ArticleNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2013
Inhibition of the PKCγ-ε pathway relieves from meningeal nociception in an animal model: an innovative perspective for migraine therapy?
Article in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- New insight into DAVF pathology-Clues from meningeal immunity.Frontiers in immunology · 2022Review
- Expression of PIAS Genes in Migraine Patients.Journal of molecular neuroscience : MN · 2021Article
- Genetic variants related to successful migraine prophylaxis with verapamil.Molecular genetics & genomic medicine · 2021Article
- Effect of Electroacupuncture on Hyperalgesia and Vasoactive Neurotransmitters in a Rat Model of Conscious Recurrent Migraine.Evidence-based complementary and alternative medicine : eCAM · 2019Article
- Protein Kinase C γ Contributes to Central Sensitization in a Rat Model of Chronic Migraine.Journal of molecular neuroscience : MN · 2017Article
- Involvement of BDNF/TrkB and ERK/CREB axes in nitroglycerin-induced rat migraine and effects of estrogen on these signals in the migraine.Biology open · 2017Article
- Association of serum levels of intercellular adhesion molecule-1 and interleukin-6 with migraine.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2015Article
- Modelling headache and migraine and its pharmacological manipulation.British journal of pharmacology · 2014Review
- Gabapentin inhibits central sensitization during migraine.Neural regeneration research · 2013Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
There is convincing evidence that nitric oxide (NO) may be a causative factor in the pathogenesis of migraine. We investigated the consequences of NO donors' administration on meningeal processes related to the development of migraine pain in an animal model of meningeal nociception. The administration in mice of the NO donors nitroglycerin (GTN) and sodium nitroprusside (SNP) produced a delayed meningeal upregulation of interleukin-1ß and inducible NO synthase. A thermal allodynia and hyperalgesia devoid of side effects was produced 1 to 4 h after administration. To clarify the cellular pathways modulated by GTN and SNP, we examined the expression of cellular factors involved in pain modulation, such as protein kinase C (PKC) and its downstream effectors. Western blotting experiments showed an upregulation and increased phosphorylation of PKCγ and PKCε within dura mater after NO donors' administration. A dramatic PKC-dependent increase of the phosphorylation of cyclic AMP response element binding protein (CREB) and signal transducer and activator of transcription (STAT)-1 was observed, along with an activation of the nuclear factor-κB (NF-κB) pathway, as reflected by a reduction of the inhibitory protein-κ-Bα (IκBα). Furthermore, the PKC blocker, Calphostin C, prevented the GTN and SNP-induced pain hypersensitivity. These results suggest the relevance of the PKC-mediated pathway in the induction of meningeal nociception and might help clarify the etiopathology of migraines. We can suggest PKC as a new target for migraine pain.
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