 at the tenth *** neurons extracted from SAMP8 were in a poor state in contrast to the SAMPR1,most processes broken and presented "bead-like" *** administration significantly reduced the levels of phosphorylated p70S6K at Thr389 in SAMP8 contrast to SAMRl in both treated *** treated with 0.5 uM rapamycin for 3 d,a mTOR inhibitor,the neurons from SAMP8 seems better than non-treated group,part of processes were smooth and slender,although part of neurons almost all processes broken and *** presentation of Tau [pS199]and Tau[pS396]both decreased significantly contrast to the control *** treated with 1.0 uM rapamycin,cell state was worse than the untreated group,most neurons were

关键词： senescence accelerated mouse prone 8 mTOR signaling phosphorylated Tau rapamycin

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Effect of inhibition of GABA uptake in the tuberomamillary nucleus on sleep-waking states following the ventrolateral preoptic area lesion in rats

Effect of inhibition of GABA uptake in the tuberomamillary n...

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中国神经科学学会第九届全国学术会议暨第五次会员代表大会

作者： Min ZHANG,Kun FAN,Peng ZHAO,Yu-Feng SHAO,Xiang-Pan KONG,Qiong YAN,Yi-Ping HOU~* Department of Neuroscience,Anatomy,Histology and Embryology,Key Laboratory of Preclinical Study for New Drugs of Gansu Province,School of Basic Medical Sciences,Lanzhou University,Lanzhou 730000,China

Objective Neurons containing gamma-aminobutyric acid(GABA) play an important role in the regulation from wakefulness to *** evidences have demonstrated that the interaction between GABAergic neurons in ventrolateral preoptic area(VLPO) and histaminergic(HA) neurons in the tuberomammillary nucleus(TMN) play a key role for regulating sleep-wakefulness *** neurons also in the TMN have been recently documented. However,GABAergic neurons in TMN have not received much attention for their role in sleep-wakefulness cycle. The present study was to investigate the effect of inhibition of GABA uptake in the TMN nucleus on sleep-waking states following the VLPO lesion and further understand the role of the GABAergic neurons in the TMN in sleep-wakefulness *** Thirty adult and male SD rats were used in this *** anesthesia,4 EEG screw electrodes were implanted into the skull and 3 flexible EMG wire electrodes were placed into the nuchal muscles. After 24 h basal record of sleep-wake cycle,microliter syringes containing ibotenic acid(IA,Sigma,***,USA) solution(10 nmol/0.5μL/side) were bilaterally injected into the VLPO for specific cells *** VLPO lesion, nipecotic acid(NPA,Sigma,***,USA),a GABA uptake inhibitor(1 mmol/0.5μL/side),was bilaterally injected into the TMN at 10:00 or 22:00 h for observing the changes of sleep-waking states in light period(8:00-20:00 h) and dark period(20:00-8:00 h) on day 8,10,12 and 14,*** recording,histological Nissl staining and immunohistochemical Fos and glutamate decarboxylase(GAD) staining were respectively performed for determining the loss number of cell and GABA neurons in the *** immunoreactivity(IR) and histidine decarboxylase (HDC)-IR were performed determining the distributions and morphologic characteristics of GABAergic and HAergic neurons in the ***(1) Effect of VLPO lesion on sleep-waking cycle and cortical EEG *** VLPO lesion,the sleep-wakin

关键词： GABAergic neuron GABA uptake inhibitor histaminergic neuron lesion glutamate decarboxylaseimmunoreactivity histidine decarboxylase-immunoreactivity tuberomammillary nucles ventrolateral preoptic area

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Neuroprotective effect of Val8-GLP-1（7-36） against a 1-40-induced neurotoxicity and its possible mechanism

Neuroprotective effect of Val8-GLP-1（7-36） against a 1-40-...

