PSD-95与老化相关学习记忆能力下降关系研究进展
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摘要
学习记忆能力下降是老年人群脑老化的主要特征之一,这部分归因于突触结构和功能的改变而非神经元的死亡。突触后致密蛋白95(PSD-95)是突触后结构中的一种支架蛋白,其表达对于维持突触结构及突触可塑性十分重要。最近的研究发现PSD-95与脑老化密切相关,对PSD-95与脑老化的关系作一综述,重点关注PSD-95与脑老化相关学习记忆能力下降的关系,以期为脑老化机制的深入研究及相关疾病的防治提供参考。
Brain aging is associated with impairments in learning and memory, which can be explained partly by alterations in synaptic structure and function rather than neuronal loss. Postsynaptic density protein 95(PSD-95) is a major scaffolding protein in postsynaptic density and is important for maintaining the synaptic structure and plasticity. PSD-95 is considered to be associated with brain aging in recent studies. Thus, we reviewed the relationship of PSD-95 and brain aging, mainly focusing on impairments in learning and memory, hoping to provide a new sight for further researches in the mechanisms of brain aging and in preventing the related diseases.
Brain aging is associated with impairments in learning and memory, which can be explained partly by alterations in synaptic structure and function rather than neuronal loss. Postsynaptic density protein 95(PSD-95) is a major scaffolding protein in postsynaptic density and is important for maintaining the synaptic structure and plasticity. PSD-95 is considered to be associated with brain aging in recent studies. Thus, we reviewed the relationship of PSD-95 and brain aging, mainly focusing on impairments in learning and memory, hoping to provide a new sight for further researches in the mechanisms of brain aging and in preventing the related diseases.
引文
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[18]EHRLICH I, KLEIN M, RUMPEL S, et al. PSD-95 is required for activity-driven synapse stabilization[J]. PNAS,2007, 104: 4176-4181.
[19]NIKONENKO I, BODA B, STEEN S, et al. PSD-95 promotes synaptogenesis and multiinnervated spine formation through nitric oxide signaling[J]. The Journal of Cell Biology, 2008, 183: 1115-1127.
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[23]EHRLICH I, MALINOW R. Postsynaptic density 95 controls AMPA receptor incorporation during long-term potentiation and experience-driven synaptic plasticity[J]. Journal of Neuroscience, 2004, 24: 916-927.
[24]ELIAS G M, FUNKE L, STEIN V, et al. Synapse-specific and developmentally regulated targeting of AMPA receptors by a family of MAGUK scaffolding proteins[J]. Neuron, 2006, 52: 307-320.
[25]BRADLEY S A, STEINERT J R. Nitric oxide-mediated posttranslational modifications: Impacts at the synapse[J]. Oxidative Medicine and Celluar Longevity, 2016, 2016: 5681036.
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[27]MOHAN A, MATHER K A, THALAMUTHU A, et al. Gene expression in the aging human brain: an overview[J]. Current Opinion in Psychiatry,2016, 29: 159-167.
[28]PANDEY S P, RAI R, GAUR P, et al. Development- and age-related alterations in the expression of AMPA receptor subunit GluR2 and its trafficking proteins in the hippocampus of male mouse brain[J]. Biogerontology,2015, 16: 317-328.
[29]ROGERS J T, LIU C C, ZHAO N, et al. Subacute ibuprofen treatment rescues the synaptic and cognitive deficits in advanced-aged mice[J]. Neurobiology of Aging,2017, 53: 112-121.
[30]MIGAUD M, CHARLESWORTH P, DEMPSTER M, et al. Enhanced long-term potentiation and impaired learning in mice with mutant postsynaptic density-95 protein[J]. Nature, 1998, 396: 433-439.
[2]ZHENG C Y, SEABOLD G K, HORAK M, et al. MAGUKs, synaptic development, and synaptic plasticity[J]. Neuroscientist, 2011, 17: 493-512.
[3]MORRISON J H, BAXTER M G. The ageing cortical synapse: hallmarks and implications for cognitive decline[J]. Nature Reviews Neuroscience, 2012, 13: 240-250.
[4]GRILLO F W. Long live the axon. Parallels between ageing and pathology from a presynaptic point of view[J]. Joumal of Chemical Neuroanatomy, 2016, 76: 28-34.
[5]PETERS A, SETHARES C, LUEBKE J I. Synapses are lost during aging in the primate prefrontal cortex[J]. Neuroscience, 2008, 152: 970-981.
[6]HONGPAISAN J, XU C, SEN A, et al. PKC activation during training restores mushroom spine synapses and memory in the aged rat[J]. Neurobiology of Disease, 2013, 55: 44-62.
[7]LYNCH M A. Long-term potentiation and memory[J]. Physiology Reviews, 2004, 84: 87-136.
[8]STATHAKIS D G, UDAR N, SANDGREN O, et al. Genomic organization of human DLG4, the gene encoding postsynaptic density 95[J]. Journal of Neurochemistry,1999, 73: 2250-2265.
