ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007
Presynaptic Ca2+/calmodulin-dependent protein kinase II modulates neurotransmitter release by activating BK channels at Caenorhabditis elegans neuromuscular junction.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 74 citations in OpenAlex.
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- Shank promotes action potential repolarization by recruiting BK channels to calcium microdomains.eLife · 2022Article
- The Calcium/Calmodulin-Dependent Kinases II and IV as Therapeutic Targets in Neurodegenerative and Neuropsychiatric Disorders.International journal of molecular sciences · 2021Review
- CaMKII binding to GluN2B at S1303 has no role in acute or inflammatory pain.Brain research · 2021Article
- The Role of Calmodulin vs. Synaptotagmin in Exocytosis.Frontiers in molecular neuroscience · 2021Review
- Coordination between Calcium/Calmodulin-Dependent Protein Kinase II and Neuronal Nitric Oxide Synthase in Neurons.International journal of molecular sciences · 2020Review
- Slo2 potassium channel function depends on RNA editing-regulated expression of a SCYL1 protein.eLife · 2020Article
- Increased calcium-mediated cerebral processes after peripheral injury: possible role of the brain in complex regional pain syndrome.The Korean journal of pain · 2020Article
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- Article
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4 authors at 1 institution in 1 country.
Funding
Abstract
Although Ca2+/calmodulin-dependent protein kinase II (CaMKII) is enriched at the presynaptic nerve terminal, its role in neurotransmitter release is poorly defined. We assessed the function of presynaptic CaMKII in neurotransmitter release and tested the hypothesis that BK channel is a mediator of presynaptic CaMKII function by analyzing miniature and evoked postsynaptic currents at the Caenorhabditis elegans neuromuscular junction. Both loss-of-function (lf) and gain-of-function (gf) of unc-43, the gene encoding CaMKII, inhibited neurotransmitter release. The inhibitory effect of unc-43(gf) was reversed by mutation or blockade of the BK channel SLO-1. SLO-1 expressed in Xenopus oocytes could be activated by recombinant rat alpha-CaMKII, and this effect of CaMKII was abolished by mutating a threonine residue (T425) at a consensus CaMKII phosphorylation site in the first RCK (regulator of conductance for K+) domain of the channel. Expression of slo-1(T425A) in neurons antagonized the inhibitory effect of unc-43(gf) on neurotransmitter release as slo-1(lf) did. The inhibitory effect of unc-43(gf) was not reversed by unc-103(lf), dgk-1(lf), or eat-16(lf), which reportedly suppress behavioral phenotypes of unc-43(gf). These observations suggest that presynaptic CaMKII is a bidirectional modulator of neurotransmitter release, presumably by phosphorylating different molecular targets, and that its negative modulatory effect on the release is mainly mediated by SLO-1 activation.
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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.