Amyloid β-protein fragment 31–35 suppresses long-term potentiation in hippocampal CA1 region of rats in vivo

Synapse ◽  
2006 ◽  
Vol 60 (4) ◽  
pp. 307-313 ◽  
Author(s):  
Jian-Mei Zhang ◽  
Mei-Na Wu ◽  
Jin-Shun Qi ◽  
Jian-Tian Qiao
Keyword(s):  
Amyloid Β ◽  
Long Term Potentiation ◽  
Amyloid Β Protein ◽  
Ca1 Region ◽  
Hippocampal Ca1 Region ◽  
Β Protein ◽  
Term Potentiation ◽  
Hippocampal Ca1

[Gly14]-humanin rescues long-term potentiation from amyloid β protein-induced impairment in the rat hippocampal CA1 region in vivo

Synapse ◽  
2010 ◽  
Vol 64 (1) ◽  
pp. 83-91 ◽  
Author(s):  
Fen Guo ◽  
Wei Jing ◽  
Cun-Gen Ma ◽  
Mei-Na Wu ◽  
Jun-Fang Zhang ◽  
...  
Keyword(s):  
Amyloid Β ◽  
Long Term Potentiation ◽  
Amyloid Β Protein ◽  
Ca1 Region ◽  
Hippocampal Ca1 Region ◽  
Β Protein ◽  
Term Potentiation ◽  
Hippocampal Ca1

Amyloid β-protein fragments 25-35 and 31-35 potentiate long-term depression in hippocampal CA1 region of rats in vivo

Synapse ◽  
2009 ◽  
Vol 63 (3) ◽  
pp. 206-214 ◽  
Author(s):  
Li Cheng ◽  
Wen-Juan Yin ◽  
Jun-Fang Zhang ◽  
Jin-Shun Qi
Keyword(s):  
Amyloid Β ◽  
Amyloid Β Protein ◽  
Long Term Depression ◽  
Protein Fragments ◽  
Ca1 Region ◽  
Hippocampal Ca1 Region ◽  
Β Protein ◽  
Hippocampal Ca1

Naturally secreted oligomers of amyloid β protein potently inhibit hippocampal long-term potentiation in vivo

Nature ◽  
2002 ◽  
Vol 416 (6880) ◽  
pp. 535-539 ◽  
Author(s):  
Dominic M. Walsh ◽  
Igor Klyubin ◽  
Julia V. Fadeeva ◽  
William K. Cullen ◽  
Roger Anwyl ◽  
...  
Keyword(s):  
Amyloid Β ◽  
Long Term Potentiation ◽  
Amyloid Β Protein ◽  
Β Protein ◽  
Term Potentiation

Amyloid-β oligomers: their production, toxicity and therapeutic inhibition

2002 ◽  
Vol 30 (4) ◽  
pp. 552-557 ◽  
Author(s):  
D. M. Walsh ◽  
I. Klyubin ◽  
J. V. Fadeeva ◽  
M. J. Rowan ◽  
D. J. Selkoe
Keyword(s):  
Amyloid Β ◽  
Long Term Potentiation ◽  
Specific Form ◽  
Amyloid Β Protein ◽  
Β Protein ◽  
Term Potentiation ◽  
Modelling Data

Despite extensive genetic and animal modelling data that support a central role for the amyloid β-protein (Aβ) in the genesis of Alzheimer's disease, the specific form(s) of Aβ which causes injury to neurons in vivo has not been identified. In the present study, we examine the importance of soluble, pre-fibrillar assemblies of Aβ as mediators of neurotoxicity. Specifically, we review the role of cell-derived SDS-stable oligomers, their blocking of hippocampal long-term potentiation in vivo and the finding that this blocking can be prevented by prior treatment of oligomer-producing cells withγ-secretase inhibitors.

Arginine vasopressin prevents amyloid β protein-induced impairment of long-term potentiation in rat hippocampus in vivo

2009 ◽  
Vol 450 (3) ◽  
pp. 306-310 ◽  
Author(s):  
Wei Jing ◽  
Fen Guo ◽  
Li Cheng ◽  
Jun-Fang Zhang ◽  
Jin-Shun Qi
Keyword(s):  
Arginine Vasopressin ◽  
Amyloid Β ◽  
Long Term Potentiation ◽  
Rat Hippocampus ◽  
Amyloid Β Protein ◽  
Β Protein ◽  
Term Potentiation

scholarly journals Phosphatidylinositol 3-Kinase Is Required for the Expression But Not for the Induction or the Maintenance of Long-Term Potentiation in the Hippocampal CA1 Region

2002 ◽  
Vol 22 (9) ◽  
pp. 3359-3365 ◽  
Author(s):  
Pietro Paolo Sanna ◽  
Maurizio Cammalleri ◽  
Fulvia Berton ◽  
Cindy Simpson ◽  
Robert Lutjens ◽  
...  
Keyword(s):  
Long Term Potentiation ◽  
Phosphatidylinositol 3 Kinase ◽  
Ca1 Region ◽  
Hippocampal Ca1 Region ◽  
Term Potentiation ◽  
Hippocampal Ca1 ◽  
Phosphatidylinositol 3

AMPA Silencing Is a Prerequisite for Developmental Long-Term Potentiation in the Hippocampal CA1 Region

2008 ◽  
Vol 100 (5) ◽  
pp. 2605-2614 ◽  
Author(s):  
Therése Abrahamsson ◽  
Bengt Gustafsson ◽  
Eric Hanse
Keyword(s):  
Developmental Stages ◽  
Long Term Potentiation ◽  
Synaptic Strength ◽  
Ca1 Region ◽  
Hippocampal Ca1 Region ◽  
Silent Synapses ◽  
Term Potentiation ◽  
Hippocampal Ca1 ◽  
Hippocampal Ca3

AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) unsilencing is an often proposed expression mechanism both for developmental long-term potentiation (LTP), involved in circuitry refinement during brain development, and for mature LTP, involved in learning and memory. In the hippocampal CA3–CA1 connection naïve (nonstimulated) synapses are AMPA signaling and AMPA-silent synapses are created from naïve AMPA-signaling (AMPA-labile) synapses by test-pulse synaptic activation (AMPA silencing). To investigate to what extent LTPs at different developmental stages are explained by AMPA unsilencing, the amount of LTP obtained at these different developmental stages was related to the amount of AMPA silencing that preceded the induction of LTP. When examined in the second postnatal week Hebbian induction was found to produce no more stable potentiation than that causing a return to the naïve synaptic strength existing prior to the AMPA silencing. Moreover, in the absence of a preceding AMPA silencing Hebbian induction produced no stable potentiation above the naïve synaptic strength. Thus this early, or developmental, LTP is nothing more than an unsilencing (dedepression) and stabilization of the AMPA signaling that was lost by the prior AMPA silencing. This dedepression and stabilization of AMPA signaling was mimicked by the presence of the protein kinase A activator forskolin. As the relative degree of AMPA silencing decreased with development, LTP manifested itself more and more as a “genuine” potentiation (as opposed to a dedepression) not explained by unsilencing and stabilization of AMPA-labile synapses. This “genuine,” or mature, LTP rose from close to nothing of total LTP prior to postnatal day (P)13, to about 70% of total LTP at P16, and to about 90% of total LTP at P30. Developmental LTP, by stabilization of AMPA-labile synapses, thus seems adapted to select synaptic connections to the growing synaptic network. Mature LTP, by instead strengthening existing stable connections between cells, may then create functionally tightly connected cell assemblies within this network.

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