ArticleFrontiers in computational neuroscience2013
The energy cost of action potential propagation in dopamine neurons: clues to susceptibility in Parkinson's disease.
Article in Frontiers in computational neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 204 papers.
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.
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.
Who cites it
204 citing papers in PubMed, 340 citations in OpenAlex.
- Regulation and roles of mammalian mitophagy.Nature reviews. Molecular cell biology · 2026Review
- Engineering functional ventral midbrain dopaminergic neurons in human organoids through WNT modulation and bioreactor culture.Molecular psychiatry · 2026Article
- Species-dependent activities of the PINK1-parkin axis.Translational neurodegeneration · 2026Review
- Intranasal Delivery of Gallium-Quercetin Nanoparticles for Multi-Target Ferroptosis Inhibition in Parkinson's Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Rewiring Lipid Metabolism: PINK1 as a Central Regulator of Mitochondrial Homeostasis in Parkinson's Disease.International journal of molecular sciences · 2026Review
- Reimagining the contribution of iron in Parkinson's disease.Neurobiology of disease · 2026Review
- The Long Haul: Microtubule Motors as the Essential Supply Line for Neuronal Longevity.Journal of neurochemistry · 2026Review
- Early GPR81/MCT1 rise and late lactate-NAD(H) Build-up in an LPS model of PD.Metabolic brain disease · 2026Article
- Neurovascular Uncoupling in Alzheimer's and Parkinson's Diseases: Mechanisms and Therapeutic Strategies.Brain sciences · 2026Review
- The Brain-Gut Axis in Parkinson's Disease Pathology.Comprehensive Physiology · 2026Review
- Long-range axon branching: contributions to brain network plasticity and repair.Nature reviews. Neuroscience · 2026Review
- Sex differences in neuromodulatory subcortical systems and their implications for Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Methamphetamine-Driven Neuroinflammation and Parkinson's Disease Pathology: Mechanistic Insight into Nrf2 and NFĸB Signaling.Molecular neurobiology · 2026Review
- Knowledge and Misconceptions About Parkinson's Disease in Lebanon: A Cross-Sectional Survey.Parkinson's disease · 2026Article
- Research progress on the α-synuclein-lysosome axis in Parkinson's disease: molecular mechanisms of protein aggregation, autophagy dysfunction, and therapeutic targeting.Frontiers in neuroscience · 2026Review
- The role of energy deficit in autophagy failure in Parkinson's disease.Frontiers in aging neuroscience · 2026Review
- Chronic stress-induced LC-NE dysfunction: cellular and axonal mechanisms underlying impaired neuromodulation.Frontiers in neuroscience · 2026Review
- Mitochondrial resilience: a convergent framework for pathogenesis and neuroprotection in Parkinson's disease.Frontiers in pharmacology · 2026Review
- Pathological tau alters head direction signaling and induces spatial disorientation.Cell reports · 2025Article
- Movement disorders: a brief overview from an evolutionary perspective.Journal of neural transmission (Vienna, Austria : 1996) · 2025Review
144 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 3 countries.
Funding
Abstract
Dopamine neurons of the substantia nigra pars compacta (SNc) are uniquely sensitive to degeneration in Parkinson's disease (PD) and its models. Although a variety of molecular characteristics have been proposed to underlie this sensitivity, one possible contributory factor is their massive, unmyelinated axonal arbor that is orders of magnitude larger than other neuronal types. We suggest that this puts them under such a high energy demand that any stressor that perturbs energy production leads to energy demand exceeding supply and subsequent cell death. One prediction of this hypothesis is that those dopamine neurons that are selectively vulnerable in PD will have a higher energy cost than those that are less vulnerable. We show here, through the use of a biology-based computational model of the axons of individual dopamine neurons, that the energy cost of axon potential propagation and recovery of the membrane potential increases with the size and complexity of the axonal arbor according to a power law. Thus SNc dopamine neurons, particularly in humans, whose axons we estimate to give rise to more than 1 million synapses and have a total length exceeding 4 m, are at a distinct disadvantage with respect to energy balance which may be a factor in their selective vulnerability in PD.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.