ArticleAnesthesiology2006
Painful peripheral nerve injury decreases calcium current in axotomized sensory neurons.
Article in Anesthesiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 69 citations in OpenAlex.
- Tmem45b modulates itch via endoplasmic reticulum calcium regulation.Frontiers in physiology · 2025Article
- In Vitro Models for Peripheral Nerve Regeneration.Advanced healthcare materials · 2024Review
- PDX1, a transcription factor essential for organ differentiation, regulates SERCA-dependent CaCell calcium · 2024Article
- Selective block of sensory neuronal T-type/Cav3.2 activity mitigates neuropathic pain behavior in a rat model of osteoarthritis pain.Arthritis research & therapy · 2022Article
- Targeted ubiquitination of sensory neuron calcium channels reduces the development of neuropathic pain.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Sigma-1 receptor activity in primary sensory neurons is a critical driver of neuropathic pain.Gene therapy · 2022Article
- Automatic Electrodiagnosis of Carpal Tunnel Syndrome Using Machine Learning.Bioengineering (Basel, Switzerland) · 2021Article
- Article
- Diabetic neuropathy research: from mouse models to targets for treatment.Neural regeneration research · 2019Review
- Effectiveness of dorsal root ganglion stimulation and dorsal column spinal cord stimulation in a model of experimental painful diabetic polyneuropathy.CNS neuroscience & therapeutics · 2019Article
- Identification of key genes and pathways involved in response to pain in goat and sheep by transcriptome sequencing.Biological research · 2018Article
- Coping with Phantom Limb Pain.Molecular neurobiology · 2018Review
- Increased thrombospondin-4 after nerve injury mediates disruption of intracellular calcium signaling in primary sensory neurons.Neuropharmacology · 2017Article
- Impact of gabapentin on neuronal high voltage-activated CaExperimental and therapeutic medicine · 2017Article
- Proteolytic maturation of αeLife · 2016Article
- Article
- Effect of knockout of α2δ-1 on action potentials in mouse sensory neurons.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2016Article
- Painful nerve injury upregulates thrombospondin-4 expression in dorsal root ganglia.Journal of neuroscience research · 2015Article
- Divergent effects of painful nerve injury on mitochondrial Ca(2+) buffering in axotomized and adjacent sensory neurons.Brain research · 2014Article
- Sigma-1 receptor antagonism restores injury-induced decrease of voltage-gated Ca2+ current in sensory neurons.The Journal of pharmacology and experimental therapeutics · 2014Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundReports of Ca(2+) current I(Ca) loss after injury to peripheral sensory neurons do not discriminate between axotomized and spared neurons. The spinal nerve ligation model separates axotomized from spared neurons innervating the same site. The authors hypothesized that I(Ca) loss is a result of neuronal injury, so they compared axotomized L5 dorsal root ganglion neurons to spared L4 neurons, as well as neurons from rats undergoing skin incision alone.
methodsAfter behavioral testing, dissociated neurons from L4 and L5 dorsal root ganglia were studied in both current and voltage patch clamp modes. The biophysical consequence of I(Ca) loss on the action potential was confirmed using selective I(Ca) antagonists. Data were grouped into small, medium, and large cells for comparison.
resultsReduced I(Ca) was predominantly a consequence of axotomy (L5 after spinal nerve ligation) and was most evident in small and medium neurons. ICa losses were associated with action potential prolongation in small and medium cells, whereas the amplitude and duration of after hyperpolarization was reduced in medium and large neurons. Blockade with Ca(2+) channel antagonists showed that action potential prolongation and after hyperpolarization diminution were alike, attributable to the loss of I(Ca).
conclusionAxotomy is required for I(Ca) loss. I(Ca) loss correlated with changes in the biophysical properties of sensory neuron membranes during action potential generation, which were due to I(Ca) loss leading to decreased outward Ca(2+)-sensitive K currents. Taken together, these results suggest that neuropathic pain may be mediated, in part, by loss of I(Ca) and the cellular processes dependent on Ca(2+).
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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.