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中国神经科学学会第九届全国学术会议暨第五次会员代表大会

作者： Xiao-Hui WANG,Zhao-Jun WANG,Dong YANG,Li YUAN,Shao-Feng LI,Jin-Shun QI~* Department of Physiology,Shanxi Medical University,Taiyuan 030001,China

Objective One of the neuropathological features of Alzheimer's disease（AD） is high density of senile plaques,mainly composed of amyloid P protein（Aβ）.It has been found that type 2 diabetes mellitus（T2DM） is a risk factor for developing *** promising treatment for AD is using glucagon-like peptide-1（GLP-1）,a modulator used in T2DM *** characterize the neuroprotective role and possible mechanism of GLP-1 in the brain, we investigated the effects of Val-GLP-1（7-36）,a GLP-1 analogue with greater biological activity,on the Aβ1-40- induced *** We investigated:（1） the effects of Intracerebraventricular（i.e.v.） injection of Val- GLP-1（7-36） on the Aβ1-40-induced impairment of spatial learning and memory of rats in Morris water maze test;（2） the effects of *** of Val-GLP-1（7-36） on the Aβ1-40-induced impairment of in vivo late phase of long-term potentiation（L-LTP） in rat hippocampal CA1 region;（3） the effects of Val-GLP-1（7-36） on the Aβ1-40-induced changes in miniature postsynaptic currents（mEPSCs and mlPSCs） in rat hippocampal CA1 pyramidal neurons;（4） the effects of pretreatment with Val-GLP-1（7-36） on Aβ1-40-induced elevation of[Ca] in cultured primary rat cortical ***（1） Pretreatment with Val-GLP-1（7-36）(0.05 pmol,0.5 pmol or 5 pmol) effectively reversed Aβ1-40（5 nmol）-induced impairment of cognitive function in a dose dependent manner.（2） Pretreatment with Val- GLP-l（7-36） effectively reversed Aβ1-40（5 nmol）-induced suppression of L-LTP in a dose-dependent manner.（3） Pretreatment with Val-GLP-1（7-36）(10 nM) prevented the Aβ1-40（100 nM）-induced decrease of frequency of mEPSCs and mlPSCs.（4） Pretreatment with Val-GLP-l（7-36）(10 nM,100 nM or 1000 nM) effectively protected against Aβ1-40（10μM）-induced elevation of[Ca] in a dose-dependent *** GLP-1 plays an important positive role in attenuating Aβ-induced deficits and stable GLP-1 analogues such as Val-GLP-1（7-36） could be an effective promising strategy for

关键词： Val8-GLP-1(7-36) neuroprotective effect Aβ1-40

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Effects of memantine on amyloid oligomer-induced impairment of synapticplasticity in vitro and in vivo

Effects of memantine on amyloid oligomer-induced impairment ...

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中国神经科学学会第九届全国学术会议暨第五次会员代表大会

作者： Tianxiang DENG,Ruyi LIN,Guilan LIU,Shujun XU,Xaiowei CHEN,Xiaofei WEI,Qinwen WANG~* Medical School,Ningbo University,Ningbo 315211,China

