ArticleMolecular pain2013
Effect of amitriptyline on tetrodotoxin-resistant Nav1.9 currents in nociceptive trigeminal neurons.
Article in Molecular pain, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 32 citations in OpenAlex.
- Discovery of E0199: A novel compound targeting both peripheral NaJournal of pharmaceutical analysis · 2025Article
- Effect of topical application of amitriptyline and nortriptyline on irreversible pulpitis pain in teeth with failed pulpal anesthesia after a successful inferior alveolar nerve block: A randomized clinical trial.Dental research journal · 2024Article
- Isoliquiritigenin, an active ingredient of Glycyrrhiza, elicits antinociceptive effects via inhibition of NaNaunyn-Schmiedeberg's archives of pharmacology · 2021Article
- Sodium Channel Blockers Modulate Abnormal Activity of Regenerating Nociceptive Corneal Nerves After Surgical Lesion.Investigative ophthalmology & visual science · 2021Article
- Postherpetic Neuralgia: Current Evidence on the Topical Film-Forming Spray with Bupivacaine Hydrochloride and a Review of Available Treatment Strategies.Advances in therapy · 2020Review
- Depression and anxiety behaviour in a rat model of chronic migraine.The journal of headache and pain · 2017Article
- Pain transduction: a pharmacologic perspective.Expert review of clinical pharmacology · 2016Review
- Update of chronic tension-type headache.Current pain and headache reports · 2015Review
- Blockade of Nav1.8 currents in nociceptive trigeminal neurons contributes to anti-trigeminovascular nociceptive effect of amitriptyline.Neuromolecular medicine · 2014Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAmitriptyline (AMI) is tricyclic antidepressant that has been widely used to manage various chronic pains such as migraines. Its efficacy is attributed to its blockade of voltage-gated sodium channels (VGSCs). However, the effects of AMI on the tetrodotoxin-resistant (TTX-r) sodium channel Nav1.9 currents have been unclear to present.
resultsUsing a whole-cell patch clamp technique, this study showed that AMI efficiently inhibited Nav1.9 currents in a concentration-dependent manner and had an IC50 of 15.16 μM in acute isolated trigeminal ganglion (TG) neurons of the rats. 10 μM AMI significantly shifted the steady-state inactivation of Nav1.9 channels in the hyperpolarizing direction without affecting voltage-dependent activation. Surprisingly, neither 10 nor 50 μM AMI caused a use-dependent blockade of Nav1.9 currents elicited by 60 pulses at 1 Hz.
conclusionThese data suggest that AMI is a state-selective blocker of Nav1.9 channels in rat nociceptive trigeminal neurons, which likely contributes to the efficacy of AMI in treating various pains, including migraines.
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