scholarly journals Role of amyloid β protein receptors in mediating synaptic plasticity

2017 ◽  
Vol 6 (4) ◽  
pp. 379-386 ◽  
Author(s):  
Yu Li ◽  
Zhongqing Sun ◽  
Qiaoyu Cao ◽  
Meiwan Chen ◽  
Huanmin Luo ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Amyloid Β ◽  
Amyloid Β Protein ◽  
Β Protein ◽  
Protein Receptors

Amyloid-β Protein Precursor Deficiency Changes Neuronal Electrical Activity and Levels of Mitochondrial Proteins in the Medial Prefrontal Cortex

2021 ◽  
pp. 1-14
Author(s):  
Qingwei Huo ◽  
Sidra Tabassum ◽  
Ming Chen ◽  
Mengyao Sun ◽  
Yueming Deng ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Amyloid Β ◽  
Neuronal Firing ◽  
Mitochondrial Proteins ◽  
Amyloid Β Protein ◽  
Protein Precursor ◽  
Β Protein ◽  
Neuronal Electrical Activity

Background: Neuropathological features of Alzheimer’s disease are characterized by the deposition of amyloid-β (Aβ) plaques and impairments in synaptic activity and memory. However, we know little about the physiological role of amyloid-β protein precursor (AβPP) from which Aβ derives. Objective: Evaluate APP deficiency induced alterations in neuronal electrical activity and mitochondrial protein expression. Methods: Utilizing electrophysiological, biochemical, pharmacological, and behavioral tests, we revealed aberrant local field potential (LFP), extracellular neuronal firing and levels of mitochondrial proteins. Result: We show that APP knockout (APP -/- ) leads to increased gamma oscillations in the medial prefrontal cortex (mPFC) at 1-2 months old, which can be restored by baclofen (Bac), a γ-aminobutyric acid type B receptor (GABABR) agonist. A higher dose and longer exposure time is required for Bac to suppress neuronal firing in APP -/-  mice than in wild type animals, indicating enhanced GABABR mediated activity in the mPFC of APP -/-  mice. In line with increased GABABR function, the glutamine synthetase inhibitor, L-methionine sulfonate, significantly increases GABABR levels in the mPFC of APP -/-  mice and this is associated with a significantly lower incidence of death. The results suggest that APP -/-  mice developed stronger GABABR mediated inhibition. Using HEK 293 as an expression system, we uncover that AβPP functions to suppress GABABR expression. Furthermore, APP -/-  mice show abnormal expression of several mitochondrial proteins. Conclusion: APP deficiency leads to both abnormal network activity involving defected GABABR and mitochondrial dysfunction, suggesting critical role of AβPP in synaptic and network function.

scholarly journals Amyloid-β protein dimers isolated directly from Alzheimer's brains impair synaptic plasticity and memory

2008 ◽  
Vol 14 (8) ◽  
pp. 837-842 ◽  
Author(s):  
Ganesh M Shankar ◽  
Shaomin Li ◽  
Tapan H Mehta ◽  
Amaya Garcia-Munoz ◽  
Nina E Shepardson ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Amyloid Β ◽  
Amyloid Β Protein ◽  
Protein Dimers ◽  
Β Protein

scholarly journals Role of Aromatic Side Chains in Amyloid β-Protein Aggregation

2012 ◽  
Vol 3 (12) ◽  
pp. 1008-1016 ◽  
Author(s):  
Risto Cukalevski ◽  
Barry Boland ◽  
Birgitta Frohm ◽  
Eva Thulin ◽  
Dominic Walsh ◽  
...  
Keyword(s):  
Protein Aggregation ◽  
Amyloid Β ◽  
Side Chains ◽  
Amyloid Β Protein ◽  
Β Protein ◽  
Aromatic Side Chains

scholarly journals GLP-1 analogue CJC-1131 prevents amyloid β protein-induced impirments of spatial memory and synaptic plasticity in rats

2017 ◽  
Vol 326 ◽  
pp. 237-243 ◽  
Author(s):  
Sheng-Xiao Zhang ◽  
Hong-Yan Cai ◽  
Xiao-Wen Ma ◽  
Li Yuan ◽  
Jun Zhang ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Spatial Memory ◽  
Amyloid Β ◽  
Amyloid Β Protein ◽  
Β Protein

scholarly journals Effects of secreted oligomers of amyloid β-protein on hippocampal synaptic plasticity: a potent role for trimers

2006 ◽  
Vol 572 (2) ◽  
pp. 477-492 ◽  
Author(s):  
Matthew Townsend ◽  
Ganesh M. Shankar ◽  
Tapan Mehta ◽  
Dominic M. Walsh ◽  
Dennis J. Selkoe
Keyword(s):  
Synaptic Plasticity ◽  
Amyloid Β ◽  
Amyloid Β Protein ◽  
Hippocampal Synaptic Plasticity ◽  
Β Protein
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