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- W3150996800 abstract "Amitriptyline (AMI), a tricyclic antidepressant, has been widely used to prevent migraine attacks and alleviate other various chronic pain, but the underlying mechanism remains unclear. Accumulated evidence sug- gests that the efficacy of AMI is related to the blockade of voltage-gated sodium channels. The aim of the present study was to investigate the effect of AMI on Nav1.8 currents in nociceptive trigeminal neurons and trigemino- vascular nociception induced by electrical stimulation of the dura mater surrounding the superior sagittal sinus (SSS) in rats, as in the animal model of vascular headaches such as migraines. Using a whole-cell voltage recording tech- nique, we showed that Nav1.8 currents were blocked by AMI in a concentration-dependent manner, with an IC50 value of 6.82 lM in acute isolated trigeminal ganglion neurons of the rats. AMI caused a hyperpolarizing shift in the voltage-dependent activation and steady-state inacti- vation and significantly blocked in a use-dependent manner and slowed the recovery from the inactivation of Nav1.8 currents. In addition, the systemic administration of AMI and A-803467 (a selective Nav1.8 channel blocker) potently alleviated the nociceptive behaviors (head flicks and grooming) induced by the electrical stimulation of the dura mater surrounding the SSS. Taken together, our data suggest that Nav1.8 currents in nociceptive trigeminal neurons are blocked by AMI through modulating the activation and inactivation kinetics, which may contribute to anti-nociceptive effect of AMI in animal models of migraines." @default.
- W3150996800 created "2021-04-13" @default.
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- W3150996800 date "2014-01-01" @default.
- W3150996800 modified "2023-09-26" @default.
- W3150996800 title "Blockade of Na v 1.8 Currents in Nociceptive Trigeminal Neurons Contributes to Anti-trigeminovascular Nociceptive Effect of Amitriptyline" @default.
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