CaMKII-dependent dendrite ramification and spine generation promote spatial training-induced memory improvement in a rat model of sporadic Alzheimer's disease
Participation in cognitively stimulating activities can preserve memory capacities in patients with Alzheimer's disease (AD), but the mechanism is not fully understood. Here, we used a rat model with hyperhomocysteinemia, an independent risk factor of AD, to study whether spatial training could...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Jiang, Xia [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2015transfer abstract |
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| Schlagwörter: |
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| Umfang: |
10 |
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| Übergeordnetes Werk: |
Enthalten in: Corrigendum to “Electrical and thermal transport properties of Fe–Ni based ternary alloys in the earth's inner core: An ab initio study” [Physics of the Earth and Planetary Interiors - Zidane, Mustapha ELSEVIER, 2021, Amsterdam [u.a.] |
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| Übergeordnetes Werk: |
volume:36 ; year:2015 ; number:2 ; pages:867-876 ; extent:10 |
| Links: |
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| DOI / URN: |
10.1016/j.neurobiolaging.2014.10.018 |
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| 245 | 1 | 0 | |a CaMKII-dependent dendrite ramification and spine generation promote spatial training-induced memory improvement in a rat model of sporadic Alzheimer's disease |
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| 520 | |a Participation in cognitively stimulating activities can preserve memory capacities in patients with Alzheimer's disease (AD), but the mechanism is not fully understood. Here, we used a rat model with hyperhomocysteinemia, an independent risk factor of AD, to study whether spatial training could remodel the synaptic and/or dendritic plasticity and the key molecular target(s) involved. We found that spatial training in water maze remarkably improved the subsequent short-term and long-term memory performance in contextual fear conditioning and Barnes maze. The trained rats showed an enhanced dendrite ramification, spine generation and plasticity in dentate gyrus (DG) neurons, and stimulation of long-term potentiation between perforant path and DG circuit. Spatial training also increased the levels of postsynaptic GluA1, GluN2A, GluN2B, and PSD93 with selective activation of calcium/calmodulin-dependent protein kinase II (CaMKII), although inhibition of CaMKII by stereotaxic injection of KN93 into hippocampal DG, abolished the training-induced cognitive improvement, dendrite ramification, and spine generation. We conclude that spatial training can preserve the cognitive function by CaMKII-dependent remodeling of dendritic plasticity in hyperhomocysteinemia-induced sporadic AD-like rats. | ||
| 520 | |a Participation in cognitively stimulating activities can preserve memory capacities in patients with Alzheimer's disease (AD), but the mechanism is not fully understood. Here, we used a rat model with hyperhomocysteinemia, an independent risk factor of AD, to study whether spatial training could remodel the synaptic and/or dendritic plasticity and the key molecular target(s) involved. We found that spatial training in water maze remarkably improved the subsequent short-term and long-term memory performance in contextual fear conditioning and Barnes maze. The trained rats showed an enhanced dendrite ramification, spine generation and plasticity in dentate gyrus (DG) neurons, and stimulation of long-term potentiation between perforant path and DG circuit. Spatial training also increased the levels of postsynaptic GluA1, GluN2A, GluN2B, and PSD93 with selective activation of calcium/calmodulin-dependent protein kinase II (CaMKII), although inhibition of CaMKII by stereotaxic injection of KN93 into hippocampal DG, abolished the training-induced cognitive improvement, dendrite ramification, and spine generation. We conclude that spatial training can preserve the cognitive function by CaMKII-dependent remodeling of dendritic plasticity in hyperhomocysteinemia-induced sporadic AD-like rats. | ||
| 650 | 7 | |a Dendrite ramification |2 Elsevier | |
| 650 | 7 | |a Calcium/calmodulin-dependent protein kinase II |2 Elsevier | |
| 650 | 7 | |a Spine generation |2 Elsevier | |
| 650 | 7 | |a Spatial training |2 Elsevier | |
| 650 | 7 | |a Alzheimer's disease |2 Elsevier | |
| 650 | 7 | |a Spatial memory |2 Elsevier | |
| 700 | 1 | |a Chai, Gao-Shang |4 oth | |
| 700 | 1 | |a Wang, Zhi-Hao |4 oth | |
| 700 | 1 | |a Hu, Yu |4 oth | |
| 700 | 1 | |a Li, Xiao-Guang |4 oth | |
| 700 | 1 | |a Ma, Zhi-Wei |4 oth | |
