ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Mitochondrial Ca(2+) uptake is essential for synaptic plasticity in pain.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed.
- Oxidative Stress as a Physiological Pain Response in Full-Term Newborns.Oxidative medicine and cellular longevity · 2017Trial
- Beat-locked ATP microdomains in the sinoatrial node map a Ca2+-timed energetic hierarchy and regional pacemaker roles.The Journal of general physiology · 2026Article
- CALB2 Overexpression Attenuates Neuropathic Pain by Inhibiting Oxidative Stress and Modulating Microglia M1/M2 Polarization Through Activation of the cAMP/CREB Pathway.Neurochemical research · 2025Article
- Mechanism of action behind the pain-relief effects of extracellular vesicles in microfragmented adipose tissue: an in vitro and in vivo study.Journal of translational medicine · 2025Article
- Microalgae and exercise: from molecular mechanisms and brain health to clinical perspectives in the context of 3P medicine.The EPMA journal · 2025Review
- Pathogenic synergy: dysfunctional mitochondria and neuroinflammation in neurodegenerative diseases associated with aging.Frontiers in aging · 2025Review
- Activity-dependent mitochondrial ROS signaling regulates recruitment of glutamate receptors to synapses.eLife · 2024Article
- Differential timing of mitochondrial activation in rat dorsal striatum induced by procedural learning and swimming.Frontiers in molecular neuroscience · 2024Article
- Spinal antinociceptive effect of the PnTx4(5-5) peptide is possibly mediated by the NMDA autoreceptors.The journal of venomous animals and toxins including tropical diseases · 2024Article
- Repeated episodes of postictal hypoxia are a mechanism for interictal cognitive impairments.Scientific reports · 2023Article
- Neither too much nor too little: mitochondrial calcium concentration as a balance between physiological and pathological conditions.Frontiers in molecular biosciences · 2023Review
- Psychostimulants influence oxidative stress and redox signatures: the role of DNA methylation.Redox report : communications in free radical research · 2022Review
- Mitochondrial CaCommunications biology · 2022Article
- Mitochondrial Reactive Oxygen Species Elicit Acute and Chronic Itch via Transient Receptor Potential Canonical 3 Activation in Mice.Neuroscience bulletin · 2022Article
- Calcium Signalling in Breast Cancer Associated Bone Pain.International journal of molecular sciences · 2022Review
- Mitochondria and sensory processing in inflammatory and neuropathic pain.Frontiers in pain research (Lausanne, Switzerland) · 2022Review
- Reactive Oxygen Species (ROS) are Critical for Morphine Exacerbation of HIV-1 gp120-Induced Pain.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2021Article
- Mitochondria focused neurotherapeutics for spinal cord injury.Experimental neurology · 2020Review
- Mechanisms and roles of mitochondrial localisation and dynamics in neuronal function.Neuronal signaling · 2020Review
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Authors and funding
8 authors.
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Abstract
The increase of cytosolic free Ca(2+) ([Ca(2+)](c)) due to NMDA receptor activation is a key step for spinal cord synaptic plasticity by altering cellular signal transduction pathways. We focus on this plasticity as a cause of persistent pain. To provide a mechanism for these classic findings, we report that [Ca(2+)](c) does not trigger synaptic plasticity directly but must first enter into mitochondria. Interfering with mitochondrial Ca(2+) uptake during a [Ca(2+)](c) increase blocks induction of behavioral hyperalgesia and accompanying downstream cell signaling, with reduction of spinal long-term potentiation (LTP). Furthermore, reducing the accompanying mitochondrial superoxide levels lessens hyperalgesia and LTP induction. These results indicate that [Ca(2+)](c) requires downstream mitochondrial Ca(2+) uptake with consequent production of reactive oxygen species (ROS) for synaptic plasticity underlying chronic pain. These results suggest modifying mitochondrial Ca(2+) uptake and thus ROS as a type of chronic pain therapy that should also have broader biologic significance.
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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.