ArticleBrain research2007
Brevetoxin-induced phosphorylation of Pyk2 and Src in murine neocortical neurons involves distinct signaling pathways.
Article in Brain research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 18 citations in OpenAlex.
- The Non-receptor Tyrosine Kinase Pyk2 in Brain Function and Neurological and Psychiatric Diseases.Frontiers in synaptic neuroscience · 2021Review
- Src family tyrosine kinase inhibitors suppress Nav1.1 expression in cultured rat spiral ganglion neurons.Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology · 2016Article
- Early mitochondrial abnormalities in hippocampal neurons cultured from Fmr1 pre-mutation mouse model.Journal of neurochemistry · 2012Article
- Clustered burst firing in FMR1 premutation hippocampal neurons: amelioration with allopregnanolone.Human molecular genetics · 2012Article
- Mechanisms of pyrethroid insecticide-induced stimulation of calcium influx in neocortical neurons.The Journal of pharmacology and experimental therapeutics · 2011Article
- Involvement of caspase activation in azaspiracid-induced neurotoxicity in neocortical neurons.Toxicological sciences : an official journal of the Society of Toxicology · 2010Article
- Hoiamide a, a sodium channel activator of unusual architecture from a consortium of two papua new Guinea cyanobacteria.Chemistry & biology · 2009Article
- Sodium channel activation augments NMDA receptor function and promotes neurite outgrowth in immature cerebrocortical neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Brevetoxins (PbTx-1 to PbTx-10) are potent lipid soluble polyether neurotoxins produced by the marine dinoflagellate Karenia brevis. Brevetoxins bind to site 5 of the alpha-subunit of voltage-gated sodium channels (VGSCs) and augment Na(+) influx. In neocortical neurons brevetoxins elevate intracellular Ca(2+) and augment NMDA receptor signaling. In this study, we explored the effects of PbTx-2 on Pyk2 and Src activation in neocortical neurons. We found that both Pyk2 and Src were activated following PbTx-2 exposure. PbTx-2-induced Pyk2 Tyr402 phosphorylation was dependent on elevation of Ca(2+) influx through NMDA receptors. Moreover, Pyk2 Tyr402 phosphorylation was also found to require PKC activation inasmuch as RO-31-8425 and GF 109203x both attenuated the response. In contrast, PbTx-2-induced Src Tyr416 phosphorylation involved a Gq-coupled receptor inasmuch as U73122, a specific PLC inhibitor, abolished the response. This Gq-coupled receptor appears to be mGluR 5. The PKCdelta inhibitor rottlerin abolished PbTx-2-induced Src activation demonstrating that this isoform of PKC is involved in the activation of Src by PbTx-2. Considered together these data suggest that although activation of neuronal Pyk2 and Src result from PbTx-2 stimulation of VGSC, engagement of these two non-receptor tyrosine kinases involves distinct signaling pathways.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.