| 700 | 1 | |a Wang, Qun |4 oth | |
| 700 | 1 | |a Wang, Jian-Zhi |4 oth | |
| 700 | 1 | |a Liu, Gong-Ping |4 oth | |
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10.1016/j.neurobiolaging.2014.10.018 doi GBVA2015008000023.pica (DE-627)ELV018419410 (ELSEVIER)S0197-4580(14)00675-7 DE-627 ger DE-627 rakwb eng 610 610 DE-600 550 520 VZ 38.70 bkl 39.53 bkl Jiang, Xia verfasserin aut CaMKII-dependent dendrite ramification and spine generation promote spatial training-induced memory improvement in a rat model of sporadic Alzheimer's disease 2015transfer abstract 10 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Participation in cognitively stimulating activities can preserve memory capacities in patients with Alzheimer's disease (AD), but the mechanism is not fully understood. Here, we used a rat model with hyperhomocysteinemia, an independent risk factor of AD, to study whether spatial training could remodel the synaptic and/or dendritic plasticity and the key molecular target(s) involved. We found that spatial training in water maze remarkably improved the subsequent short-term and long-term memory performance in contextual fear conditioning and Barnes maze. The trained rats showed an enhanced dendrite ramification, spine generation and plasticity in dentate gyrus (DG) neurons, and stimulation of long-term potentiation between perforant path and DG circuit. Spatial training also increased the levels of postsynaptic GluA1, GluN2A, GluN2B, and PSD93 with selective activation of calcium/calmodulin-dependent protein kinase II (CaMKII), although inhibition of CaMKII by stereotaxic injection of KN93 into hippocampal DG, abolished the training-induced cognitive improvement, dendrite ramification, and spine generation. We conclude that spatial training can preserve the cognitive function by CaMKII-dependent remodeling of dendritic plasticity in hyperhomocysteinemia-induced sporadic AD-like rats. Participation in cognitively stimulating activities can preserve memory capacities in patients with Alzheimer's disease (AD), but the mechanism is not fully understood. Here, we used a rat model with hyperhomocysteinemia, an independent risk factor of AD, to study whether spatial training could remodel the synaptic and/or dendritic plasticity and the key molecular target(s) involved. We found that spatial training in water maze remarkably improved the subsequent short-term and long-term memory performance in contextual fear conditioning and Barnes maze. The trained rats showed an enhanced dendrite ramification, spine generation and plasticity in dentate gyrus (DG) neurons, and stimulation of long-term potentiation between perforant path and DG circuit. Spatial training also increased the levels of postsynaptic GluA1, GluN2A, GluN2B, and PSD93 with selective activation of calcium/calmodulin-dependent protein kinase II (CaMKII), although inhibition of CaMKII by stereotaxic injection of KN93 into hippocampal DG, abolished the training-induced cognitive improvement, dendrite ramification, and spine generation. We conclude that spatial training can preserve the cognitive function by CaMKII-dependent remodeling of dendritic plasticity in hyperhomocysteinemia-induced sporadic AD-like rats. Dendrite ramification Elsevier Calcium/calmodulin-dependent protein kinase II Elsevier Spine generation Elsevier Spatial training Elsevier Alzheimer's disease Elsevier Spatial memory Elsevier Chai, Gao-Shang oth Wang, Zhi-Hao oth Hu, Yu oth Li, Xiao-Guang oth Ma, Zhi-Wei oth Wang, Qun oth Wang, Jian-Zhi oth Liu, Gong-Ping oth Enthalten in Elsevier Science Zidane, Mustapha ELSEVIER Corrigendum to “Electrical and thermal transport properties of Fe–Ni based ternary alloys in the earth's inner core: An ab initio study” [Physics of the Earth and Planetary Interiors 2021 Amsterdam [u.a.] (DE-627)ELV005660645 volume:36 year:2015 number:2 pages:867-876 extent:10 https://doi.org/10.1016/j.neurobiolaging.2014.10.018 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-GGO SSG-OPC-GEO SSG-OPC-AST 38.70 Geophysik: Allgemeines VZ 39.53 Planeten VZ AR 36 2015 2 867-876 10 045F 610 |