Soluble amyloid-P protein(Aβ) plays a central pathogenic role in Alzheimer's disease(AD).Memantine,a low-affinity N-methyl-D-aspartate receptor(NMDAR) antagonist,exerts neural protective effects in *** this study, we investigated protection of memantine against the neurotoxicity of oligomeric Aβusing electrophysiology methods in vitro and in vivo and behavioral *** vitro,incubation of Aβ1-42 oligomers(500 nM) for 40 min prior to HFS strongly prevented *** inhibition can be partially reversed by an appropriate dose of mementine(20 mg/kg,i.p.) treatment for 7 ***,animals treated with a higher dose(40 mg/kg/day,i.p.) of memantine showed complete abolishment of LTP ***,inhibition of LTP by Aβ1-42 is partially restored when we pretreated with memantine(1μM) for 2 h,but alone treatment use this concentration of memantine for 2 h before HFS would partial inhibited the induction of *** vivo,we found acute injection of soluble Aβ1-42(40 pmol in 5μL,i.e.v.) alone 10 min before HFS inhibited LTP, the inhibitory effect of Aβ1-42 was partially prevented when 10 mg/kg memantine was injected 30 min before Aβ1- *** injection of twice this dose(20 mg/kg) alone completely inhibited *** behavioral testing,systemic treatment with memantine(3 mg/kg,i.p) alone impaired performance of operant learning task,but Aβ1-42 failed to strongly increase perseveration errors when the rats also received an injection of the subthreshold dose of memantine (1 mg/kg) if injection of soluble Aβ1-42(60 pmol in 10μL) alone before testing expand errors *** findings indicate that memantine restore Aβoligomers-mediated inhibition of hippocampal LTP in a concentration-related manner both in vitro and in vivo,it also prevented disruptive effect of Aβ1-42 on learned behavior,differences does-related in vitro and in vivo may be due to the different experimental environments and brain regions(the dentate gyrus in vitro and CA1 area in vivo).Thus,th

关键词： Aβ AD synapse plasticity NMDA memantine

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Extensive brain structural network abnormality in first-episode treatment-na(i)ve patients with schizophrenia:Morphological and covariation study

Extensive brain structural network abnormality in first-epis...

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中国神经科学学会第九届全国学术会议暨第五届会员代表大会

作者： Zhuangfei CHEN Yingcheng WANG Siew E Chua Charlton Cheung Gráinne M.McAlonan Pak C Sham David A Collier Marco Picchioni Stefania Benetti Andrea Mechelli Nicolas Crossley Wei DENG Joseph P.Kambeitz Paul Allen Philip McGuire Tao LI Qiyong GONG Chaohua HUANG Lijun JIANG Mingli LI Zongling HE Qiang WANG Xiaohong MA St Andrew''s Academic Centre Institute of Psychiatry King''s College London NN1 5BG Division of Psychological Medicine and Psychiatry Section of Neuroimaging Institute of Psychiatry King''s College London London SE5 8AF UK Division of Psychological Medicine and Psychiatry Section of Neuroimaging Institute of Psychiatry King''s College London London SE5 8AF UK The Mental Health Center & Psychiatric laboratory West China Hospital Sichuan University Chengdu China The State Key Laboratory of Biotherapy West China Hospital Sichuan University Chengdu China Department of Psychiatry The University of Hong Kong Pokfulam S.A.R.China MRC SGDP Centre Institute of Psychiatry King''s College London London SE5 8AF UK Division of Psychological Medicine and Psychiatry Section of Neuroimaging Institute of Psychiatry King''s College London London SE5 8AF UK Department of Psychosis Study Institute of Psychiatry King''s College London London SE5 8AF UK Huaxi MR Research Center Department of Radiology West China Hospital Sichuan University Chengdu China

Objective With a particular focus on putative cortico-striatal-thalamic-cortical (CSTC) networks current study aimed to explore robust gray matter volume (GMV) changes in non-medicated first-episode schizophrenia (FES) *** High-resolution T1-weighted images were obtained using 3.0 Tesla magnetic resonance imaging from 86 first-episode drug-naive schizophrenia patients and 86 healthy controls (CON).Severity of symptoms in patients was evaluated by using Positive and Negative Syndrome Scale (PANSS).Fourteen spherical region of interest (ROI) GMV in the CSTC loop were acquired after optimized voxel-based morphometry (VBM) *** of Spherical ROIs and corresponding correlation coefficients were compared between FES and CON *** associations of GMV with PANSS subscale score and symptom dimension scores were also *** GMV reduction was detected in bilateral hippocampus in FES group by VBM *** located in left inferior frontal gyrus (Brodmann's area 47) and right thalamus (medial dosal nucleus) present GMV *** of ROIs revealed more extensive GMV loss and disassociation between *** Our study support that schizophrenia involves distributed rather than focal pathology and disordered *** analysis could make compensation to VBM and ROI method to uncover more subtle aberrations in regional correlation.

