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NaN/Nav1.9: a sodium channel with unique properties

Trends in Neurosciences, 2002
The Na(v)1.9 Na(+) channel (also known as NaN) is preferentially expressed in nociceptive neurons of the dorsal root ganglia (DRG) and trigeminal ganglia. Na(v)1.9 produces a persistent, tetrodotoxin-resistant current with wide overlap between activation and steady-state inactivation, and appears to modulate resting potential and to amplify small ...
Sulayman, Dib-Hajj   +3 more
openaire   +2 more sources

NaV1.9: a sodium channel linked to human pain

Nature Reviews Neuroscience, 2015
The voltage-gated sodium channel Na(V)1.9 is preferentially expressed in nociceptors and has been shown in rodent models to have a major role in inflammatory and neuropathic pain. These studies suggest that by selectively targeting Na(V)1.9, it might be possible to ameliorate pain without inducing adverse CNS side effects such as sedation, confusion ...
Sulayman D, Dib-Hajj   +2 more
openaire   +2 more sources

Heterologous expression of NaV1.9 chimeras in various cell systems

Pflügers Archiv - European Journal of Physiology, 2015
SCN11A encodes the voltage-gated sodium channel NaV1.9, which deviates most strongly from the other eight NaV channels expressed in mammals. It is characterized by resistance to the prototypic NaV channel blocker tetrodotoxin and exhibits slow activation and inactivation gating.
R Oliver, Goral   +3 more
openaire   +2 more sources

Na+ channel Nav1.9: in search of a gating mechanism

Trends in Neurosciences, 2003
Voltage-gated Na(+) channels play key roles in generating and propagating action potentials. Their gating is believed to rely exclusively on changes in membrane potential. However, recent data from Blum, Kafitz and Konnerth provide direct evidence that the opening of Na(v)1.9, a member of the voltage-gated Na(+) channel family, is mediated by ligand ...
Patrick, Delmas, Bertrand, Coste
openaire   +2 more sources

Nav1.9 expression in magnocellular neurosecretory cells of supraoptic nucleus

Experimental Neurology, 2014
Osmoregulation in mammals is tightly controlled by the release of vasopressin and oxytocin from magnocellular neurosecretory cells (MSC) of the supraoptic nucleus (SON). The release of vasopressin and oxytocin in the neurohypophysis by axons of MSC is regulated by bursting activity of these neurons, which is influenced by multiple sources, including ...
J A, Black   +3 more
openaire   +2 more sources

Expression of Nav1.9 Channels in Human Dental Pulp and Trigeminal Ganglion

Journal of Endodontics, 2007
There is a higher incidence of local anesthetic failure in endodontic patients experiencing pulpal hyperalgesia. Up-regulation of Nav1.9, a voltage-gated sodium channel isoform, might play a key role in local anesthetic failure because Nav1.9 channels increase neuronal excitability and have low sensitivity to blockade by local anesthetics ...
Jason E, Wells   +3 more
openaire   +2 more sources

Modulations of Nav1.8 and Nav1.9 Channels in Monosodium Urate–Induced Gouty Arthritis in Mice

Inflammation, 2021
The aim of the present study was to observe the changes of TTX-R, Nav1.8, and Nav1.9 Na+ currents in MSU-induced gouty arthritis mice, and to explore the possibility of Nav1.8 and Nav1.9 channels as potential targets for gout pain treatment. Acute gouty arthritis was induced by monosodium urate (MSU) in mice.
Jie Qiu   +4 more
openaire   +2 more sources

Persistent modification of Nav1.9 following chronic exposure to insecticides and pyridostigmine bromide

Toxicology and Applied Pharmacology, 2014
Many veterans of the 1991 Gulf War (GW) returned from that conflict with a widespread chronic pain affecting deep tissues. Recently, we have shown that a 60day exposure to the insecticides permethrin, chlorpyrifos, and pyridostigmine bromide (NTPB) had little influence on nociceptor action potential forming Nav1.8, but increased Kv7 mediated inhibitory
Thomas J, Nutter, Brian Y, Cooper
openaire   +2 more sources

Reduced excitability and impaired nociception in peripheral unmyelinated fibers from Nav1.9-null mice

Pain, 2016
AbstractThe upregulation of the tetrodotoxin-resistant voltage-gated sodium channel NaV1.9 has previously been associated with inflammatory hyperalgesia. Na1.9 knockout (KO) mice, however, did not seem insensitive in conventional tests of acute nociception.
Tal, Hoffmann   +5 more
openaire   +2 more sources

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