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10.1016/j.neurobiolaging.2014.10.018 doi GBVA2015008000023.pica (DE-627)ELV018419410 (ELSEVIER)S0197-4580(14)00675-7 DE-627 ger DE-627 rakwb eng 610 610 DE-600 550 520 VZ 38.70 bkl 39.53 bkl Jiang, Xia verfasserin aut CaMKII-dependent dendrite ramification and spine generation promote spatial training-induced memory improvement in a rat model of sporadic Alzheimer's disease 2015transfer abstract 10 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Participation in cognitively stimulating activities can preserve memory capacities in patients with Alzheimer's disease (AD), but the mechanism is not fully understood. Here, we used a rat model with hyperhomocysteinemia, an independent risk factor of AD, to study whether spatial training could remodel the synaptic and/or dendritic plasticity and the key molecular target(s) involved. We found that spatial training in water maze remarkably improved the subsequent short-term and long-term memory performance in contextual fear conditioning and Barnes maze. The trained rats showed an enhanced dendrite ramification, spine generation and plasticity in dentate gyrus (DG) neurons, and stimulation of long-term potentiation between perforant path and DG circuit. Spatial training also increased the levels of postsynaptic GluA1, GluN2A, GluN2B, and PSD93 with selective activation of calcium/calmodulin-dependent protein kinase II (CaMKII), although inhibition of CaMKII by stereotaxic injection of KN93 into hippocampal DG, abolished the training-induced cognitive improvement, dendrite ramification, and spine generation. We conclude that spatial training can preserve the cognitive function by CaMKII-dependent remodeling of dendritic plasticity in hyperhomocysteinemia-induced sporadic AD-like rats. Participation in cognitively stimulating activities can preserve memory capacities in patients with Alzheimer's disease (AD), but the mechanism is not fully understood. Here, we used a rat model with hyperhomocysteinemia, an independent risk factor of AD, to study whether spatial training could remodel the synaptic and/or dendritic plasticity and the key molecular target(s) involved. We found that spatial training in water maze remarkably improved the subsequent short-term and long-term memory performance in contextual fear conditioning and Barnes maze. The trained rats showed an enhanced dendrite ramification, spine generation and plasticity in dentate gyrus (DG) neurons, and stimulation of long-term potentiation between perforant path and DG circuit. Spatial training also increased the levels of postsynaptic GluA1, GluN2A, GluN2B, and PSD93 with selective activation of calcium/calmodulin-dependent protein kinase II (CaMKII), although inhibition of CaMKII by stereotaxic injection of KN93 into hippocampal DG, abolished the training-induced cognitive improvement, dendrite ramification, and spine generation. We conclude that spatial training can preserve the cognitive function by CaMKII-dependent remodeling of dendritic plasticity in hyperhomocysteinemia-induced sporadic AD-like rats. Dendrite ramification Elsevier Calcium/calmodulin-dependent protein kinase II Elsevier Spine generation Elsevier Spatial training Elsevier Alzheimer's disease Elsevier Spatial memory Elsevier Chai, Gao-Shang oth Wang, Zhi-Hao oth Hu, Yu oth Li, Xiao-Guang oth Ma, Zhi-Wei oth Wang, Qun oth Wang, Jian-Zhi oth Liu, Gong-Ping oth Enthalten in Elsevier Science Zidane, Mustapha ELSEVIER Corrigendum to “Electrical and thermal transport properties of Fe–Ni based ternary alloys in the earth's inner core: An ab initio study” [Physics of the Earth and Planetary Interiors 2021 Amsterdam [u.a.] (DE-627)ELV005660645 volume:36 year:2015 number:2 pages:867-876 extent:10 https://doi.org/10.1016/j.neurobiolaging.2014.10.018 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-GGO SSG-OPC-GEO SSG-OPC-AST 38.70 Geophysik: Allgemeines VZ 39.53 Planeten VZ AR 36 2015 2 867-876 10 045F 610 |
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10.1016/j.neurobiolaging.2014.10.018 doi GBVA2015008000023.pica (DE-627)ELV018419410 (ELSEVIER)S0197-4580(14)00675-7 DE-627 ger DE-627 rakwb eng 610 610 DE-600 550 520 VZ 38.70 bkl 39.53 bkl Jiang, Xia verfasserin aut CaMKII-dependent dendrite ramification and spine generation promote spatial training-induced memory improvement in a rat model of sporadic Alzheimer's disease 2015transfer abstract 10 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Participation in cognitively stimulating activities can preserve memory capacities in patients with Alzheimer's disease (AD), but the mechanism is not fully understood. Here, we used a rat model with hyperhomocysteinemia, an independent risk factor of AD, to study whether spatial training could remodel the synaptic and/or dendritic plasticity and the key molecular target(s) involved. We found that spatial training in water maze remarkably improved the subsequent short-term and long-term memory performance in contextual fear conditioning and Barnes maze. The trained rats showed an enhanced dendrite ramification, spine generation and plasticity in dentate gyrus (DG) neurons, and stimulation of long-term potentiation between perforant path and DG circuit. Spatial training also increased the levels of postsynaptic GluA1, GluN2A, GluN2B, and PSD93 with selective