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Mitochondrial Dynamics in Neurons
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Mitochondrial Dynamics in Neurons

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (31 July 2022) | Viewed by 15239

Special Issue Editors

Dr. Ramon Trullas

E-Mail Website
Guest Editor
1. Neurobiology Unit, Institut d’Investigacions Biomèdiques de Barcelona (CSIC), 08036 Barcelona, Spain
2. Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), 08036 Barcelona, Spain
Interests: mitochondrial DNA; neurodegeneration; mitochondrial dynamics; synaptopathies; mito-nuclear communication
Dr. Anna Colell

E-Mail Website
Guest Editor
Neurobiology Unit, Institut d'Investigacions Biomèdiques de Barcelona, Consejo Superior de Investigaciones Científicas (CSIC), and Centro de Investigación en Red de Enfermedades Neurodegenerativas (CIBERNED), Spain
Interests: Alzheimer’s disease; cholesterol in neurodegeneration; mitochondria; mitochondrial oxidative stress; autophagy/mitophagy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The chemical energy provided by the mitochondria is essential for proper neuronal function. Once differentiated, neurons depend on their communication through synaptic transmission to survive, and synapses consume most of the neural energy. To ensure that there is no shortage, neurons send mitochondria from their soma to the energy-hungry synapses through long axonal and dendritic tracts. Conversely, exhausted mitochondria travel long distances back from synapses to the soma to recover. The continuous distribution of mitochondrial energy required by neurons involves several biochemical processes that are closely coordinated by mito-nuclear communication, which adjusts neuronal bioenergetics in an activity-dependent manner. These biochemical processes include mitochondrial fusion, fission, and transport; mitochondrial quality control; and replication, transcription, and translation of mitochondrial DNA. The alteration of any of these processes is at the root of various neurodegenerative diseases. Consequently, the biochemical mechanisms involved in neuronal mitochondrial bioenergetics are now the subject of intense investigation.

The Special Issue “Mitochondrial Dynamics in Neurons” aims to cover research on cellular and molecular mechanisms involved in the regulation of mitochondrial dynamics and the mitochondrial DNA copy number in neurons, including the influence of glial cells on the function of neuronal mitochondria. The Special Issue will also incorporate research that aims to ascertain the role of mito-nuclear communication, mitochondrial quality control, and mitochondrial dynamics in neurodegenerative diseases. The main objective of this Special Issue is to bring together research on the different fields of mitochondrial biology to advance our knowledge of the physio-pathological effects of mitochondria in neuronal function.

Dr. Ramon Trullas
Dr. Anna Colell
Guest Editors

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • mitochondrial dynamics
  • mitochondrial DNA
  • mito-nuclear communication
  • mitophagy
  • mitochondrial transport
  • mitochondrial oxidative stress
  • neurodegenerative disorders
  • mitochondrial cholesterol
  • neuronal bioenergetics
  • mitofusion
  • OPA1
  • DRP1
  • mitochondrial fission
  • mitochondrial fusion

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Published Papers (2 papers)

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14 pages, 3261 KiB  
Article
Mfn2 Overexpression Attenuates MPTP Neurotoxicity In Vivo
by Fanpeng Zhao, Quillan Austria, Wenzhang Wang and Xiongwei Zhu
Int. J. Mol. Sci. 2021, 22(2), 601; https://doi.org/10.3390/ijms22020601 - 9 Jan 2021
Cited by 11 | Viewed by 3012
Abstract
Mitochondrial dysfunction represents a critical event in the pathogenesis of Parkinson’s disease (PD). Increasing evidence demonstrates that disturbed mitochondrial dynamics and quality control play an important role in mitochondrial dysfunction in PD. Our previous study demonstrated that MPP+ induces mitochondrial fragmentation in [...] Read more.
Mitochondrial dysfunction represents a critical event in the pathogenesis of Parkinson’s disease (PD). Increasing evidence demonstrates that disturbed mitochondrial dynamics and quality control play an important role in mitochondrial dysfunction in PD. Our previous study demonstrated that MPP+ induces mitochondrial fragmentation in vitro. In this study, we aimed to assess whether blocking MPTP-induced mitochondrial fragmentation by overexpressing Mfn2 affords neuroprotection in vivo. We found that the significant loss of dopaminergic neurons in the substantia nigra (SN) induced by MPTP treatment, as seen in wild-type littermate control mice, was almost completely blocked in mice overexpressing Mfn2 (hMfn2 mice). The dramatic reduction in dopamine neuronal fibers and dopamine levels in the striatum caused by MPTP administration was also partially inhibited in hMfn2 mice. MPTP-induced oxidative stress and inflammatory response in the SN and striatum were significantly alleviated in hMfn2 mice. The impairment of motor function caused by MPTP was also blocked in hMfn2 mice. Overall, our work demonstrates that restoration of mitochondrial dynamics by Mfn2 overexpression protects against neuronal toxicity in an MPTP-based PD mouse model, which supports the modulation of mitochondrial dynamics as a potential therapeutic target for PD treatment. Full article
(This article belongs to the Special Issue Mitochondrial Dynamics in Neurons)
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Review

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11 pages, 1037 KiB  
Review
Mitochondrial Biogenesis in Neurons: How and Where
by Carlos Cardanho-Ramos and Vanessa Alexandra Morais
Int. J. Mol. Sci. 2021, 22(23), 13059; https://doi.org/10.3390/ijms222313059 - 2 Dec 2021
Cited by 79 | Viewed by 11369
Abstract
Neurons rely mostly on mitochondria for the production of ATP and Ca2+ homeostasis. As sub-compartmentalized cells, they have different pools of mitochondria in each compartment that are maintained by a constant mitochondrial turnover. It is assumed that most mitochondria are generated in [...] Read more.
Neurons rely mostly on mitochondria for the production of ATP and Ca2+ homeostasis. As sub-compartmentalized cells, they have different pools of mitochondria in each compartment that are maintained by a constant mitochondrial turnover. It is assumed that most mitochondria are generated in the cell body and then travel to the synapse to exert their functions. Once damaged, mitochondria have to travel back to the cell body for degradation. However, in long cells, like motor neurons, this constant travel back and forth is not an energetically favourable process, thus mitochondrial biogenesis must also occur at the periphery. Ca2+ and ATP levels are the main triggers for mitochondrial biogenesis in the cell body, in a mechanism dependent on the Peroxisome-proliferator-activated γ co-activator-1α-nuclear respiration factors 1 and 2-mitochondrial transcription factor A (PGC-1α-NRF-1/2-TFAM) pathway. However, even though of extreme importance, very little is known about the mechanisms promoting mitochondrial biogenesis away from the cell body. In this review, we bring forward the evoked mechanisms that are at play for mitochondrial biogenesis in the cell body and periphery. Moreover, we postulate that mitochondrial biogenesis may vary locally within the same neuron, and we build upon the hypotheses that, in the periphery, local protein synthesis is responsible for giving all the machinery required for mitochondria to replicate themselves. Full article
(This article belongs to the Special Issue Mitochondrial Dynamics in Neurons)
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