Brain mitochondrial ATP-insensitive large conductance Ca+2-activated K+ channel properties are altered in a rat model of amyloid-β neurotoxicity-Reference-Cited by-同舟云学术

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Brain mitochondrial ATP-insensitive large conductance Ca+2-activated K+ channel properties are altered in a rat model of amyloid-β neurotoxicity

Published:2015-07 Issue: Volume:269 Page:8-16
ISSN:0014-4886
Container-title:Experimental Neurology
language:en
Short-container-title:Experimental Neurology

Author:

Jafari A.,Noursadeghi E.,Khodagholi F.,Saghiri R.,Sauve R.,Aliaghaei A.,Eliassi A.

Funder

Neuroscience Research Center of Shahid Beheshti University of Medical Sciences

Publisher

Elsevier BV

Subject

Developmental Neuroscience,Neurology

Reference53 articles.

1. Beta-amyloid peptides induce mitochondrial dysfunction and oxidative stress in astrocytes and death of neurons through activation of NADPH oxidase;Abramov;J. Neurosci.,2004

2. Potassium channels in brain mitochondria;Bednarczyk;Acta Biochim. Pol.,2009

3. Putative structural and functional coupling of the mitochondrial BKCa channel to the respiratory chain;Bednarczyk;PLoS ONE,2013

4. Proteomic identification of proteins specifically oxidized by intracerebral injection of amyloid beta-peptide (1–42) into rat brain: implications for Alzheimer's disease;Boyd-Kimball;Neuroscience,2005

5. BK channel beta4 subunit reduces dentate gyrus excitability and protects against temporal lobe seizures;Brenner;Nat. Neurosci.,2005

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