activation of calcium/calmodulin-dependent protein kinase II (CaMKII), although inhibition of CaMKII by stereotaxic injection of KN93 into hippocampal DG, abolished the training-induced cognitive improvement, dendrite ramification, and spine generation. We conclude that spatial training can preserve the cognitive function by CaMKII-dependent remodeling of dendritic plasticity in hyperhomocysteinemia-induced sporadic AD-like rats. Participation in cognitively stimulating activities can preserve memory capacities in patients with Alzheimer's disease (AD), but the mechanism is not fully understood. Here, we used a rat model with hyperhomocysteinemia, an independent risk factor of AD, to study whether spatial training could remodel the synaptic and/or dendritic plasticity and the key molecular target(s) involved. We found that spatial training in water maze remarkably improved the subsequent short-term and long-term memory performance in contextual fear conditioning and Barnes maze. The trained rats showed an enhanced dendrite ramification, spine generation and plasticity in dentate gyrus (DG) neurons, and stimulation of long-term potentiation between perforant path and DG circuit. Spatial training also increased the levels of postsynaptic GluA1, GluN2A, GluN2B, and PSD93 with selective activation of calcium/calmodulin-dependent protein kinase II (CaMKII), although inhibition of CaMKII by stereotaxic injection of KN93 into hippocampal DG, abolished the training-induced cognitive improvement, dendrite ramification, and spine generation. We conclude that spatial training can preserve the cognitive function by CaMKII-dependent remodeling of dendritic plasticity in hyperhomocysteinemia-induced sporadic AD-like rats. Dendrite ramification Elsevier Calcium/calmodulin-dependent protein kinase II Elsevier Spine generation Elsevier Spatial training Elsevier Alzheimer's disease Elsevier Spatial memory Elsevier Chai, Gao-Shang oth Wang, Zhi-Hao oth Hu, Yu oth Li, Xiao-Guang oth Ma, Zhi-Wei oth Wang, Qun oth Wang, Jian-Zhi oth Liu, Gong-Ping oth Enthalten in Elsevier Science Zidane, Mustapha ELSEVIER Corrigendum to “Electrical and thermal transport properties of Fe–Ni based ternary alloys in the earth's inner core: An ab initio study” [Physics of the Earth and Planetary Interiors 2021 Amsterdam [u.a.] (DE-627)ELV005660645 volume:36 year:2015 number:2 pages:867-876 extent:10 https://doi.org/10.1016/j.neurobiolaging.2014.10.018 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-GGO SSG-OPC-GEO SSG-OPC-AST 38.70 Geophysik: Allgemeines VZ 39.53 Planeten VZ AR 36 2015 2 867-876 10 045F 610 |
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10.1016/j.neurobiolaging.2014.10.018 doi GBVA2015008000023.pica (DE-627)ELV018419410 (ELSEVIER)S0197-4580(14)00675-7 DE-627 ger DE-627 rakwb eng 610 610 DE-600 550 520 VZ 38.70 bkl 39.53 bkl Jiang, Xia verfasserin aut CaMKII-dependent dendrite ramification and spine generation promote spatial training-induced memory improvement in a rat model of sporadic Alzheimer's disease 2015transfer abstract 10 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Participation in cognitively stimulating activities can preserve memory capacities in patients with Alzheimer's disease (AD), but the mechanism is not fully understood. Here, we used a rat model with hyperhomocysteinemia, an independent risk factor of AD, to study whether spatial training could remodel the synaptic and/or dendritic plasticity and the key molecular target(s) involved. We found that spatial training in water maze remarkably improved the subsequent short-term and long-term memory performance in contextual fear conditioning and Barnes maze. The trained rats showed an enhanced dendrite ramification, spine generation and plasticity in dentate gyrus (DG) neurons, and stimulation of long-term potentiation between perforant path and DG circuit. Spatial training also increased the levels of postsynaptic GluA1, GluN2A, GluN2B, and PSD93 with selective activation of calcium/calmodulin-dependent protein kinase II (CaMKII), although inhibition of CaMKII by stereotaxic injection of KN93 into hippocampal DG, abolished the training-induced cognitive improvement, dendrite ramification, and spine generation. We conclude that spatial training can preserve the cognitive function by CaMKII-dependent remodeling of dendritic plasticity in hyperhomocysteinemia-induced sporadic AD-like rats. Participation in cognitively stimulating activities can preserve memory capacities in patients with Alzheimer's disease (AD), but the mechanism is not fully understood. Here, we used a rat model with hyperhomocysteinemia, an independent risk factor of AD, to study whether spatial training could remodel the synaptic