FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2038862511> ?p ?o ?g. }

• W2038862511 endingPage "22923" @default.
• W2038862511 startingPage "22913" @default.
• W2038862511 abstract "Nociceptive dorsal root ganglion (DRG) neurons express tetrodotoxin-sensitive (TTX-S) and -resistant (TTX-R) Na+ current (INa) mediated by voltage-gated Na+ channels (VGSCs). In nociceptive DRG neurons, VGSC β2 subunits, encoded by Scn2b, selectively regulate TTX-S α subunit mRNA and protein expression, ultimately resulting in changes in pain sensitivity. We hypothesized that VGSCs in nociceptive DRG neurons may also be regulated by β1 subunits, encoded by Scn1b. Scn1b null mice are models of Dravet Syndrome, a severe pediatric encephalopathy. Many physiological effects of Scn1b deletion on CNS neurons have been described. In contrast, little is known about the role of Scn1b in peripheral neurons in vivo. Here we demonstrate that Scn1b null DRG neurons exhibit a depolarizing shift in the voltage dependence of TTX-S INa inactivation, reduced persistent TTX-R INa, a prolonged rate of recovery of TTX-R INa from inactivation, and reduced cell surface expression of Nav1.9 compared with their WT littermates. Investigation of action potential firing shows that Scn1b null DRG neurons are hyperexcitable compared with WT. Consistent with this, transient outward K+ current (Ito) is significantly reduced in null DRG neurons. We conclude that Scn1b regulates the electrical excitability of nociceptive DRG neurons in vivo by modulating both INa and IK. Nociceptive dorsal root ganglion (DRG) neurons express tetrodotoxin-sensitive (TTX-S) and -resistant (TTX-R) Na+ current (INa) mediated by voltage-gated Na+ channels (VGSCs). In nociceptive DRG neurons, VGSC β2 subunits, encoded by Scn2b, selectively regulate TTX-S α subunit mRNA and protein expression, ultimately resulting in changes in pain sensitivity. We hypothesized that VGSCs in nociceptive DRG neurons may also be regulated by β1 subunits, encoded by Scn1b. Scn1b null mice are models of Dravet Syndrome, a severe pediatric encephalopathy. Many physiological effects of Scn1b deletion on CNS neurons have been described. In contrast, little is known about the role of Scn1b in peripheral neurons in vivo. Here we demonstrate that Scn1b null DRG neurons exhibit a depolarizing shift in the voltage dependence of TTX-S INa inactivation, reduced persistent TTX-R INa, a prolonged rate of recovery of TTX-R INa from inactivation, and reduced cell surface expression of Nav1.9 compared with their WT littermates. Investigation of action potential firing shows that Scn1b null DRG neurons are hyperexcitable compared with WT. Consistent with this, transient outward K+ current (Ito) is significantly reduced in null DRG neurons. We conclude that Scn1b regulates the electrical excitability of nociceptive DRG neurons in vivo by modulating both INa and IK." @default.
• W2038862511 created "2016-06-24" @default.
• W2038862511 creator A5008675517 @default.
• W2038862511 creator A5023299117 @default.
• W2038862511 creator A5058935937 @default.
• W2038862511 creator A5088221049 @default.
• W2038862511 date "2011-07-01" @default.
• W2038862511 modified "2023-09-27" @default.
• W2038862511 title "Na+ Channel Scn1b Gene Regulates Dorsal Root Ganglion Nociceptor Excitability in Vivo" @default.
• W2038862511 cites W1497499431 @default.
• W2038862511 cites W163561699 @default.
• W2038862511 cites W1844967107 @default.
• W2038862511 cites W1965950761 @default.
• W2038862511 cites W1970739996 @default.
• W2038862511 cites W1971045205 @default.
• W2038862511 cites W1972220619 @default.
• W2038862511 cites W1982950553 @default.
• W2038862511 cites W1989812125 @default.
• W2038862511 cites W1995100344 @default.
• W2038862511 cites W1997480818 @default.
• W2038862511 cites W2000574545 @default.
• W2038862511 cites W2000702493 @default.
• W2038862511 cites W2024390133 @default.
• W2038862511 cites W2035451747 @default.
