ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2012
Systemic administration of anti-NGF increases A-type potassium currents and decreases pancreatic nociceptor excitability in a rat model of chronic pancreatitis.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- The Efficacy of Nerve Growth Factor Antibody for the Treatment of Osteoarthritis Pain and Chronic Low-Back Pain: A Meta-Analysis.Frontiers in pharmacology · 2020Pooled it
- From Inflammation to Neuroplasticity: Molecular Mechanisms of Pain in Acute, Recurrent and Chronic Pancreatitis.International journal of molecular sciences · 2026Review
- Navigating chronic pancreatitis pain: a pathophysiological and therapeutic overview.Frontiers in physiology · 2025Review
- Recent advances in the understanding and management of chronic pancreatitis pain.Journal of pancreatology · 2024Review
- KFrontiers in cellular neuroscience · 2020Review
- Animal Models: Challenges and Opportunities to Determine Optimal Experimental Models of Pancreatitis and Pancreatic Cancer.Pancreas · 2019Review
- The Importance of Peripheral Nerves in Adipose Tissue for the Regulation of Energy Balance.Biology · 2019Review
- Anti-nerve growth factor monoclonal antibodies for the control of pain in dogs and cats.The Veterinary record · 2019Review
- Neuronal Transforming Growth Factor beta Signaling via SMAD3 Contributes to Pain in Animal Models of Chronic Pancreatitis.Gastroenterology · 2018Article
- Towards a neurobiological understanding of pain in chronic pancreatitis: mechanisms and implications for treatment.Pain reports · 2017Review
- Exploiting the Ref-1-APE1 node in cancer signaling and other diseases: from bench to clinic.NPJ precision oncology · 2017Article
- Current understanding of the neuropathophysiology of pain in chronic pancreatitis.World journal of gastrointestinal pathophysiology · 2015Review
- Neural plasticity in pancreatitis and pancreatic cancer.Nature reviews. Gastroenterology & hepatology · 2015Review
- Upregulation of nav1.7 through high salt loading: (mol pain 2013;9:39).Journal of neurogastroenterology and motility · 2014Article
- Opening paths to novel analgesics: the role of potassium channels in chronic pain.Trends in neurosciences · 2014Review
- Kv2 dysfunction after peripheral axotomy enhances sensory neuron responsiveness to sustained input.Experimental neurology · 2014Article
- Hydrogen sulfide increases excitability through suppression of sustained potassium channel currents of rat trigeminal ganglion neurons.Molecular pain · 2013Article
- Vertical transmission of respiratory syncytial virus modulates pre- and postnatal innervation and reactivity of rat airways.PloS one · 2013Article
- Article
- Transforming growth factor beta induces sensory neuronal hyperexcitability, and contributes to pancreatic pain and hyperalgesia in rats with chronic pancreatitis.Molecular pain · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
We have previously shown that pancreatic sensory neurons in rats with chronic pancreatitis (CP) display increased excitability associated with a decrease in transient inactivating potassium currents (I(A)), thus accounting in part for the hyperalgesia associated with this condition. Because of its well known role in somatic hyperalgesia, we hypothesized a role for the nerve growth factor (NGF) in driving these changes. CP was induced by intraductal injection of trinitrobenzene sulfonic acid (TNBS) in rats. After 3 wk, anti-NGF antibody or control serum was injected intra-peritoneally daily for 1 wk. This protocol was repeated in another set of experiments in control rats (receiving intraductal PBS instead of TNBS). Pancreatic nociceptors labeled with the dye Dil were identified, and patch-clamp recordings were made from acutely dissociated DRG neurons. Sensory neurons from anti-NGF-treated rats displayed a lower resting membrane potential, increased rheobase, decreased burst discharges in response to stimulatory current, and decreased input resistance compared with those treated with control serum. Under voltage-clamp condition, neuronal I(A) density was increased in anti-NGF-treated rats compared with rats treated with control serum. However, anti-NGF treatment had no effect on electrophysiological parameters in neurons from control rats. The expression of Kv-associated channel or ancillary genes Kv1.4, 4.1, 4.2, 4.3, and DPP6, DPP10, and KCHIPs 1-4 in pancreas-specific nociceptors was examined by laser-capture microdissection and real-time PCR quantification of mRNA levels. No significant differences were seen among those. These findings emphasize a key role for NGF in maintaining neuronal excitability in CP specifically via downregulation of I(A) by as yet unknown mechanisms.
Indexed as
Identifiers
What OpenQuestion holds
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.