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Foxo1 selectively regulates static mechanical pain by interacting with Nav1.7

Pain, 2020
Abstract Mechanical allodynia is a debilitating condition for millions of patients with chronic pain. Mechanical allodynia can manifest in distinct forms, including brush-evoked dynamic and filament-evoked static allodynia. In the nervous system, the forkhead protein Foxo1 plays a critical role in neuronal structures and functions.
Xiao-Long, Zhang   +9 more
openaire   +2 more sources

Differential modulation of Nav1.7 and Nav1.8 channels by antidepressant drugs

European Journal of Pharmacology, 2015
Antidepressant drugs of the SSRI family are used as a third-line treatment for neuropathic pain. In contrast MAOi antidepressants, that also increase extracellular serotonin bioavailability have little or no effects on this condition. In addition to their action of the serotonin transporter, some SSRI have been shown to inhibit voltage gated sodium ...
Olivier, Thériault   +3 more
openaire   +2 more sources

Neuropathische Schmerzen durch Nav1.7-Mutationen

Der Nervenarzt, 2013
K. Doppler, C. Sommer
openaire   +1 more source

NaV1.7 and pain: contribution of peripheral nerves

2020
The sodium channel NaV1.7 contributes to action potential (AP) generation and propagation. Loss-of-function mutations in patients lead to congenital indifference to pain, though it remains unclear where on the way from sensory terminals to central nervous system the signalling is disrupted.
openaire   +1 more source

The link between an Nav1.7 mutation and erythromelalgia

2018
The landmark paper discussed in this chapter is ‘Gain-of-function mutation in Nav1.7 in familial erythromelalgia induces bursting of sensory neurons’, published by Dib-Hajj et al. in 2005. The voltage-dependent sodium channels Nav1.7, Nav1.8, and Nav1.9 have a restricted pattern of expression in sensory neurons in the periphery and are concentrated in ...
openaire   +1 more source

156 NAV1.7 POLYMORPHISMS AND INFLAMMATORY PAIN

European Journal of Pain, 2006
openaire   +1 more source

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