SK channel activation is neuroprotective in conditions of enhanced ER-mitochondrial coupling.

ABSTRACT: Alterations in the strength and interface area of contact sites between the endoplasmic reticulum (ER) and mitochondria contribute to calcium (Ca²⁺) dysregulation and neuronal cell death, and have been implicated in the pathology of several neurodegenerative diseases. Weakening this physical linkage may reduce Ca²⁺ uptake into mitochondria, while fortifying these organelle contact sites may promote mitochondrial Ca²⁺ overload and cell death. Small conductance Ca²⁺-activated K⁺ (SK) channels regulate mitochondrial respiration, and their activation attenuates mitochondrial damage in paradigms of oxidative stress. In the present study, we enhanced ER-mitochondrial coupling and investigated the impact of SK channels on survival of neuronal

SUBMITTER: Honrath B 

PROVIDER: S-EPMC5964177 | biostudies-literature | 2018 May

REPOSITORIES: biostudies-literature