Abstract
Addition of 200 nM β-amyloid 1-42 (Abeta) to a rat hippocampal slice impairs the induction of a long-term post-tetanic potentiation (LTP) of population spike (PS) in pyramidal neurons of the CA1 field of hippocampus. Intraperitoneal injection into the rat of the mitochondria-targeted plastoquinone derivative SkQR1 (1 µmol/kg of weight given 24 h before the slices were made) abolishes the deleterious effect of Abeta on LTP. These data demonstrate that SkQR1 therapy is able to compensate the Abeta-induced impairments of long-term synaptic plasticity in the hippocampus, which are the main cause of loss of memory and other cognitive functions associated with Alzheimer's disease.
© Pleiades Publishing, Ltd., 2011.
MeSH terms
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Alzheimer Disease / drug therapy
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Alzheimer Disease / metabolism
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Alzheimer Disease / physiopathology*
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Amyloid beta-Peptides / toxicity*
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Animals
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Antioxidants / administration & dosage*
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CA1 Region, Hippocampal / cytology
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CA1 Region, Hippocampal / drug effects*
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CA1 Region, Hippocampal / physiopathology
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Disease Models, Animal
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Humans
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Long-Term Potentiation / drug effects*
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Male
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Mitochondria / drug effects*
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Mitochondria / metabolism
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Neurons / drug effects
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Neurons / physiology
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Plastoquinone / administration & dosage
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Plastoquinone / analogs & derivatives*
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Rats
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Rats, Wistar
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Rhodamines / administration & dosage*
Substances
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10-(6'-plastoquinonyl) decylrhodamine 19
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Amyloid beta-Peptides
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Antioxidants
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Rhodamines
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Plastoquinone