ArticleAnesthesiology2009
Axotomy depletes intracellular calcium stores in primary sensory neurons.
Article in Anesthesiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 52 citations in OpenAlex.
- STIM Proteins: The Gas and Brake of Calcium Entry in Neurons.Neuroscience bulletin · 2025Review
- PDX1, a transcription factor essential for organ differentiation, regulates SERCA-dependent CaCell calcium · 2024Article
- Article
- Sensory neuron dysfunction in orthotopic mouse models of colon cancer.Journal of neuroinflammation · 2022Article
- Calcium in Neuronal and Glial Response to Axotomy.International journal of molecular sciences · 2021Review
- In Vivo Gene Delivery of STC2 Promotes Axon Regeneration in Sciatic Nerves.Molecular neurobiology · 2021Article
- Functional Electrical Stimulation and the Modulation of the Axon Regeneration Program.Frontiers in cell and developmental biology · 2020Review
- Mechanism and role of the intra-axonal Calreticulin translation in response to axonal injury.Experimental neurology · 2020Article
- Maintenance of homeostatic plasticity at theeLife · 2019Article
- From Mechanism to Cure: Renewing the Goal to Eliminate the Disease of Pain.Pain medicine (Malden, Mass.) · 2018Review
- Increased thrombospondin-4 after nerve injury mediates disruption of intracellular calcium signaling in primary sensory neurons.Neuropharmacology · 2017Article
- Sexual Dimorphism in a Reciprocal Interaction of Ryanodine and IPThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Orai1 and Orai3 Mediate Store-Operated Calcium Entry Contributing to Neuronal Excitability in Dorsal Root Ganglion Neurons.Frontiers in cellular neuroscience · 2017Article
- Differential expression of CaMKII isoforms and overall kinase activity in rat dorsal root ganglia after injury.Neuroscience · 2015Article
- Involvement of endoplasmic reticulum stress response in orofacial inflammatory pain.Experimental neurobiology · 2014Article
- Divergent effects of painful nerve injury on mitochondrial Ca(2+) buffering in axotomized and adjacent sensory neurons.Brain research · 2014Article
- The properties, distribution and function of Na(+)-Ca(2+) exchanger isoforms in rat cutaneous sensory neurons.The Journal of physiology · 2014Article
- Selective cleavage of SNAREs in sensory neurons unveils protein complexes mediating peptide exocytosis triggered by different stimuli.Molecular neurobiology · 2014Article
- Remote neurodegeneration: multiple actors for one play.Molecular neurobiology · 2014Review
- Axon-soma communication in neuronal injury.Nature reviews. Neuroscience · 2014Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe cellular mechanisms of neuropathic pain are inadequately understood. Previous investigations have revealed disrupted Ca signaling in primary sensory neurons after injury. The authors examined the effect of injury on intracellular Ca stores of the endoplasmic reticulum, which critically regulate the Ca signal and neuronal function.
methodsIntracellular Ca levels were measured with Fura-2 or mag-Fura-2 microfluorometry in axotomized fifth lumbar (L5) dorsal root ganglion neurons and adjacent L4 neurons isolated from hyperalgesic rats after L5 spinal nerve ligation, compared to neurons from control animals.
resultsEndoplasmic reticulum Ca stores released by the ryanodine-receptor agonist caffeine decreased by 46% in axotomized small neurons. This effect persisted in Ca-free bath solution, which removes the contribution of store-operated membrane Ca channels, and after blockade of the mitochondrial, sarco-endoplasmic Ca-ATPase and the plasma membrane Ca ATPase pathways. Ca released by the sarco-endoplasmic Ca-ATPase blocker thapsigargin and by the Ca-ionophore ionomycin was also diminished by 25% and 41%, respectively. In contrast to control neurons, Ca stores in axotomized neurons were not expanded by neuronal activation by K depolarization, and the proportionate rate of refilling by sarco-endoplasmic Ca-ATPase was normal. Luminal Ca concentration was also reduced by 38% in axotomized neurons in permeabilized neurons. The adjacent neurons of the L4 dorsal root ganglia showed modest and inconsistent changes after L5 spinal nerve ligation.
conclusionsPainful nerve injury leads to diminished releasable endoplasmic reticulum Ca stores and a reduced luminal Ca concentration. Depletion of Ca stores may contribute to the pathogenesis of neuropathic pain.
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Registered trials
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