ArticleBritish journal of pharmacology2007
Chronic exposure of sensory neurones to increased levels of nerve growth factor modulates CB1/TRPV1 receptor crosstalk.
Article in British journal of pharmacology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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
17 citing papers in PubMed, 41 citations in OpenAlex.
- Article
- Maladaptive changes in the homeostasis of AEA-TRPV1/CB1R induces pain-related hyperactivity of nociceptors after spinal cord injury.Cell & bioscience · 2025Article
- Systematic Review of Systemic and Neuraxial Effects of Acetaminophen in Preclinical Models of Nociceptive Processing.Journal of pain research · 2021Review
- The Endocannabinoid/Endovanilloid System in Bone: From Osteoporosis to Osteosarcoma.International journal of molecular sciences · 2019Review
- An insight into paracetamol and its metabolites using molecular docking and molecular dynamics simulation.Journal of molecular modeling · 2018Article
- Spatial Distribution of the Cannabinoid Type 1 and Capsaicin Receptors May Contribute to the Complexity of Their Crosstalk.Scientific reports · 2016Article
- Glucose concentration in culture medium affects mRNA expression of TRPV1 and CB1 receptors and changes capsaicin toxicity in PC12 cells.Iranian journal of basic medical sciences · 2014Article
- Cannabinoid 1 and transient receptor potential vanilloid 1 receptors discretely modulate evoked glutamate separately from spontaneous glutamate transmission.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Neurotrophins in the lower urinary tract: becoming of age.Current neuropharmacology · 2011Article
- The cannabinergic system is implicated in the upregulation of central NGF protein by psychotropic drugs.Psychopharmacology · 2011Article
- Capsaicin in the periaqueductal gray induces analgesia via metabotropic glutamate receptor-mediated endocannabinoid retrograde disinhibition.British journal of pharmacology · 2011Article
- Chemical synthesis, pharmacological characterization, and possible formation in unicellular fungi of 3-hydroxy-anandamide.Journal of lipid research · 2009Article
- Role of ionotropic cannabinoid receptors in peripheral antinociception and antihyperalgesia.Trends in pharmacological sciences · 2009Review
- Constitutive activity at the cannabinoid CB1 receptor is required for behavioral response to noxious chemical stimulation of TRPV1: antinociceptive actions of CB1 inverse agonists.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- TRPV1: on the road to pain relief.Current molecular pharmacology · 2008Review
- Modulation of sensory neuron potassium conductances by anandamide indicates roles for metabolites.British journal of pharmacology · 2008Article
- Interaction Between the Cannabinoid and Vanilloid Systems on Anxiety in Male Rats.Basic and clinical neuroscienceArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAnandamide (AEA) activates both cannabinoid CB(1) and TRPV1 receptors, which are expressed on cultured dorsal root ganglion neurones. Increased levels of nerve growth factor (NGF) are associated with chronic pain states. EXPERIMENTAL APPROACH: The aim of this study was to compare of the effects of AEA on CB(1) receptor signalling and TRPV1-CB(1) crosstalk in low and high concentrations of NGF, using voltage-clamp electrophysiology and Fura-2 calcium imaging. KEY
resultsChronic exposure to high NGF (200 ng ml(-1)) as compared to low NGF (20 ng ml(-1)) increases the proportion of neurones that exhibit an inward current in response to AEA (1 microM), from 7 to 29%. In contrast, inhibition of voltage-gated calcium currents by AEA is not significantly different in low NGF (33+/-9%, compared to high NGF 28+/-6%). Crosstalk between CB and TRPV1 receptors is modulated by exposure to high NGF. In low NGF, exposure to the CB(1) receptor antagonist, SR141716A, (100 nM) increases the percentage of neurones in which AEA elicits an increase in [Ca(2+)](i), from 10 to 23%. In high NGF, the antagonist does not alter the percentage of responders (33 to 30%). In low NGF, exposure to the CB receptor agonist, WIN55 (1 microM) reduces capsaicin-mediated increases in [Ca(2+)](i) to 28+/-8% of control as compared to an enhancement to 172+/-26% of control observed in high NGF. CONCLUSIONS AND IMPLICATIONS: We conclude that cannabinoid-mediated modulation of TRPV1 receptor activation is altered after exposure to high NGF.
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.