In vivo injected mitochondria-targeted plastoquinone antioxidant SkQR1 prevents β-amyloid-induced decay of long-term potentiation in rat hippocampal slices

Biochemistry (Mosc). 2011 Dec;76(12):1367-70. doi: 10.1134/S0006297911120108.

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.

MeSH terms

  • Alzheimer Disease / drug therapy
  • Alzheimer Disease / metabolism
  • Alzheimer Disease / physiopathology*
  • Amyloid beta-Peptides / toxicity*
  • Animals
  • Antioxidants / administration & dosage*
  • CA1 Region, Hippocampal / cytology
  • CA1 Region, Hippocampal / drug effects*
  • CA1 Region, Hippocampal / physiopathology
  • Disease Models, Animal
  • Humans
  • Long-Term Potentiation / drug effects*
  • Male
  • Mitochondria / drug effects*
  • Mitochondria / metabolism
  • Neurons / drug effects
  • Neurons / physiology
  • Plastoquinone / administration & dosage
  • Plastoquinone / analogs & derivatives*
  • Rats
  • Rats, Wistar
  • Rhodamines / administration & dosage*

Substances

  • 10-(6'-plastoquinonyl) decylrhodamine 19
  • Amyloid beta-Peptides
  • Antioxidants
  • Rhodamines
  • Plastoquinone