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Modulation of KCNQ potassium channels by a novel opener pyrazolo[l,5-a]pyrimidin-7(4H)-one compound QO-58

Modulation of KCNQ potassium channels by a novel opener pyra...

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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： Fan ZHANG,Jing-Jing MA,Yi MI,Jin-Long QI,Qing-Zhong JIA,Xiao-Na DU,Hai-Lin ZHANG 1 Department of Pharmacology,2 Department of New Drug Development,Hebei Medical University,Shijiazhuang 050017,China

Voltage-gated Kv7/KCNQ/M-potassium channels play an essential role in setting the resting membrane potential and in controlling the excitability of *** or depression of KCNQ channels results in neuronal hyperactivity and *** function is also indicated in nociceptive sensory ***,modulation of KCNQ2/3 function represents a potentially new strategy to treat neuronal excitability disorders such as epilepsy and neuropathic *** designed and synthesized a novel serial compounds of pyrazolo[1,5-a]pyrimidin-7（4H）- ones（PPOs）which activate KCNQ ***,in this study,we characterized one of these compounds,QO- 58's effect and mechanism underlying the activation of KCNQ channels using patch clamp technique.（1）QO-58 activated KCNQ2/Q3 currents at-40 mV concentration-dependently with a ECof 2.3±0.8μM.（2）QO-58 shifted the voltage-dependent activation of the KCNQ2/Q3 channel,and the Vwas shifted approximately-40 mV towards more negative potential in the presence 10 uM QO-58.（3）QO-58 significantly slowed channel activation and deactivation kinetics.（4）Among KCNQ channels,QO-58 increased homomeric KCNQ1-4 and heteromeric KCNQ3/Q5 currents recorded at-40 mV;The ECs value were 7.05±1.0,1.31±1.0,9.70±2.4,0.60±0.1,5.16±2.2μM,for KCNQ1, KCNQ2,KCNQ3,KCNQ4 and KCNQ3/Q5,respectively.（5）QO-58 enhanced native M currents from rat DRG neurons.（6）QO-58 dose-dependently prevented seizures induced by electroshock in rats,with a 73.3%reduction of seizures obtained at a dose of 50 mg/*** results indicate QO-58 is a potent KCNQ channel opener with more selective effect on KCNQ2 and ***-58 activates KCNQ channels through enhancing voltage-dependent activation and slowing channel ***-58 shows potent anti-seizure effects and can be developed further to treat disease related with neuronal hyperexcitability.

关键词： KCNQ channels M channel opener QO-58 seizures

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High glucose exacerbates β-amyloid production and the beneficial role of benfotiamine in vitro

High glucose exacerbates β-amyloid production and the benef...

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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-Jing SUN,Lei ZHAO,Na ZHAO,Chun-Jiu ZHONG~* Department of Neurology,Zhongshan Hospital & Shanghai Medical College State Key Laboratory of Medical Neurobiology Institute of Brain Science Fudan University.

Our previous study has demonstrated that benfotiamine,a protective agent for diabetes complications, significantly decreases p-amyloid(Aβ) production through enhancing the phosphorylation levels and reduced enzymatic activities of both GSK-3αand GSK-3βin the APP/PS1 transgenic *** evidence from a population- based study also shows a link between Alzheimer's disease(AD) and diabetes mellitus(DM).The prevelance rate of AD is high as much as 2 to 5 times in population suffering from DM compared with non-DM control subjects. Experimental investigations suggest that the abnormality of cerebral glucose metabolism is the key etiological factor for *** we explored the effect of benfotiamine on high glucose exacerbating Aβproduction and the possible mechanism using HEK293 APPsw overexpression *** results showed that Aβproduction was first rising and then dropping along with the increased concentrations of glucose in the cell culture medium(1 g/L,3 g/L,4.5 g/ L,5.5 g/L,6.5 g/L,7.5 g/L,8.5 g/L,10.5 g/L) and the prolongation of incubated time(6,12,and 24 h).After being incubated for 6 h or 12 h,the Aβproduction of cells incubated in 5.5 g/L glucose was higher significantly compared with those of cells in 1 g/L glucose(6 h,P<0.05;12 h,P<0.01).It was associated with high glucose up-regulating the activities of GSK-3:The ratios of p-GSK-3a/GSK-3a and p-GSK-3β/GSK-3βin 5.5 g/L group were significantly decreased(p-GSK-3α/GSK-3α,P<0.01;p-GSK-3β/GSK-3β,P<0.05),and the activities of GSK-3a and GSK- 3βwere significantly increased compared with those in 1.0 g/L group(P<0.05).Benfotiamine significantly reduced Aβproduction enhanced by high glucose compared with control group(20 ug/mL group P<0.05,40μg/mL group P<0.01).The mechanisms may be through modulating GSK-3 activities:Benfotiamine(40μg/mL) significantly decreased the activities of GSK-3a and GSK-3βcompared with control group(P<0.05).Increased Aβproduction induced by high glucose is associated with the up-regulatio

关键词： Alzheimer's disease diabetes mellitus benfotiamene glycogen synthase kinase-3

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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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The effects of NMDAR and mGluR on Ap-mediated synaptic plasticity disruption in vitro

The effects of NMDAR and mGluR on Ap-mediated synaptic plast...

