ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Calcium-dependent isoforms of protein kinase C mediate glycine-induced synaptic enhancement at the calyx of Held.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Neurotensin speeds inhibition of dopamine neurons through temporal modulation of GABANeuropharmacology · 2018Article
- Biphasic modulation of parallel fibre synaptic transmission by co-activation of presynaptic GABAA and GABAB receptors in mice.The Journal of physiology · 2016Article
- Molecular Machines Regulating the Release Probability of Synaptic Vesicles at the Active Zone.Frontiers in synaptic neuroscience · 2016Review
- Cocaine-seeking is associated with PKC-dependent reduction of excitatory signaling in accumbens shell D2 dopamine receptor-expressing neurons.Neuropharmacology · 2015Article
- Platelet Activating Factor Enhances Synaptic Vesicle Exocytosis Via PKC, Elevated Intracellular Calcium, and Modulation of Synapsin 1 Dynamics and Phosphorylation.Frontiers in cellular neuroscience · 2015Article
- Synaptic gain-of-function effects of mutant Cav2.1 channels in a mouse model of familial hemiplegic migraine are due to increased basal [Ca2+]i.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Calcium-dependent PKC isoforms have specialized roles in short-term synaptic plasticity.Neuron · 2014Article
- Distribution of glycine receptors on the surface of the mature calyx of Held nerve terminal.Frontiers in neural circuits · 2014Article
- Reelin mobilizes a VAMP7-dependent synaptic vesicle pool and selectively augments spontaneous neurotransmission.Neuron · 2013Article
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5 authors.
Funding
Abstract
Depolarization of presynaptic terminals that arises from activation of presynaptic ionotropic receptors, or somatic depolarization, can enhance neurotransmitter release; however, the molecular mechanisms mediating this plasticity are not known. Here we investigate the mechanism of this enhancement at the calyx of Held synapse, in which presynaptic glycine receptors depolarize presynaptic terminals, elevate resting calcium levels, and potentiate release. Using knock-out mice of the calcium-sensitive PKC isoforms (PKC(Ca)), we find that enhancement of evoked but not spontaneous synaptic transmission by glycine is mediated primarily by PKC(Ca). Measurements of calcium at the calyx of Held indicate that deficits in synaptic modulation in PKC(Ca) knock-out mice occur downstream of presynaptic calcium increases. Glycine enhances synaptic transmission primarily by increasing the effective size of the pool of readily releasable vesicles. Our results reveal that PKC(Ca) can enhance evoked neurotransmitter release in response to calcium increases caused by small presynaptic depolarizations.
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