[9]SHENG M, KIM E. The postsynaptic organization of synapses[J]. Cold Spring Harbor Perspectives in Biology, 2011, 3.
[10]VALLEJO D, CODOCEDO J F, INESTROSA N C. Posttranslational modifications regulate the postsynaptic localization of PSD-95[J]. Molecular Neurobiology, 2017, 54: 1759-1776.
[11]LAMBERT J T, HILL T C, PARK D K, et al. Protracted and asynchronous accumulation of PSD95-family MAGUKs during maturation of nascent dendritic spines[J]. Developmental Neurobiology, 2017, 77: 1161-1174.
[12]BAO J, LIN H, OUYANG Y, et al. Activity-dependent transcription regulation of PSD-95 by neuregulin-1 and Eos[J]. Nature Neuroscience, 2004, 7: 1250-1258.
[13]CHEN X, WINTERS C, AZZAM R, et al. Organization of the core structure of the postsynaptic density[J]. PNAS, 2008, 105: 4453-4458.
[14]HAN K, KIM E. Synaptic adhesion molecules and PSD-95[J]. Progress in Neurobiology, 2008, 84: 263-283.
[15]GIANNONE G, MONDIN M, GRILLO-BOSCH D, et al. Neurexin-1beta binding to neuroligin-1 triggers the preferential recruitment of PSD-95 versus gephyrin through tyrosine phosphorylation of neuroligin-1[J]. Cell Reports, 2013, 3: 1996-2007.
[16]PRANGE O, WONG T P, GERROW K, et al. A balance between excitatory and inhibitory synapses is controlled by PSD-95 and neuroligin[J]. PNAS, 2004, 101: 13915-13920.
[17]EL-HUSSEINI A E, SCHNELL E, CHETKOVICH D M, et al. PSD-95 involvement in maturation of excitatory synapses[J]. Science,2000, 290: 1364-1368.
[18]EHRLICH I, KLEIN M, RUMPEL S, et al. PSD-95 is required for activity-driven synapse stabilization[J]. PNAS,2007, 104: 4176-4181.
[19]NIKONENKO I, BODA B, STEEN S, et al. PSD-95 promotes synaptogenesis and multiinnervated spine formation through nitric oxide signaling[J]. The Journal of Cell Biology, 2008, 183: 1115-1127.
[20]WU Q, SUN M, BERNARD L P, et al. Postsynaptic density 95 (PSD-95) serine 561 phosphorylation regulates a conformational switch and bidirectional dendritic spine structural plasticity[J]. The Journal of Biological Chemistry, 2017, 292: 16150-16160.
[21]B QUE JC A R. PSD-95 regulates synaptic transmission and plasticity in rat cerebral cortex[J]. The Journal of Physiology,2003, 546: 859-867.
[22]STEIN V, HOUSE D R, BREDT D S, et al. Postsynaptic density-95 mimics and occludes hippocampal long-term potentiation and enhances long-term depression[J]. Journal of Neuroscience, 2003, 23: 5503-5506.
[23]EHRLICH I, MALINOW R. Postsynaptic density 95 controls AMPA receptor incorporation during long-term potentiation and experience-driven synaptic plasticity[J]. Journal of Neuroscience, 2004, 24: 916-927.
[24]ELIAS G M, FUNKE L, STEIN V, et al. Synapse-specific and developmentally regulated targeting of AMPA receptors by a family of MAGUK scaffolding proteins[J]. Neuron, 2006, 52: 307-320.
[25]BRADLEY S A, STEINERT J R. Nitric oxide-mediated posttranslational modifications: Impacts at the synapse[J]. Oxidative Medicine and Celluar Longevity, 2016, 2016: 5681036.
[26]NAGURA H, DOI T, FUJIYOSHI Y. Characterization of physiological phenotypes of dentate gyrus synapses of PDZ1/2 domain-deficient PSD-95-knockin mice[J]. Eurpean Journal Neuroscience, 2016, 43: 618-625.
[27]MOHAN A, MATHER K A, THALAMUTHU A, et al. Gene expression in the aging human brain: an overview[J]. Current Opinion in Psychiatry,2016, 29: 159-167.
[28]PANDEY S P, RAI R, GAUR P, et al. Development- and age-related alterations in the expression of AMPA receptor subunit GluR2 and its trafficking proteins in the hippocampus of male mouse brain[J]. Biogerontology,2015, 16: 317-328.
[29]ROGERS J T, LIU C C, ZHAO N, et al. Subacute ibuprofen treatment rescues the synaptic and cognitive deficits in advanced-aged mice[J]. Neurobiology of Aging,2017, 53: 112-121.
[30]MIGAUD M, CHARLESWORTH P, DEMPSTER M, et al. Enhanced long-term potentiation and impaired learning in mice with mutant postsynaptic density-95 protein[J]. Nature, 1998, 396: 433-439.