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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： Ru-Yi LIN,Tian-Xiang DENG,Gui-Lan LIU,Shu-Jun XU,Xaio-Wei CHEN,Xiao-Fei WEI,Qin-Wen WANG Medical School,Ningbo University,Ningbo 315211,China

Apart from anticholinesterases,memantine,a low-affinity NMDA receptor(NMDAR) antagonist,is the only currently approved treatment for clinical dementia of the Alzheimer *** we examined if subtype-preferring NMDA receptor antagonists could preferentially protect against the inhibition of NMDA receptor-dependent plasticity of excitatory synaptic transmission by Aβin the hippocampus by electrophysiology methods in *** selective for NMDA receptors containing NR2B but not NR2A subunits prevented Aβ-mediated inhibition of plasticity and showed *** AB,pretreatment with a high dose of NR2B antagonist ifenprodil(1μM) and Ro 25-6981(200 nM) completely inhibited *** experiments indicated that a lower dose of ifenprodil(400 nM) could partially block LTP(131±7%) and reverse Aβinhibition on LTP(139±6%).However,Ro 25-6981(50 nM) didn't block LTP(143±10%) but did prevent Aβinhibition on LTP(132±8%).The selective antagonist NVP-AAM077 for NMDA receptors containing NR2A did not affect LTP on its own,and failed to prevent the inhibition of LTP by Aβ.Furthermore,we also investigated LTD which was induced by strong LFS but not weak LFS,however,weak LFS plus Aβpresented a steady LTD in both the dentate gyrus and the CA1 region of the hippocampus.D-AP5(a specific NMDAR antagonist) could not block the LTD induced by Aβwith weak LFS in the CA1 *** contrary to the D-AP5,weak LFS with Aβ-induced LTD was completely abrogated by LY341495(the group I metabotropic glutamate receptor antagonist).Moreover,the enhancement of LTD by Ap was reversed by SB203580(p38 Mitogen-Activated Protein Kinase inhibitor) and phenylarsine oxide(membrane-permeable protein-tyrosine phosphatase inhibitor).The present data suggest that preferentially targeting NR2B subunit-containing NMDARs with a selective antagonist may provide an effective means of preventing cognitive deficits in Alzheimer's disease and LTD induced by Aβwith weak LFS was not NMDAR-dependent,but mGluR

关键词： Aβ AD synapse plasticity NMDA mGluR

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Alpha-band modulation during intersensory selective attention

Alpha-band modulation during intersensory selective attentio...

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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： Xiang-Fei HONG,Shan-Bao TONG~* Neural Engineering Laboratory,Med-X Research Institute,Shanghai Jiao Tong University,Shanghai 200030,China

Objective Human can focus attention to one sensory modality（*** or visual） and reach a biased attentional state in a top-down manner,which will facilitate information processing in that sensory *** activity in human EEG was related to this intersensory selective attention in previous *** we study the time course of intersensory selective attention by analyzing alpha-band ERD（event-related desynchronization） during the *** Ten subjects（4 females） with a mean age of（21.3±2.7） years participated in the ***-target paradigm was used,in which there were 3 kinds of cues:auditory（A）,visual（V） and audiovisual（AV）.In each trial,the cue was firstly presented on a display and the subject was required to direct his/ her attention to a sensory modality as *** a variable cue-target interval（CTI）,a compound audiovisual stimulus appeared as the *** performed a GO/NoGo task to detect the cued sensory part of the target in A or V condition,and detect both sensory parts in AV *** EEG data were recorded from 30 scalp electrodes mounted in an elastic cap(EasyCap,BrainAmp amplifier,Brain Products GmbH,Munich,Germany). EEG was segmented to epochs according to different ***-band ERD was calculated based on the artifact-free EEG epochs and then smoothed by averaging over time samples with a moving averaging *** calculate the statistical significance of alpha-band ERD,30 electrodes were divided to 13 cortical regions:PF（Fpl,Fp2）,LF（F7, F3）,MF（Fz）,RF（F4,F8）,LT（T7）,RT（T8）,LC（FC5,FC1,C3,CP5,CP1）,MC（Cz）,RC（FC6,FC2,C4,CP6,CP2）, LP（P7,P3,TP9）,MP（Pz）,RP（P4,P8,TP10）,and 0（01,02,Oz）.In addition to the pre-cue baseline,post-cue CTI was divided to three periods:begin,middle and ***-way repeated measures ANOVA was performed using SPSS, and the within-subject factors were defined as Sequence（baseline,begin,middle,end）,Cue（A,V,AV） and Area（13 cortical regions listed above）.Results Three-way repeated m

关键词： intersensory selective attention alpha-band ERD

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Modulatory effect of prokineticin 2 on GABA-activated currents in rat primary sensory neurons

Modulatory effect of prokineticin 2 on GABA-activated curren...

