ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2022
HCN2 Ion Channels Drive Pain in Rodent Models of Migraine.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Sildenafil provokes headache but not migraine in men with migraine without aura: a randomized, placebo-controlled crossover trial.The journal of headache and pain · 2026Trial
- Sex-dependent central amygdala physiology after supradural CGRP exposure is associated with migraine-like behaviors.The journal of headache and pain · 2026Article
- MMP1 and PRSS23 induce PARCommunications biology · 2026Article
- Dual block evidence of the effects of topiramate, a sulfamate-substituted monosaccharide, on voltage-gated sodium current and hyperpolarization-activated cation current.BMC pharmacology & toxicology · 2025Article
- Impaired touch sensation on hairy skin in HCN3-deficient mice.Frontiers in neuroscience · 2025Article
- De Novo Genome Assemblies From Two Indigenous Americans from Arizona Identify New Polymorphisms in Non-Reference Sequences.Genome biology and evolution · 2024Article
- Opioid-Induced Hyperalgesia and Tolerance Are Driven by HCN Ion Channels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Migraine is believed to be initiated by neuronal activity in the CNS, that triggers excitation of nociceptive trigeminal ganglion (TG) nerve fibers innervating the meninges and thus causes a unilateral throbbing headache. Drugs that precipitate or potentiate migraine are known to elevate intracellular levels of the cyclic nucleotides cAMP or cGMP, while anti-migraine treatments couple to signaling pathways that reduce cAMP or cGMP, suggesting an involvement of these cyclic nucleotides in migraine. Members of the HCN ion channel family are activated by direct binding of cAMP or cGMP, suggesting in turn that a member of this family may be a critical trigger of migraine. Here, we show that pharmacological block or targeted genetic deletion of HCN2 abolishes migraine-like pain in three rodent migraine models (in both sexes). Induction of migraine-like pain in these models triggered expression of the protein C-FOS, a marker of neuronal activity, in neurons of the trigeminocervical complex (TCC), where TG neurons terminate, and C-FOS expression was reversed by peripheral HCN2 inhibition. HCN2 block
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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.