Ndufs4 ablation decreases synaptophysin expression in hippocampus
Subrata Kumar Shil1, Yoshiteru Kagawa2, Banlanjo Abdulaziz Umaru1
1Department of Organ Anatomy, Tohoku University Graduate School of Medicine, 2-1 Seiryo-machi, Aoba-ku, Sendai, Miyagi, 980-8575, Japan.
Scientific Reports
|May 27, 2021
Summary
Mitochondrial protein Ndufs4 is crucial for neuronal health. Its deficiency impairs mitochondrial respiration and reduces synaptophysin expression, impacting neuroplasticity.
Area of Science:
- Neuroscience
- Mitochondrial Biology
- Cellular Neuroscience
Background:
- Mitochondrial dysfunction is linked to neurodegenerative diseases.
- NADH Dehydrogenase (Ubiquinone) Fe-S protein 4 (Ndufs4) is a key mitochondrial complex I subunit implicated in Leigh syndrome.
- The precise role of Ndufs4 in neuronal function remains unclear.
Purpose of the Study:
- To investigate the role of Ndufs4 in neuronal function and neuroplasticity.
- To elucidate the molecular mechanisms underlying Ndufs4's impact on neurons.
Main Methods:
- Confirmation of Ndufs4 expression in mouse hippocampal neurons and astrocytes.
- Analysis of mitochondrial respiration in Ndufs4-knockout (Ndufs4-KO) mouse hippocampus.
- Assessment of neuronal morphology and synaptophysin expression in Ndufs4-silenced cells.
- Western blot analysis of ERK signaling pathway activity.
Main Results:
- Ndufs4-KO mice exhibited decreased mitochondrial respiration in the hippocampus.
- No change in neuronal number, but decreased synaptophysin expression in Ndufs4-KO hippocampus.
- Ndufs4 silencing in Neuro-2a cells led to shorter neurites and reduced synaptophysin.
- Ndufs4 silencing decreased extracellular regulated kinase (ERK) signaling activity.
Conclusions:
- Ndufs4 is essential for maintaining mitochondrial respiration in neurons.
- Ndufs4 influences neuroplasticity by regulating synaptophysin expression.
- Ndufs4-mediated mitochondrial activity impacts neuronal function via the ERK signaling pathway.