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Neuronal nitric oxide synthase alteration accounts for the role of 5-HT1A-receptor in modulating anxiety-related behaviors

Neuronal nitric oxide synthase alteration accounts for the r...

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中国神经科学学会第九届全国学术会议暨第五次会员代表大会

作者： Jing ZHANG~1,Xin-Yan HUANG~(1,3),Min-Li YE~1,Chun-Xia LUO~(1,2),Hai-Yin WU~2,Yao HU~1,Qi-Gang ZHOU~(1,2), Dan-Lian WU~1,Li-Juan ZHU~1,Dong-Ya ZHU~(1,2,*) 1 Department of Pharmacology,School of Pharmacy,2 Laboratory of Cerebrovascular Disease,3 Nanjing Maternal and Child Health Hospital,Nanjing Medical University,Nanjing 210029,China.

Objection Epidemiological studies of anxiety disorders have indicated that as many as 29%of people will,at some point in their lives,suffer from anxiety *** serotonergic system is essential for regulating affects and moods,and has long been implicated in the pathogenesis of *** activity of serotonergic pathways is critically regulated by plasma membrane serotonin transporter and serotonin *** various 5-HT receptor subtypes,5-HT receptors have been predominantly involved in anxiety-related ***,the mechanism underlying the role of 5-HT receptors in these diseases remains *** Here we show that 5-HTR-selective agonist 8-OH-DPAT and selective serotonin reuptake inhibitor（SSRI） fluoxetine down-regulated hippocampal neuronal nitric oxide synthase（nNOS） expression,whereas 5-HT1AR-selective antagonist NAN-190 up-regulated hippocampal nNOS *** assessing anxiety-related behaviors using the novelty suppressed feeding,open-field and elevated plus maze tests,we show that mice lacking nNOS gene（KO） or treated with nNOSselective inhibitor 7-NI（i.p.,30 mg/kg/d for 28 days,or intrahippocampal microinjection,16.31μg/1.0μL） displayed an anxiolytic-like phenotype,implicating nNOS *** also show that,in wild-type（WT） mice,adminstrations of 8-OH-DPAT（i.p.,0.1 mg/kg/d） or fluoxetine（i.p.,10 mg/kg/d） for 28 days caused anxiolytic-like effects,whereas NAN-190（i.p.,0.3 mg/kg/d for 28 days） caused anxiogenic-like *** KO mice however,these drugs were ***,intrahippocampal infusion of 8-OH-DPAT（45.963μg/100μL） using 14-day osmotic minipump produced anxiolytic *** microinjection of 7-NI（16.31μg/1.0μL） abolished the anxiogenic-like effects of intrahippocampal NAN-190（4.74μg/1.0μL）.Additionally,NAN-190 decreased and 8-OH-DPAT increased phosphorylated CREB levels in WT mice but not in KO *** of hippocampal CREB phosphorylation by microinjection of H89（5.19μg/1.0μL）,a PKA inhi

关键词： neuronal nitric oxide synthase 5-HT,5-HT1A-receptor anxiety-related behavior CREB hippocampus

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Expression of TRPV1 in peripheral blood in adult chronic visceral hypersensitivety rats induced by neonatal colon irritation

Expression of TRPV1 in peripheral blood in adult chronic vis...

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中国神经科学学会第九届全国学术会议暨第五次会员代表大会

作者： Wei-Ying ZOU~1,Bei YANG~1,Ting CHEN~1,Ming-Di XIONG~1,Lei WU~1,Da-Lei ZHANG~1,Ting ZOU~(1,*),Xin-Yan GAO~2,Ri-Xin CHEN~3 1 Department of Physiology,Medical College of Nanchang University,Nanchang,Nanchang 330006,China 2 Institute of Acupuncture & Moxibustion,China Academy of Chinese Medical Sciences,Beijing 100700,China 3 Department of Acupuncture and Rehabilitation,Affiliated Hospital of Jiangxi College of Traditional Chinese Medicine,Nanchang,Nanchang 330006,China