• W2038862511 cites W2035500508 @default.
• W2038862511 cites W2037170098 @default.
• W2038862511 cites W2046511019 @default.
• W2038862511 cites W2048832552 @default.
• W2038862511 cites W2054036590 @default.
• W2038862511 cites W2056531158 @default.
• W2038862511 cites W2058501926 @default.
• W2038862511 cites W2062176870 @default.
• W2038862511 cites W2068216219 @default.
• W2038862511 cites W2082952610 @default.
• W2038862511 cites W2085957678 @default.
• W2038862511 cites W2088094161 @default.
• W2038862511 cites W2092933077 @default.
• W2038862511 cites W2140695849 @default.
• W2038862511 cites W2145540995 @default.
• W2038862511 cites W2147699570 @default.
• W2038862511 cites W2154917087 @default.
• W2038862511 cites W2162723169 @default.
• W2038862511 cites W2172027567 @default.
• W2038862511 cites W2331570632 @default.
• W2038862511 doi "https://doi.org/10.1074/jbc.m111.242370" @default.
• W2038862511 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3123059" @default.
• W2038862511 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21555511" @default.
• W2038862511 hasPublicationYear "2011" @default.
• W2038862511 type Work @default.
• W2038862511 sameAs 2038862511 @default.
• W2038862511 citedByCount "41" @default.
• W2038862511 countsByYear W20388625112012 @default.
• W2038862511 countsByYear W20388625112013 @default.
• W2038862511 countsByYear W20388625112014 @default.
• W2038862511 countsByYear W20388625112015 @default.
• W2038862511 countsByYear W20388625112016 @default.
• W2038862511 countsByYear W20388625112017 @default.
• W2038862511 countsByYear W20388625112018 @default.
• W2038862511 countsByYear W20388625112019 @default.
• W2038862511 countsByYear W20388625112020 @default.
• W2038862511 countsByYear W20388625112021 @default.
• W2038862511 countsByYear W20388625112022 @default.
• W2038862511 countsByYear W20388625112023 @default.
• W2038862511 crossrefType "journal-article" @default.
• W2038862511 hasAuthorship W2038862511A5008675517 @default.
• W2038862511 hasAuthorship W2038862511A5023299117 @default.
• W2038862511 hasAuthorship W2038862511A5058935937 @default.
• W2038862511 hasAuthorship W2038862511A5088221049 @default.
• W2038862511 hasBestOaLocation W20388625111 @default.
• W2038862511 hasConcept C126322002 @default.
• W2038862511 hasConcept C134018914 @default.
• W2038862511 hasConcept C15490471 @default.
• W2038862511 hasConcept C169760540 @default.
• W2038862511 hasConcept C170493617 @default.
• W2038862511 hasConcept C172659308 @default.
• W2038862511 hasConcept C178790620 @default.
• W2038862511 hasConcept C185592680 @default.
• W2038862511 hasConcept C2776281502 @default.
• W2038862511 hasConcept C2776741303 @default.
• W2038862511 hasConcept C2777589315 @default.
• W2038862511 hasConcept C50952357 @default.
• W2038862511 hasConcept C537181965 @default.
• W2038862511 hasConcept C71924100 @default.
• W2038862511 hasConcept C86803240 @default.
• W2038862511 hasConcept C94487597 @default.
• W2038862511 hasConcept C95444343 @default.
• W2038862511 hasConceptScore W2038862511C126322002 @default.
• W2038862511 hasConceptScore W2038862511C134018914 @default.
• W2038862511 hasConceptScore W2038862511C15490471 @default.
• W2038862511 hasConceptScore W2038862511C169760540 @default.
• W2038862511 hasConceptScore W2038862511C170493617 @default.
• W2038862511 hasConceptScore W2038862511C172659308 @default.
• W2038862511 hasConceptScore W2038862511C178790620 @default.
• W2038862511 hasConceptScore W2038862511C185592680 @default.
• W2038862511 hasConceptScore W2038862511C2776281502 @default.
• W2038862511 hasConceptScore W2038862511C2776741303 @default.
• W2038862511 hasConceptScore W2038862511C2777589315 @default.
• W2038862511 hasConceptScore W2038862511C50952357 @default.

• next