ArticleJournal of cellular and molecular medicine2015
Botulinum neurotoxin type A modulates vesicular release of glutamate from satellite glial cells.
Article in Journal of cellular and molecular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- Pooled it
- Glial cells in neuropathic pain.Physiological reviews · 2026Review
- Calcitonin gene-related peptide differentially modulates intracellular calcium levels in response to depolarizing stimuli in trigeminal ganglion neurons and glial cells.Neuroscience · 2025Article
- Intradermally injected abobotulinumtoxinA administered preemptively before surgery alleviates post-surgical pain and normalizes behavior in a translational animal model.Scientific reports · 2025Article
- Article
- OnabotulinumtoxinA effects on trigeminal nociceptors.Cephalalgia : an international journal of headache · 2023Article
- Increase of glutamate in satellite glial cells of the trigeminal ganglion in a rat model of craniofacial neuropathic pain.Frontiers in neuroanatomy · 2023Article
- Review
- How Does Botulinum Toxin Inhibit Itch?Toxins · 2022Review
- Peripheral role of glutamate in orofacial pain.Frontiers in neuroscience · 2022Review
- Dysregulation of the peripheral glutamatergic system: A key player in migraine pathogenesis?Cephalalgia : an international journal of headache · 2021Review
- Emerging Opportunities in Human Pluripotent Stem-Cells Based Assays to Explore the Diversity of Botulinum Neurotoxins as Future Therapeutics.International journal of molecular sciences · 2021Review
- Direct Inhibition of Microglia Activation by Pretreatment With Botulinum Neurotoxin A for the Prevention of Neuropathic Pain.Frontiers in neuroscience · 2021Article
- Satellite Glial Cells in Pain Research: A Targeted Viewpoint of Potential and Future Directions.Frontiers in pain research (Lausanne, Switzerland) · 2021Review
- Mechanisms of Botulinum Toxin Type A Action on Pain.Toxins · 2019Review
- OnabotulinumtoxinA in Migraine and Other Headaches: Review and Update.Current treatment options in neurology · 2019Review
- Intra-articular botulinum toxin A (BoNT/A) for pain management in dogs with osteoarthritis secondary to hip dysplasia: A randomized controlled clinical trial.The Journal of veterinary medical science · 2019Article
- Therapeutic use of botulinum toxin in pain treatment.Neuronal signaling · 2018Review
- Review
- Antipruritic Effects of Botulinum Neurotoxins.Toxins · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study investigated the presence of cell membrane docking proteins synaptosomal-associated protein, 25 and 23 kD (SNAP-25 and SNAP-23) in satellite glial cells (SGCs) of rat trigeminal ganglion; whether cultured SGCs would release glutamate in a time- and calcium-dependent manner following calcium-ionophore ionomycin stimulation; and if botulinum neurotoxin type A (BoNTA), in a dose-dependent manner, could block or decrease vesicular release of glutamate. SGCs were isolated from the trigeminal ganglia (TG) of adult Wistar rats and cultured for 7 days. The presence of SNAPs in TG sections and isolated SGCs were investigated using immunohistochemistry and immunocytochemistry, respectively. SGCs were stimulated with ionomycin (5 μM for 4, 8, 12 and 30 min.) to release glutamate. SGCs were then pre-incubated with BoNTA (24 hrs with 0.1, 1, 10 and 100 pM) to investigate if BoNTA could potentially block ionomycin-stimulated glutamate release. Glutamate concentrations were measured by ELISA. SNAP-25 and SNAP-23 were present in SGCs in TG sections and in cultured SGCs. Ionomycin significantly increased glutamate release from cultured SGCs 30 min. following the treatment (P < 0.001). BoNTA (100 pM) significantly decreased glutamate release (P < 0.01). Results from this study demonstrated that SGCs, when stimulated with ionomycin, released glutamate that was inhibited by BoNTA, possibly through cleavage of SNAP-25 and/or SNAP-23. These novel findings demonstrate the existence of vesicular glutamate release from SGCs, which could potentially play a role in the trigeminal sensory transmission. In addition, interaction of BoNTA with non-neuronal cells at the level of TG suggests a potential analgesic mechanism of action of BoNTA.
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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.