ArticleNeuroscience2025
Calcitonin gene-related peptide differentially modulates intracellular calcium levels in response to depolarizing stimuli in trigeminal ganglion neurons and glial cells.
Article in Neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Elevated levels of calcitonin gene-related peptide (CGRP) are implicated in migraine pathology, but its effects on the excitability state of trigeminal ganglion Aδ and C-fiber neurons and glia have not been fully investigated. The goal of this study was to determine changes mediated by CGRP on intracellular calcium levels in trigeminal neurons and glia in response to depolarizing stimulation. Intracellular calcium levels were determined in Aδ and C-fiber neurons of primary trigeminal ganglion cultures obtained from neonatal Sprague Dawley rats using Fura-2 and fluorescent microscopy. Cells were left untreated or preincubated for 2 h with CGRP, then incubated with the depolarizing stimuli KCl or ATP. Data analysis was performed using Olympus CellSens Dimension software and JASP. CGRP greatly increased the calcium amplitude in response to 60 mM KCl and 100 µM ATP in Aδ neurons, while causing a smaller, similar response in C-fiber neurons. CGRP also increased the percentage of Aδ neurons responsive to 60 mM KCl and enhanced the magnitude of the calcium response. In glial cells, CGRP increased the magnitude of the 60 mM KCl-mediated response. However, CGRP suppressed the stimulatory calcium response to 15 mM KCl in neurons and glial cells and differentially modulated the calcium response to 30 mM KCl in Aδ and C-fiber neurons. These results provide evidence of a novel role of CGRP to regulate the excitability state of Aδ and C-fiber neurons and glial cells implicated in pain signaling in migraine differently in response to the strength of the depolarizing stimulus.
Indexed as
Identifiers
What Socratic 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 Socratic graph.