Synaptic dysfunction, memory deficits and hippocampal atrophy due to ablation of mitochondrial fission in adult forebrain neurons

Well-balanced mitochondrial fission and fusion processes are essential for nervous system development. Loss of function of the main mitochondrial fission mediator, dynamin-related protein 1 (Drp1), is lethal early during embryonic development or around birth, but the role of mitochondrial fission in...

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Veröffentlicht in:Cell death and differentiation 2016-01, Vol.23 (1), p.18-28
Hauptverfasser: Oettinghaus, B, Schulz, J M, Restelli, L M, Licci, M, Savoia, C, Schmidt, A, Schmitt, K, Grimm, A, Morè, L, Hench, J, Tolnay, M, Eckert, A, D'Adamo, P, Franken, P, Ishihara, N, Mihara, K, Bischofberger, J, Scorrano, L, Frank, S
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container_end_page 28
container_issue 1
container_start_page 18
container_title Cell death and differentiation
container_volume 23
creator Oettinghaus, B
Schulz, J M
Restelli, L M
Licci, M
Savoia, C
Schmidt, A
Schmitt, K
Grimm, A
Morè, L
Hench, J
Tolnay, M
Eckert, A
D'Adamo, P
Franken, P
Ishihara, N
Mihara, K
Bischofberger, J
Scorrano, L
Frank, S
description Well-balanced mitochondrial fission and fusion processes are essential for nervous system development. Loss of function of the main mitochondrial fission mediator, dynamin-related protein 1 (Drp1), is lethal early during embryonic development or around birth, but the role of mitochondrial fission in adult neurons remains unclear. Here we show that inducible Drp1 ablation in neurons of the adult mouse forebrain results in progressive, neuronal subtype-specific alterations of mitochondrial morphology in the hippocampus that are marginally responsive to antioxidant treatment. Furthermore, DRP1 loss affects synaptic transmission and memory function. Although these changes culminate in hippocampal atrophy, they are not sufficient to cause neuronal cell death within 10 weeks of genetic Drp1 ablation. Collectively, our in vivo observations clarify the role of mitochondrial fission in neurons, demonstrating that Drp1 ablation in adult forebrain neurons compromises critical neuronal functions without causing overt neurodegeneration.
doi_str_mv 10.1038/cdd.2015.39
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subjects 631/378
Animals
Antioxidants - administration & dosage
Apoptosis
Atrophy - genetics
Atrophy - metabolism
Atrophy - pathology
Biochemistry
Biomedical and Life Sciences
Cell Biology
Cell Cycle Analysis
Dynamins - biosynthesis
Dynamins - genetics
Hippocampus - growth & development
Hippocampus - metabolism
Hippocampus - pathology
Life Sciences
Memory Disorders - genetics
Memory Disorders - pathology
Mice
Mitochondria - metabolism
Mitochondria - pathology
Mitochondrial Dynamics - genetics
Nerve Degeneration - genetics
Nerve Degeneration - metabolism
Nerve Degeneration - pathology
Nervous System - growth & development
Nervous System - pathology
Neurons - metabolism
Neurons - pathology
Original Paper
Prosencephalon - growth & development
Prosencephalon - metabolism
Prosencephalon - pathology
Stem Cells
title Synaptic dysfunction, memory deficits and hippocampal atrophy due to ablation of mitochondrial fission in adult forebrain neurons
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