ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006
Physiological activity depresses synaptic function through an effect on vesicle priming.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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38 citing papers in PubMed.
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- GABAeLife · 2023Article
- Axonal α7* nicotinic acetylcholine receptors modulate glutamatergic signaling and synaptic vesicle organization in ventral hippocampal projections.Frontiers in neural circuits · 2022Article
- The soluble neurexin-1β ectodomain causes calcium influx and augments dendritic outgrowth and synaptic transmission.Scientific reports · 2020Article
- Homeostatic control of Drosophila neuromuscular junction function.Synapse (New York, N.Y.) · 2020Review
- Homeostatic Presynaptic Plasticity Is Specifically Regulated by P/Q-type CaCell reports · 2017Article
- Presynaptic inhibition upon CB1 or mGlu2/3 receptor activation requires ERK/MAPK phosphorylation of Munc18-1.The EMBO journal · 2016Article
- Fluorescent false neurotransmitter reveals functionally silent dopamine vesicle clusters in the striatum.Nature neuroscience · 2016Article
- Regulation of density of functional presynaptic terminals by local energy supply.Molecular brain · 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
- Depression biased non-Hebbian spike-timing-dependent synaptic plasticity in the rat subiculum.The Journal of physiology · 2014Article
- Innervation by a GABAergic neuron depresses spontaneous release in glutamatergic neurons and unveils the clamping phenotype of synaptotagmin-1.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Cannabinoid type 1 receptors transiently silence glutamatergic nerve terminals of cultured cerebellar granule cells.PloS one · 2014Article
- Molecular mechanisms driving homeostatic plasticity of neurotransmitter release.Frontiers in cellular neuroscience · 2013Review
- Short-term synaptic plasticity compensates for variability in number of motor neurons at a neuromuscular junction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Astrocyte-derived thrombospondins mediate the development of hippocampal presynaptic plasticity in vitro.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- The presynaptic active zone protein RIM1α controls epileptogenesis following status epilepticus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Presynaptically silent synapses: dormancy and awakening of presynaptic vesicle release.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2012Review
- Differential requirement for protein synthesis in presynaptic unmuting and muting in hippocampal glutamate terminals.PloS one · 2012Article
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Abstract
Neurons engage compensatory, homeostatic synaptic changes to maintain their overall firing rate. We examined the induction and expression of a persistent presynaptic adaptation. We explored the effect of mild extracellular potassium elevation to increase hippocampal pyramidal neuron spiking over a physiological range. With several days of mild depolarization, glutamate release adapted, as revealed by an increased mismatch between the number of active, FM1-43-positive, glutamatergic synapses and the total number of synapses defined by vesicular glutamate transporter-1 antibody staining. Surprisingly, the adaptation of glutamate terminals was all-or-none; recycling vesicle pool size at remaining active synapses was not significantly altered by the adaptation. Tetrodotoxin (TTX), but not postsynaptic receptor blockade, reversed depolarization-induced adaptation, and TTX added to normal incubation medium increased the number of active synapses, suggesting that normal spiking activity sustains a steady-state percentage of inactive terminals. Chronic mild depolarization depressed EPSCs and decreased the size of the readily releasable pool of vesicles (RRP). Several hours of 10 Hz electrical stimulation also depressed the RRP size, confirming that spiking alone induces adaptation and that strong stimulation induces more rapid presynaptic adaptation. Despite the importance of RRP alteration to the adaptation, ultrastructural experiments revealed no changes in docked or total synaptic vesicle numbers. Furthermore, alpha-latrotoxin induced vesicle release at adapted synapses, consistent with the idea that adaptation resulted from changes in vesicle priming. These results show that glutamatergic neurotransmission persistently adapts to changes in electrical activity over a wide physiological range.
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