ArticleMolecular pain2012
Painful nerve injury increases plasma membrane Ca2+-ATPase activity in axotomized sensory neurons.
Article in Molecular pain, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 36 citations in OpenAlex.
- Aging-Related Changes in the Injury Response of the Peripheral Nervous System.Neuroscience bulletin · 2026Review
- Integrated analyses reveal evolutionarily conserved and specific injury response genes in dorsal root ganglion.Scientific data · 2022Article
- Calcium Signalling in Breast Cancer Associated Bone Pain.International journal of molecular sciences · 2022Review
- Calcium in Neuronal and Glial Response to Axotomy.International journal of molecular sciences · 2021Review
- Article
- Dorsal Root Ganglion Stimulation Alleviates Pain-related Behaviors in Rats with Nerve Injury and Osteoarthritis.Anesthesiology · 2020Article
- GCaMP as an indirect measure of electrical activity in rat trigeminal ganglion neurons.Cell calcium · 2020Article
- Bromelain reversed electrolyte imbalance in the chronically constricted sciatic nerve of Wistar rats.Naunyn-Schmiedeberg's archives of pharmacology · 2020Article
- Pathological pain processing in mouse models of multiple sclerosis and spinal cord injury: contribution of plasma membrane calcium ATPase 2 (PMCA2).Journal of neuroinflammation · 2019Article
- Evidence for a role of plasma membrane calcium pumps in neurodegenerative disease: Recent developments.Neuroscience letters · 2018Review
- Increased thrombospondin-4 after nerve injury mediates disruption of intracellular calcium signaling in primary sensory neurons.Neuropharmacology · 2017Article
- Paclitaxel-induced increase in mitochondrial volume mediates dysregulation of intracellular CaCell calcium · 2017Article
- Blockade of P2X4 Receptors Inhibits Neuropathic Pain-Related Behavior by Preventing MMP-9 Activation and, Consequently, Pronociceptive Interleukin Release in a Rat Model.Frontiers in pharmacology · 2017Article
- Sciatic nerve ligation causes impairment of mitochondria associated with changes in distribution, respiration, and cardiolipin composition in related spinal cord neurons in rats.Molecular and cellular biochemistry · 2016Article
- Article
- Paclitaxel-induced increase in NCX activity in subpopulations of nociceptive afferents: A protective mechanism against chemotherapy-induced peripheral neuropathy?Cell calcium · 2016Article
- Standardized Profiling of The Membrane-Enriched Proteome of Mouse Dorsal Root Ganglia (DRG) Provides Novel Insights Into Chronic Pain.Molecular & cellular proteomics : MCP · 2016Article
- CaMKII Controls Whether Touch Is Painful.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Trafficking of Na+/Ca2+ exchanger to the site of persistent inflammation in nociceptive afferents.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Divergent effects of painful nerve injury on mitochondrial Ca(2+) buffering in axotomized and adjacent sensory neurons.Brain research · 2014Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundThe plasma membrane Ca2+-ATPase (PMCA) is the principal means by which sensory neurons expel Ca2+ and thereby regulate the concentration of cytoplasmic Ca2+ and the processes controlled by this critical second messenger. We have previously found that painful nerve injury decreases resting cytoplasmic Ca2+ levels and activity-induced cytoplasmic Ca2+ accumulation in axotomized sensory neurons. Here we examine the contribution of PMCA after nerve injury in a rat model of neuropathic pain.
resultsPMCA function was isolated in dissociated sensory neurons by blocking intracellular Ca2+ sequestration with thapsigargin, and cytoplasmic Ca2+ concentration was recorded with Fura-2 fluorometry. Compared to control neurons, the rate at which depolarization-induced Ca2+ transients resolved was increased in axotomized neurons after spinal nerve ligation, indicating accelerated PMCA function. Electrophysiological recordings showed that blockade of PMCA by vanadate prolonged the action potential afterhyperpolarization, and also decreased the rate at which neurons could fire repetitively.
conclusionWe found that PMCA function is elevated in axotomized sensory neurons, which contributes to neuronal hyperexcitability. Accelerated PMCA function in the primary sensory neuron may contribute to the generation of neuropathic pain, and thus its modulation could provide a new pathway for peripheral treatment of post-traumatic neuropathic pain.
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