ArticleJournal of neurotrauma2016
Trigeminal Pain Molecules, Allodynia, and Photosensitivity Are Pharmacologically and Genetically Modulated in a Model of Traumatic Brain Injury.
Article in Journal of neurotrauma, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.
- Trigeminal neuralgia and genetics: A systematic review.Molecular painPooled it
- CGRP-induced migraine-like headache in persistent post-traumatic headache attributed to mild traumatic brain injury.The journal of headache and pain · 2022Trial
- Neuropathic pain in traumatic brain injury: consequences, mechanisms, and therapeutic avenues.Inflammopharmacology · 2026Review
- Phenotype-guided Management of Post-traumatic Headache: An Update on Pathophysiology and Treatment.Current pain and headache reports · 2026Review
- The effects of physical exercise on inflammation-induced maladaptive neuroplasticity in post-traumatic headache.Neuroscience · 2026Review
- OnabotulinumtoxinA inhibits dysregulation of descending pain modulation following mild traumatic brain injury in mice.The journal of headache and pain · 2025Article
- Sex differences in the effects of calcitonin gene-related peptide signaling on migraine-like behavior in animal models: a narrative review.Frontiers in neurology · 2025Review
- Biomarkers and Endophenotypes of Post-traumatic Headaches.Current pain and headache reports · 2024Review
- Approachability and Sensory Changes Following Mild Traumatic Brain Injury in Pigs.Biomedicines · 2024Article
- Onabotulinumtoxin A for the Treatment of Post-Traumatic Headache: Is It Better than Anti-CGRP Antibodies?Toxins · 2024Review
- Oxytocin Receptors on Calvarial Periosteal Innervation: Therapeutic Target for Post-Traumatic Headache?Pharmaceutics · 2024Article
- Trigeminal Sensitization in a Closed Head Model for Mild Traumatic Brain Injury.Journal of neurotrauma · 2024Article
- Inflammation, brain connectivity, and neuromodulation in post-traumatic headache.Brain, behavior, & immunity - health · 2024Review
- Conservative Management of Acute Sports-Related Concussions: A Narrative Review.Healthcare (Basel, Switzerland) · 2024Review
- Identification of brain areas in mice with peak neural activity across the acute and persistent phases of post-traumatic headache.Cephalalgia : an international journal of headache · 2023Article
- Effect of Voluntary Exercise on Endogenous Pain Control Systems and Post-traumatic Headache in Mice.The journal of pain · 2023Article
- Cannabidiol's neuroprotective properties and potential treatment of traumatic brain injuries.Frontiers in neurology · 2023Review
- Review
- Preclinical assessment of onabotulinumtoxinA for the treatment of mild traumatic brain injury-related acute and persistent post-traumatic headache.Cephalalgia : an international journal of headache · 2022Article
- Post-traumatic Headache: Pharmacologic Management and Targeting CGRP Signaling.Current neurology and neuroscience reports · 2022Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pain-signaling molecules, nitric oxide synthase (NOS) and calcitonin gene-related peptide (CGRP), are implicated in the pathophysiology of post-traumatic headache (PTH) as they are for migraine. This study assessed the changes of inducible NOS (iNOS) and its cellular source in the trigeminal pain circuit, as well as the relationship between iNOS and CGRP after controlled cortical impact (CCI) injury in mice. The effects of a CGRP antagonist (MK8825) and sumatriptan on iNOS messenger RNA (mRNA) and protein were compared to vehicle at 2 weeks postinjury. Changes in CGRP levels in the trigeminal nucleus caudalis (TNC) in iNOS knockouts with CCI were compared to wild-type (WT) mice at 3 days and 2 weeks post injury. Trigeminal allodynia and photosensitivity were measured. MK8825 and sumatriptan increased allodynic thresholds in CCI groups compared to vehicle (p < 0.01), whereas iNOS knockouts were not different from WT. Photosensitivity was attenuated in MK8825 mice and iNOS knockouts compared to WT (p < 0.05). MK8825 and sumatriptan reduced levels of iNOS mRNA and iNOS immunoreactivity in the TNC and ganglia (p < 0.01). Differences in iNOS cellular localization were found between the trigeminal ganglia and TNC. Although the knockout of iNOS attenuated CGRP at 3 days (p < 0.05), it did not reduce CGRP at 2 weeks. CGRP immunoreactivity was found in the meningeal layers post-CCI, while negligible in controls. Findings support the importance of interactions between CGRP and iNOS in mediating allodynia, as well as the individual roles in photosensitivity. Mitigating prolonged increases in CGRP may be a promising intervention for treating acute PTH.
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Registered trials
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