and/or dendritic plasticity and the key molecular target(s) involved. We found that spatial training in water maze remarkably improved the subsequent short-term and long-term memory performance in contextual fear conditioning and Barnes maze. The trained rats showed an enhanced dendrite ramification, spine generation and plasticity in dentate gyrus (DG) neurons, and stimulation of long-term potentiation between perforant path and DG circuit. Spatial training also increased the levels of postsynaptic GluA1, GluN2A, GluN2B, and PSD93 with selective activation of calcium/calmodulin-dependent protein kinase II (CaMKII), although inhibition of CaMKII by stereotaxic injection of KN93 into hippocampal DG, abolished the training-induced cognitive improvement, dendrite ramification, and spine generation. We conclude that spatial training can preserve the cognitive function by CaMKII-dependent remodeling of dendritic plasticity in hyperhomocysteinemia-induced sporadic AD-like rats. Dendrite ramification Elsevier Calcium/calmodulin-dependent protein kinase II Elsevier Spine generation Elsevier Spatial training Elsevier Alzheimer's disease Elsevier Spatial memory Elsevier Chai, Gao-Shang oth Wang, Zhi-Hao oth Hu, Yu oth Li, Xiao-Guang oth Ma, Zhi-Wei oth Wang, Qun oth Wang, Jian-Zhi oth Liu, Gong-Ping oth Enthalten in Elsevier Science Zidane, Mustapha ELSEVIER Corrigendum to “Electrical and thermal transport properties of Fe–Ni based ternary alloys in the earth's inner core: An ab initio study” [Physics of the Earth and Planetary Interiors 2021 Amsterdam [u.a.] (DE-627)ELV005660645 volume:36 year:2015 number:2 pages:867-876 extent:10 https://doi.org/10.1016/j.neurobiolaging.2014.10.018 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-GGO SSG-OPC-GEO SSG-OPC-AST 38.70 Geophysik: Allgemeines VZ 39.53 Planeten VZ AR 36 2015 2 867-876 10 045F 610 |
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10.1016/j.neurobiolaging.2014.10.018 doi GBVA2015008000023.pica (DE-627)ELV018419410 (ELSEVIER)S0197-4580(14)00675-7 DE-627 ger DE-627 rakwb eng 610 610 DE-600 550 520 VZ 38.70 bkl 39.53 bkl Jiang, Xia verfasserin aut CaMKII-dependent dendrite ramification and spine generation promote spatial training-induced memory improvement in a rat model of sporadic Alzheimer's disease 2015transfer abstract 10 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Participation in cognitively stimulating activities can preserve memory capacities in patients with Alzheimer's disease (AD), but the mechanism is not fully understood. Here, we used a rat model with hyperhomocysteinemia, an independent risk factor of AD, to study whether spatial training could remodel the synaptic and/or dendritic plasticity and the key molecular target(s) involved. We found that spatial training in water maze remarkably improved the subsequent short-term and long-term memory performance in contextual fear conditioning and Barnes maze. The trained rats showed an enhanced dendrite ramification, spine generation and plasticity in dentate gyrus (DG) neurons, and stimulation of long-term potentiation between perforant path and DG circuit. Spatial training also increased the levels of postsynaptic GluA1, GluN2A, GluN2B, and PSD93 with selective activation of calcium/calmodulin-dependent protein kinase II (CaMKII), although inhibition of CaMKII by stereotaxic injection of KN93 into hippocampal DG, abolished the training-induced cognitive improvement, dendrite ramification, and spine generation. We conclude that spatial training can preserve the cognitive function by CaMKII-dependent remodeling of dendritic plasticity in hyperhomocysteinemia-induced sporadic AD-like rats. Participation in cognitively stimulating activities can preserve memory capacities in patients with Alzheimer's disease (AD), but the mechanism is not fully understood. Here, we used a rat model with hyperhomocysteinemia, an independent risk factor of AD, to study whether spatial training could remodel the synaptic and/or dendritic plasticity and the key molecular target(s) involved. We found that spatial training in water maze remarkably improved the subsequent short-term and long-term memory performance in contextual fear conditioning and Barnes maze. The trained rats showed an enhanced dendrite ramification, spine generation and plasticity in dentate gyrus (DG) neurons, and stimulation of long-term potentiation between perforant path and DG circuit. Spatial training also increased the levels of postsynaptic GluA1, GluN2A, GluN2B, and PSD93 with selective activation of calcium/calmodulin-dependent protein kinase II (CaMKII), although inhibition of CaMKII by stereotaxic injection of KN93 into hippocampal DG, abolished the training-induced cognitive