Objective TRPV1 is a nonspecific cation channel of the transient receptor potential channel family and may be upregulated during visceral nociceptive *** expression of TRPV1 of nerve fibres,mucosa and muscular layers in gastro-intestinal tract was increased in visceral *** studies demonstrated that TRPV1 is expressed in peripheral blood cells(PBCs).The aim was to investigate whether TRPV1 expression in PBCs is increased in chronic visceral hypersensitivity in adult rats induced by colon irritation during postnatal *** Hypersensitive SD rats were generated by colorectal distension(CRD)during postnatal days 8 to *** sensitivity of the colon to balloon distention in adult was measured by grading their abdominal withdrawal reflex(AWR).The PBCs were obtained by cardiac puncture after *** cells were isolated from PBCs by density gradient ***-PCR was performed to detect the expression of TRPV1 and GAPDH *** signal intensity of each TRPV1 band was normalized by *** ODs in each sample were expressed as a ratio of TRPV1 over GAPDH densitometric *** The AWR score in response to CRD in adult rats with neonatal colorectal irritation was significantly higher than control with distension pressures of 20(Mean±SD,1.069±0.457 vs 0.1667±0.389,P<0.01),40(2.069±0.529 vs 1.25±0.753,P<0.01), 60(3.137±0.639 vs 2.20±0.63,P<0.01)and 80 mmHg(3.827±0.601 vs 3.20±0.632,P<0.05).The expression of TRPV1 mRNA of mononuclear cells of PBCs in the control group was in lower level(Mean±SD,0.148±0.084).The TRPV1 expression in neonatal CRD group was increased in adults(Mean±SD,0.724±0.593,P>0.05).Conclusions The colorectal distension in neonates can result in visceral hypersensitivity to CRD in adult rats compared with *** TRPV1 mRNA is expressed in PBCs and its expression may show up-regulation by neonatal colon *** results suggest that the TRPV1 expression in PBCs may be involved in abd

关键词： TRPV1 visceral hypersensitivity

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Identification of the role of phosphodiesterase in mediating memory:implication in Alzheimer’s disease

Identification of the role of phosphodiesterase in mediating...

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中国神经科学学会第九届全国学术会议暨第五次会员代表大会

作者： Rolf HANSEN Marco CONTI Steven P.WILSON James M.O'DONNELL Departments of Behavioral Medicine & Psychiatry and Physiology & Pharmacology West Virginia University Health Sciences CenterMorgantownWV26506USA Division of Reproductive Biology Department of Obstetrics & GynecologyUniversity of CaliforniaSan FranciscoCA 94143USA Department of Pharmacology Physiologyand NeuroscienceUniversity of South Carolina School of MedicineColumbiaSC 29208USA

＜正＞Objective Phosphodiseterase（PDE） is a superfamily of enzymes that catalyzes the hydrolysis of intracellular cAMP and/or *** the 11 PDE families（PDE1-11）,PDE4 is the most important family in the control of intracellular cAMP *** has been well established that PDE4 plays an essentia]role in the mediation of ***,it is not known whether PDE4 is involved in memory associated with Alzheimer’s disease（AD）. The objective of this study was to identify the role of PDE4 and its isoforms（PDE4A-D） in AD-related memory. Methods Mice deficient in PDE4A,PDE4B,or PDE4D were microinfused withβ-amyloid peptide 1-42（Aβ42;0.4μg/side） or vehicle into bilateral dorsal hippocampi before memory tests using the object recognition,passive avoidance,and Morris water-maze *** silencing was used to identify the role of PDE4 variants in memory. Expression of phosphorylated CREB（pCREB） in the hippocampus was also examined using Western blotting analysis. Results Mice deficient in PDE4A or PDE4D,but not PDE4B,displayed memory enhancement in one or all of the memory ***4A or PDE4D knockout mice also exhibited reversal of Aβ42-induced memory impairment, which was observed in wild-type mice in the object recognition,passive avoidance,and water-maze ***, microinfusions of lentiviral vectors containing microRNAs（miRNAs） that target long-form PDE4D splice variants mimicked the ability of PDE4D deficiency to enhance memory in normal mice;the miRNAs also reversed Aβ42- induced memory deficits in the radial arm maze test in ***,Aβ42 decreased pCREB levels in the hippocampus of wild-type mice or negative control sequence-treated rats,but not mice deficient in PDE4A or PDE4D nor rats treated with *** These results suggest that both PDE4A and PDE4D,in particular the long-form PDE4D isoforms,play an important role in the mediation of memory associated with Alzheimer’s disease. Targeting PDE4A or PDE4D may be a novel approach to tr

