ReviewNeural plasticity2016
Linking Mitochondria to Synapses: New Insights for Stress-Related Neuropsychiatric Disorders.
Review in Neural plasticity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
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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.
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Who cites it
38 citing papers in PubMed, 64 citations in OpenAlex.
- Mechanistic insights into the synaptic damage-repair and regeneration processes in neurodegenerative Alzheimer's disease: phytochemicals as neuroprotective agents.Frontiers in synaptic neuroscience · 2026Review
- Candidate Key Proteins in Tinnitus-A Bioinformatic Study of Synaptic Transmission in the Inferior Colliculus.International journal of molecular sciences · 2025Article
- Curcumin Improves Hippocampal Cell Bioenergetics, Redox and Inflammatory Markers, and Synaptic Proteins, Regulating Mitochondrial Calcium Homeostasis.Neurotoxicity research · 2025Article
- Tat-Beclin-1 Ameliorates Memory by Improving Neuronal Cytoarchitecture and Mitigating Mitochondrial Dysfunction in Scopolamine-Induced Amnesic Male Mice.ACS pharmacology & translational science · 2024Article
- Mitochondrial plasticity and synaptic plasticity crosstalk; in health and Alzheimer's disease.CNS neuroscience & therapeutics · 2024Review
- Impaired mitochondrial function in bipolar disorder and alcohol use disorder: a case study usingPsychoradiology · 2024Article
- Isolated Mitochondrial Preparations andCurrent neuropharmacology · 2023Review
- Mitochondrial Dysfunction in Attention Deficit Hyperactivity Disorder.The Eurasian journal of medicine · 2022Article
- Rhodiola Rosea Extract Counteracts Stress in an Adaptogenic Response Curve Manner via Elimination of ROS and Induction of Neurite Outgrowth.Oxidative medicine and cellular longevity · 2022Article
- Mitochondria as the target for disease related hormonal dysregulation.Brain, behavior, & immunity - health · 2021Article
- Dual imaging of dendritic spines and mitochondriaNeurobiology of stress · 2021Article
- CCL5 promotion of bioenergy metabolism is crucial for hippocampal synapse complex and memory formation.Molecular psychiatry · 2021Article
- Cell competition from development to neurodegeneration.Disease models & mechanisms · 2021Review
- Neuroinflammation as a Common Denominator of Complex Diseases (Cancer, Diabetes Type 2, and Neuropsychiatric Disorders).International journal of molecular sciences · 2021Review
- Mitochondrial Glucocorticoid Receptors and Their Actions.International journal of molecular sciences · 2021Review
- Article
- Early-Life Stress Alters Synaptic Plasticity and mTOR Signaling: Correlation With Anxiety-Like and Cognition-Related Behavior.Frontiers in genetics · 2020Article
- Prefrontal Cortical and Behavioral Adaptations to Surgical Delivery Mediated by Metabolic Principles.Cerebral cortex (New York, N.Y. : 1991) · 2019Article
- Fractionated mitochondrial magnetic separation for isolation of synaptic mitochondria from brain tissue.Scientific reports · 2019Article
- Dysfunctional Mitochondrial Bioenergetics and Synaptic Degeneration in Alzheimer Disease.International neurourology journal · 2019Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The brain evolved cellular mechanisms for adapting synaptic function to energy supply. This is particularly evident when homeostasis is challenged by stress. Signaling loops between the mitochondria and synapses scale neuronal connectivity with bioenergetics capacity. A biphasic "inverted U shape" response to the stress hormone glucocorticoids is demonstrated in mitochondria and at synapses, modulating neural plasticity and physiological responses. Low dose enhances neurotransmission, synaptic growth, mitochondrial functions, learning, and memory whereas chronic, higher doses produce inhibition of these functions. The range of physiological effects by stress and glucocorticoid depends on the dose, duration, and context at exposure. These criteria are met by neuronal activity and the circadian, stress-sensitive and ultradian, stress-insensitive modes of glucocorticoid secretion. A major hallmark of stress-related neuropsychiatric disorders is the disrupted glucocorticoid rhythms and tissue resistance to signaling with the glucocorticoid receptor (GR). GR resistance could result from the loss of context-dependent glucocorticoid signaling mediated by the downregulation of the activity-dependent neurotrophin BDNF. The coincidence of BDNF and GR signaling changes glucocorticoid signaling output with consequences on mitochondrial respiration efficiency, synaptic plasticity, and adaptive trajectories.
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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.