Evidence map›Paper›PMID 25339743›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014

Loss of mitochondrial fission depletes axonal mitochondria in midbrain dopamine neurons.

Amandine Berthet, Elyssa B Margolis, Jue Zhang, Ivy Hsieh, Jiasheng Zhang, Thomas S Hnasko, Jawad Ahmad, Robert H Edwards, Hiromi Sesaki, Eric J Huang and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers.

0numbers the graph read from it
0cells of the map it votes in
128citing papers in PubMed
12.2field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

128 citing papers in PubMed, 242 citations in OpenAlex.

  1. Article
  2. Mitochondrial molecular diversity in the brain.Current opinion in neurobiology · 2026
    Review
  3. Article
  4. Review
  5. Mitochondrial mechanics nucleates axonal jamming and swelling.bioRxiv : the preprint server for biology · 2026
    Article
  6. Article
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  8. Review
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  11. bioRxiv : the preprint server for biology · 2025
    Article
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  20. Article

68 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 4 institutions in 1 country.

Amandine BerthetGladstone Institute of Neurological Disease, San Francisco, California 94158.
Elyssa B MargolisDepartment of Neurology and.
Jue ZhangGladstone Institute of Neurological Disease, San Francisco, California 94158.
Ivy HsiehDepartment of Pathology, University of California, San Francisco, San Francisco, California 94158.
Jiasheng ZhangDepartment of Pathology, University of California, San Francisco, San Francisco, California 94158.ORCID http://orcid.org/0000-0001-6097-1384
Thomas S HnaskoDepartment of Neurosciences, Translational Neurosciences Institute, University of California, San Diego, La Jolla, California 92093.
Jawad AhmadGladstone Institute of Neurological Disease, San Francisco, California 94158.
Robert H EdwardsDepartment of Neurology and Graduate Programs in Neuroscience and Biomedical Sciences, University of California, San Francisco, San Francisco, California 94158.
Hiromi SesakiDepartment of Cell Biology, School of Medicine, Johns Hopkins University, Baltimore, Maryland 21287, and.
Eric J HuangGraduate Programs in Neuroscience and Biomedical Sciences, University of California, San Francisco, San Francisco, California 94158, Department of Pathology, University of California, San Francisco, San Francisco, California 94158.
Ken NakamuraGladstone Institute of Neurological Disease, San Francisco, California 94158, Department of Neurology and Graduate Programs in Neuroscience and Biomedical Sciences, University of California, San Francisco, San Francisco, California 94158, ken.nakamura@gladstone.ucsf.edu.
Gladstone Institutes · USUniversity of California, San Francisco · USJohns Hopkins University · USNeurosciences Institute · US

Funding

Behavioral CoreP30NS065780 · NINDS · J. DAVID GLADSTONE INSTITUTES · PI MUCKE, LENNART · 2011 to 2015
$4.0M
EXTRAMULAR RESEARCH FACILITIES CONSTRUCTIONC06RR018928 · NCRR · J. DAVID GLADSTONE INSTITUTES · PI MAHLEY, ROBERT W. · 2003 to 2003
$2.1M
Beta-cell ProliferationR01DK081472 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI HUSSAIN, MEHBOOB A, WONDISFORD, FREDRIC E. · 2009 to 2013
$2.1M
Heterogeneity of Ventral Tegmental Area Neurons and Opioid RewardR01DA030529 · NIDA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MARGOLIS, ELYSSA · 2011 to 2015
$1.8M
Novel Therapeutic Approaches to Alzheimer's DiseaseP30NS069496 · NINDS · J. DAVID GLADSTONE INSTITUTES · PI MUCKE, LENNART · 2009 to 2010
$1.7M
Regulation of mitochondrial morphology by alpha-synucleinK08NS062954 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI NAKAMURA, KEN · 2009 to 2013
$878k
Mouse models of neuroprotection in dopamine neuronsK26OD010927 · OD · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI HUANG, ERIC J · 2012 to 2013
$307k
Mechanisms of ER Stress and Neurodegeneration in Parkinson's DiseaseI01BX001108 · VA · VETERANS AFFAIRS MED CTR SAN FRANCISCO · PI Eric J Huang · 2011 to 2026
–
BLRD VA I01 BX001108NCRR NIH HHS C06 RR018928NIDA NIH HHS R01 DA030529NIDA NIH HHS R01DA030529NIDDK NIH HHS R01 DK081472NIH HHS K26 OD010927NIH HHS OD010927NINDS NIH HHS K08 NS062954NINDS NIH HHS KO8NS062954NINDS NIH HHS P30 NS065780NINDS NIH HHS P30NS065780NINDS NIH HHS P30 NS069496NINDS NIH HHS P30NS069496Wellcome Trust
6 · The paper itself

Abstract

Disruptions in mitochondrial dynamics may contribute to the selective degeneration of dopamine (DA) neurons in Parkinson's disease (PD). However, little is known about the normal functions of mitochondrial dynamics in these neurons, especially in axons where degeneration begins, and this makes it difficult to understand the disease process. To study one aspect of mitochondrial dynamics-mitochondrial fission-in mouse DA neurons, we deleted the central fission protein dynamin-related protein 1 (Drp1). Drp1 loss rapidly eliminates the DA terminals in the caudate-putamen and causes cell bodies in the midbrain to degenerate and lose α-synuclein. Without Drp1, mitochondrial mass dramatically decreases, especially in axons, where the mitochondrial movement becomes uncoordinated. However, in the ventral tegmental area (VTA), a subset of midbrain DA neurons characterized by small hyperpolarization-activated cation currents (Ih) is spared, despite near complete loss of their axonal mitochondria. Drp1 is thus critical for targeting mitochondria to the nerve terminal, and a disruption in mitochondrial fission can contribute to the preferential death of nigrostriatal DA neurons.

Indexed as

AnimalsAxonsDopaminergic NeuronsDynaminsFemaleMaleMembrane PotentialsMesencephalonMiceMice, KnockoutMitochondriaMitochondrial DynamicsOrgan Culture TechniquesDnm1l protein, mouseDynaminsaxonDrp1mitochondrianeurodegenerationParkinson's disease

Identifiers

PMID25339743
PMCPMC4205554
OpenAlexW1968522541

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.