关键词： phosphodiesterase memory Alzheimer’s disease gene knockout gene knockdown PDE4 subtypes CREB miRNAs

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The phosphodiesterase-4 inhibitor rolipram reverses Aβ-induced cognitive impairment and neuroinflammatory and apoptotic responses in rats

The phosphodiesterase-4 inhibitor rolipram reverses Aβ-indu...

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中国神经科学学会第九届全国学术会议暨第五次会员代表大会

作者： Chuang WANG~(1,3),Xue-Mei YANG~2,Ye-Ye ZHUO~1,Heng ZHOU~1,Huan-Bing LIN~1,Yu-Fang CHENG~1,Han-Ting ZHANG~(3,*),Jiang-Ping XU~(1,*) 1 Department of Pharmacology,School of Pharmaceutical Sciences,Southern Medical University,Guangzhou 510515, China 2 Hygiene Detection Center,School of Public Health and Tropical Medicine,Southern Medical University,Guangzhou 510515,China 3 Departments of Behavioral Medicine & Psychiatry and Physiology & Pharmacology,West Virginia University Health Sciences Center,Morgantown,WV 26506,USA

Objectiveβ-Amyloid(Aβ) peptides play an important role in cognition deficits,neuroinflammation,and apoptosis observed in Alzheimer's disease(AD).Activation of cyclic AMP(cAMP) signaling enhances memory and inhibits inflammatory and apoptotic ***,it is not known whether inhibition of phosphodiesterase-4 (PDE4),a critical controller of intracellular cAMP concentrations,affects AD-associated neuroinflammatory and apoptotic responses and whether these responses contribute to deficits of memory mediated by cAMP signaling. Methods The water-maze and passive avoidance tests were used to test memory in rats infused with aggregated Aβ25-35 into bilateral CA1 subregions in the presence or absence of rolipram,a prototypical PDE4 inhibitor. Levels of inflammatory factors and apoptosis-related proteins were measured in the hippocampus of these rats after behavioral tests and confirmed with Aβ1-42 *** Rats microinfused with Aβ25-35(10μg/side) into CA1 displayed deficits in learning ability and memory,as evidenced by increases in escape latency during acquisition trials and decreases in exploratory activities in the probe trial in the water-maze task and 24-h retention in the passive avoidance *** memory deficits were reversed by rolipram(0.1,0.25,and 0.5 mg/kg/d,i.p.) in a dose-dependent ***,Aβ25-35-treated rats also displayed decreases in expression of phosphorylated cAMP responseelement binding protein(pCREB) and Bcl-2,but increases in expression of NF-κB p65 and Bax in the hippocampus;these effects were also reversed by rolipram in a dose-dependent *** neurochemical results were observed by replacing Aβ25-35 with Aβ1-42,a full-length amyloid peptide that quickly forms toxic *** These results suggest that PDE4 inhibitors such as rolipram may reverse Aβ-induced memory deficits at least in part via the attenuation of neuronal inflammation and apoptosis mediated by cAMP/CREB ***4 could be a ta

关键词： CREB memory,phosphodiesterase-4 rolipram P-amyloid

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