ArticleThe Journal of physiology2004
Intracellular Na+ inhibits voltage-dependent N-type Ca2+ channels by a G protein betagamma subunit-dependent mechanism.
Article in The Journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- The modulation of emotional and social behaviors by oxytocin signaling in limbic network.Frontiers in molecular neuroscience · 2022Review
- Sodium Fluctuations in Astroglia and Their Potential Impact on Astrocyte Function.Frontiers in physiology · 2020Review
- Effect of Electroacupuncture onScientific reports · 2018Article
- Physiology of Astroglia.Physiological reviews · 2018Review
- Article
- The Epithelial Sodium Channel and the Processes of Wound Healing.BioMed research international · 2016Review
- Regulation of synaptic transmission at the photoreceptor terminal: a novel role for the cation-chloride co-transporter NKCC1.The Journal of physiology · 2013Article
- Stargazin modulates neuronal voltage-dependent Ca(2+) channel Ca(v)2.2 by a Gbetagamma-dependent mechanism.The Journal of biological chemistry · 2010Article
- Regulation of podosome formation in macrophages by a splice variant of the sodium channel SCN8A.The Journal of biological chemistry · 2009Article
- Expanding the neuron's calcium signaling repertoire: intracellular calcium release via voltage-induced PLC and IP3R activation.PLoS biology · 2007Article
- Dominant role of betagamma subunits of G-proteins in oxytocin-evoked burst firing.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
- Intracellular monovalent ions as second messengers.The Journal of membrane biology · 2006Review
- The Role of Intracellular Sodium in the Regulation of NMDA-Receptor-Mediated Channel Activity and Toxicity.Molecular neurobiology · 2006Review
- Kinetic modeling of Na(+)-induced, Gbetagamma-dependent activation of G protein-gated K(+) channels.Journal of molecular neuroscience : MN · 2005Article
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Authors and funding
7 authors.
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Abstract
N-type voltage-dependent Ca(2+) channels (N-VDCCs) play important roles in neurotransmitter release and certain postsynaptic phenomena. These channels are modulated by a number of intracellular factors, notably by Gbetagamma subunits of G proteins, which inhibit N-VDCCs in a voltage-dependent (VD) manner. Here we show that an increase in intracellular Na(+) concentration inhibits N-VDCCs in hippocampal pyramidal neurones and in Xenopus oocytes. In acutely dissociated hippocampal neurones, Ba(2+) current via N-VDCCs was inhibited by Na(+) influx caused by the activation of NMDA receptor channels. In Xenopus oocytes expressing N-VDCCs, Ba(2+) currents were inhibited by Na(+) influx and enhanced by depletion of Na(+), after incubation in a Na(+)-free extracellular solution. The Na(+)-induced inhibition was accompanied by the development of VD facilitation, a hallmark of a Gbetagamma-dependent process. Na(+)-induced regulation of N-VDCCs is Gbetagamma dependent, as suggested by the blocking of Na(+) effects by Gbetagamma scavengers and by excess Gbetagamma, and may be mediated by the Na(+)-induced dissociation of Galphabetagamma heterotrimers. N-VDCCs may be novel effectors of Na(+)ion, regulated by the Na(+) concentration via Gbetagamma.
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