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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： Wang-Ping HU~*,Yan-Cai XIONG,Xue-Mei LI,Yu-Qiang LIU,Fang QIU,Dan WU,Yun-Bo GAN Department of Pharmacology,Xianning College,Xianning 437100,China

Prokineticin 2（PK2） is a newly identified regulatory protein,which is involved in a wide range of physiological processes including pain perception in *** injection of PK2 into rats induces hyperalgesia to tactile and thermal ***2 receptors,PKR1 and PKR2,are expressed in primary sensory neurons. Mice lacking the PK2 or PKR1 gene exhibited impaired pain perception to various stimuli,including noxious heat, mechanical,capsaicin,and ***,the precise role of PK2 in nociception is yet not fully ***, we investigate the effects of PK2 on GABA receptor function in rat trigeminal ganglion neurons using whole-cell patch clamp ***2 reversibly depressed inward currents produced by GABA receptor activation(I) with an IC of（0.26±0.02） ***2 appeared to decrease the efficacy of GABA to GABA receptor but not the affinity. The maximum response of the GABA dose-response curve decreased to（71.2±7.0）%of control after pretreatment with PK2,while the threshold value and EC of curve did not alter *** effects of PK2 on I voltage ***2 depressed I at all holding potentials between -80 and 40 mV,and did not alter the reversal potentials of *** inhibition of PK2 on the amplitude of I was increased gradually when the pretreatment duration was extended from 30s to *** PK2-induced inhibition of I was removed by intracellular dialysis of either GDP-β-S（a non-hydrolyzable GDP analog）,EGTA(a Ca chelator) or GF109203X（a selective protein kinase C inhibitor）,but not by H89（a protein kinase A inhibitor）.These results suggest that PK2 down-regulates the function of the GABA receptor via G-protein and protein kinase C dependent signal pathways in primary sensory neurons and this depression might underlie the hyperalgesia induced by PK2.

关键词： prokineticin 2 GABA-activated current depression primary sensory neuron patch clamp technique intracellular dialysis

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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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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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Transplantation of Olig2-expressing neural stem cells and adoptive immunotherapy of Myelin basic protein activated T cells promotes remyelination and functional recovery after spinal cord injury

Transplantation of Olig2-expressing neural stem cells and 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： Jian-Guo HU~(1,2,3),Jian-Sheng ZHOU~3,Yu-Xin ZHANG~3,Bao-Ming ZHAO~1,Shan-Feng MA~3,He-Zuo LV~(1,2,*) 1 Center Laboratory,The First Affiliated Hospital of Bengbu Medical College,Bengbu 233004,China 2 Department of Clinical Laboratory Science,The First Affiliated Hospital of Bengbu Medical College,Bengbu 233004, China 3Anhui Key Laboratory of Tissue Transplantation,Bengbu Medical College,Bengbu 233004,China

Neural stem cell transplantation is a major focus of current research in treatment of spinal cord injury (SCI).However,it is very important to promote the transplanted neural stem cells(NSCs) differentiate into OLs and neurons in lesion *** previous studies have shown that 01ig2-overexpression can promote the differentiation of cultured NSCs into mature ***,it has been reported that myelin basic protein activated T cells(MBP-T) can produce neurotrophic factors,improve the SCI local micro-environment,and be neuroprotective to residual myelin and ***,we suppose that combination of 01ig2-modified NSC transplantation and MBP-T cell adoptive immunotherapy may have complementary roles in the treatment of *** this study,the MBP-T cells,which can express IFN-γ,IL-10,and IL-13 after activation in vitro,were passively immunized to spinal cord injured rats within one day after *** NSCs,which were infected with lentivirus expressing green fluorescent protein(GFP-NSCs) or 01ig2(01ig2-GFP-NSCs),were transplanted into injured spinal cord 9 d after *** fate of transplanted cells was tracked by GFP fluorescence after transplantation in different time *** adoptive immunotherapy,the transferred MBP-T cells(CD4-positive) could be detected in injured spinal cord from 3 d to 4 *** infiltration of the MBP-T cells was correlated with and the differentiation of resident microglia and/or infiltrating blood monocytes toward an "alternatively-activated" anti-inflammatory(M2) macrophage *** 2 to 7 weeks after transplantation,the grafted NSCs could be detected to survive and integrate into the injured spinal *** 2 weeks, the survival of grafted NSCs increased fivefold in MBP-T cell-transferred rats compared with vehicle-treated ones. The engrafted GFP-NSCs mostly differentiated into astrocytes,but not OLs and ***,the percentage of MBP-positive OLs increased 12-fold in 01ig2-GFP-NSC-engrafted rats compared with GFP-NS

关键词： spinal cord injury passive immunization Olig2 neural stem cells transplantation

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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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