Nicotine‐induced phosphorylation of ERK in mouse primary cortical neurons: evidence for involvement of glutamatergic signaling and CaMKII
Steiner RC, Heath CJ, Picciotto MR. Nicotine‐induced phosphorylation of ERK in mouse primary cortical neurons: evidence for involvement of glutamatergic signaling and CaMKII. Journal Of Neurochemistry 2007, 103: 666-678. PMID: 17666046, DOI: 10.1111/j.1471-4159.2007.04799.x.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBlotting, WesternCalcium-Calmodulin-Dependent Protein Kinase Type 2Cells, CulturedCerebral CortexCulture MediaDose-Response Relationship, DrugExtracellular Signal-Regulated MAP KinasesFemaleGlutamic AcidIndicators and ReagentsMiceMice, Inbred C57BLMice, KnockoutNeuronsNicotineNicotinic AgonistsPhosphorylationPregnancyReceptors, GlutamateReceptors, NicotinicReverse Transcriptase Polymerase Chain ReactionSignal TransductionSynaptic TransmissionConceptsNicotine-induced ERK phosphorylationExtracellular signal-regulated kinaseERK phosphorylationCAMP-dependent protein kinaseCalmodulin-dependent protein kinase IICalcium/calmodulin-dependent protein kinase IINicotinic acetylcholine receptor inhibitorNicotine-induced phosphorylationSignal-regulated kinaseCortical neuronsProtein kinase IIProtein kinase CMouse primary cortical neuronsKinase II activityAlpha3/beta4Calmodulin-dependent protein kinase II activityGlutamatergic signalingProtein kinaseVoltage-gated sodium channelsKinase IICultured mouse cortical neuronsKinase CCalcium/calmodulin-dependent protein kinase II activityPhosphorylationL-type voltage-gated calcium channels