improvement, dendrite ramification, and spine generation. We conclude that spatial training can preserve the cognitive function by CaMKII-dependent remodeling of dendritic plasticity in hyperhomocysteinemia-induced sporadic AD-like rats. Dendrite ramification Elsevier Calcium/calmodulin-dependent protein kinase II Elsevier Spine generation Elsevier Spatial training Elsevier Alzheimer's disease Elsevier Spatial memory Elsevier Chai, Gao-Shang oth Wang, Zhi-Hao oth Hu, Yu oth Li, Xiao-Guang oth Ma, Zhi-Wei oth Wang, Qun oth Wang, Jian-Zhi oth Liu, Gong-Ping oth Enthalten in Elsevier Science Zidane, Mustapha ELSEVIER Corrigendum to “Electrical and thermal transport properties of Fe–Ni based ternary alloys in the earth's inner core: An ab initio study” [Physics of the Earth and Planetary Interiors 2021 Amsterdam [u.a.] (DE-627)ELV005660645 volume:36 year:2015 number:2 pages:867-876 extent:10 https://doi.org/10.1016/j.neurobiolaging.2014.10.018 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OPC-GGO SSG-OPC-GEO SSG-OPC-AST 38.70 Geophysik: Allgemeines VZ 39.53 Planeten VZ AR 36 2015 2 867-876 10 045F 610 |
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CaMKII-dependent dendrite ramification and spine generation promote spatial training-induced memory improvement in a rat model of sporadic Alzheimer's disease |
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Participation in cognitively stimulating activities can preserve memory capacities in patients with Alzheimer's disease (AD), but the mechanism is not fully understood. Here, we used a rat model with hyperhomocysteinemia, an independent risk factor of AD, to study whether spatial training could remodel the synaptic and/or dendritic plasticity and the key molecular target(s) involved. We found that spatial training in water maze remarkably improved the subsequent short-term and long-term memory performance in contextual fear conditioning and Barnes maze. The trained rats showed an enhanced dendrite ramification, spine generation and plasticity in dentate gyrus (DG) neurons, and stimulation of long-term potentiation between perforant path and DG circuit. Spatial training also increased the levels of postsynaptic GluA1, GluN2A, GluN2B, and PSD93 with selective activation of calcium/calmodulin-dependent protein kinase II (CaMKII), although inhibition of CaMKII by stereotaxic injection of KN93 into hippocampal DG, abolished the training-induced cognitive improvement, dendrite ramification, and spine generation. We conclude that spatial training can preserve the cognitive function by CaMKII-dependent remodeling of dendritic plasticity in hyperhomocysteinemia-induced sporadic AD-like rats. |
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Participation in cognitively stimulating activities can preserve memory capacities in patients with Alzheimer's disease (AD), but the mechanism is not fully understood. Here, we used a rat model with hyperhomocysteinemia, an independent risk factor of AD, to study whether spatial training could remodel the synaptic and/or dendritic plasticity and the key molecular target(s) involved. We found that spatial training in water maze remarkably improved the subsequent short-term and long-term memory performance in contextual fear conditioning and Barnes maze. The trained rats showed an enhanced dendrite ramification, spine generation and plasticity in dentate gyrus (DG) neurons, and stimulation of long-term potentiation between perforant path and DG circuit. Spatial training also increased the levels of postsynaptic GluA1, GluN2A, GluN2B, and PSD93 with selective activation of calcium/calmodulin-dependent protein kinase II (CaMKII), although inhibition of CaMKII by stereotaxic injection of KN93 into hippocampal DG, abolished the training-induced cognitive improvement, dendrite ramification, and spine generation. We conclude that spatial training can preserve the cognitive function by CaMKII-dependent remodeling of dendritic plasticity in hyperhomocysteinemia-induced sporadic AD-like rats. |
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Participation in cognitively stimulating activities can preserve memory capacities in patients with Alzheimer's disease (AD), but the mechanism is not fully understood. Here, we used a rat model with hyperhomocysteinemia, an independent risk factor of AD, to study whether spatial training could remodel the synaptic and/or dendritic plasticity and the key molecular target(s) involved. We found that spatial training in water maze remarkably improved the subsequent short-term and long-term memory performance in contextual fear conditioning and Barnes maze. The trained rats showed an enhanced dendrite ramification, spine generation and plasticity in dentate gyrus (DG) neurons, and stimulation of long-term potentiation between perforant path and DG circuit. Spatial training also increased the levels of postsynaptic GluA1, GluN2A, GluN2B, and PSD93 with selective activation of calcium/calmodulin-dependent protein kinase II (CaMKII), although inhibition of CaMKII by stereotaxic injection of KN93 into hippocampal DG, abolished the training-induced cognitive improvement, dendrite ramification, and spine generation. We conclude that spatial training can preserve the cognitive function by CaMKII-dependent remodeling of dendritic plasticity in hyperhomocysteinemia-induced sporadic AD-like rats. |
