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Abstract

Mitochondrial dysfunction, particularly impaired calcium (Ca²⁺) regulation, is implicated in the pathology of many neurodegenerative diseases. To better understand the role of mitochondrial Ca²⁺ handling in neuronal vulnerability, this study compared mitochondrial Ca²⁺ dynamics in primary cortical neurons from adult cyclophilin D knockout (CyPD‑KO) and wild‑type (WT) mice. Neurons were transfected with a mitochondria‑targeted, ratiometric pericam Ca²⁺ indicator to measure mitochondrial Ca²⁺ responses in real time. These experiments provide insight into how the absence of cyclophilin D influences mitochondrial Ca²⁺ buffering and may clarify mechanisms linking mitochondrial dysfunction to neurodegeneration.

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