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We conclude that spatial training can preserve the cognitive function by CaMKII-dependent remodeling of dendritic plasticity in hyperhomocysteinemia-induced sporadic AD-like rats.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Participation in cognitively stimulating activities can preserve memory capacities in patients with Alzheimer's disease (AD), but the mechanism is not fully understood. Here, we used a rat model with hyperhomocysteinemia, an independent risk factor of AD, to study whether spatial training could remodel the synaptic and/or dendritic plasticity and the key molecular target(s) involved. We found that spatial training in water maze remarkably improved the subsequent short-term and long-term memory performance in contextual fear conditioning and Barnes maze. The trained rats showed an enhanced dendrite ramification, spine generation and plasticity in dentate gyrus (DG) neurons, and stimulation of long-term potentiation between perforant path and DG circuit. Spatial training also increased the levels of postsynaptic GluA1, GluN2A, GluN2B, and PSD93 with selective activation of calcium/calmodulin-dependent protein kinase II (CaMKII), although inhibition of CaMKII by stereotaxic injection of KN93 into hippocampal DG, abolished the training-induced cognitive improvement, dendrite ramification, and spine generation. We conclude that spatial training can preserve the cognitive function by CaMKII-dependent remodeling of dendritic plasticity in hyperhomocysteinemia-induced sporadic AD-like rats.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Dendrite ramification</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Calcium/calmodulin-dependent protein kinase II</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Spine generation</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Spatial training</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Alzheimer's disease</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Spatial memory</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Chai, Gao-Shang</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Wang, Zhi-Hao</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Hu, Yu</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Li, Xiao-Guang</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Ma, Zhi-Wei</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Wang, Qun</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Wang, Jian-Zhi</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Liu, Gong-Ping</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier Science</subfield><subfield code="a">Zidane, Mustapha ELSEVIER</subfield><subfield code="t">Corrigendum to “Electrical and thermal transport properties of Fe–Ni based ternary alloys in the earth's inner core: An ab initio study” [Physics of the Earth and Planetary Interiors</subfield><subfield code="d">2021</subfield><subfield code="g">Amsterdam [u.a.]</subfield><subfield code="w">(DE-627)ELV005660645</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:36</subfield><subfield code="g">year:2015</subfield><subfield code="g">number:2</subfield><subfield code="g">pages:867-876</subfield><subfield code="g">extent:10</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.neurobiolaging.2014.10.018</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OPC-GGO</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OPC-GEO</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OPC-AST</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">38.70</subfield><subfield code="j">Geophysik: Allgemeines</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">39.53</subfield><subfield code="j">Planeten</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">36</subfield><subfield code="j">2015</subfield><subfield code="e">2</subfield><subfield code="h">867-876</subfield><subfield code="g">10</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">610</subfield></datafield></record></collection>
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