ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2002
Persistent, exocytosis-independent silencing of release sites underlies homosynaptic depression at sensory synapses in Aplysia.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
16 citing papers in PubMed, 30 citations in OpenAlex.
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- Anxiety and initial value dependence in startle habituation.Psychophysiology · 2022Article
- Excitatory postsynaptic calcium transients atLearning & memory (Cold Spring Harbor, N.Y.) · 2021Article
- Persistent Associative Plasticity at an Identified Synapse Underlying Classical Conditioning Becomes Labile with Short-Term Homosynaptic Activation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Developmental Function of the PHR Protein RPM-1 Is Required for Learning in Caenorhabditis elegans.G3 (Bethesda, Md.) · 2015Article
- Persistent long-term facilitation at an identified synapse becomes labile with activation of short-term heterosynaptic plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Release properties of individual presynaptic boutons expressed during homosynaptic depression and heterosynaptic facilitation of the Aplysia sensorimotor synapse.Frontiers in cellular neuroscience · 2013Article
- Protein kinase C acts as a molecular detector of firing patterns to mediate sensory gating in Aplysia.Nature neuroscience · 2012Article
- A novel form of presynaptic plasticity based on the fast reactivation of release sites switched off during low-frequency depression.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Insights into a molecular switch that gates sensory neuron synapses during habituation in Aplysia.Neurobiology of learning and memory · 2009Review
- Parametric and non-parametric modeling of short-term synaptic plasticity. Part I: Computational study.Journal of computational neuroscience · 2009Article
- Parametric and non-parametric modeling of short-term synaptic plasticity. Part II: Experimental study.Journal of computational neuroscience · 2009Article
- Synaptic fatigue at the naive perforant path-dentate granule cell synapse in the rat.The Journal of physiology · 2005Article
- Multiple mechanisms govern the dynamics of depression at neocortical synapses of young rats.The Journal of physiology · 2004Article
- Prolonged habituation of the gill-withdrawal reflex in Aplysia depends on protein synthesis, protein phosphatase activity, and postsynaptic glutamate receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003Article
- Short-term synaptic plasticity, simulation of nerve terminal dynamics, and the effects of protein kinase C activation in rat hippocampus.The Journal of physiology · 2002Article
Corrections and comments
- Erratum issued
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The synaptic connections of Aplysia sensory neurons (SNs) undergo dramatic homosynaptic depression (HSD) with only a few low-frequency stimuli. Strong and weak SN synapses, although differing in their probabilities of release, undergo HSD at the same rate; this suggests that the major mechanism underlying HSD in these SNs may not be depletion of the releasable pool of vesicles. In computational models, we evaluated alternative mechanisms of HSD, including vesicle depletion, to determine which mechanisms enable strong and weak synapses to depress with identical time courses. Of five mechanisms tested, only release-independent, stimulus-dependent switching off of release sites resulted in HSD that was independent of initial synaptic strength. This conclusion that HSD is a release-independent phenomenon was supported by empirical results: an increase in Ca2+ influx caused by spike broadening with a K+ channel blocker did not alter HSD. Once induced, HSD persisted during 40 min of rest with no detectable recovery; thus, release does not recover automatically with rest, contrary to what would be expected if HSD represented an exhaustion of the exocytosis mechanism. The hypothesis that short-term HSD involves primarily a stepwise silencing of release sites, rather than vesicle depletion, is consistent with our earlier observation that HSD is accompanied by only a modest decrease in release probability, as indicated by little change in the paired-pulse ratio. In contrast, we found that there was a dramatic decrease in the paired-pulse ratio during serotonin-induced facilitation; this suggests that heterosynaptic facilitation primarily involves an increase in release probability, rather than a change in the number of functional release sites.
Indexed as
Identifiers
11880525PMC6758855W1752133427What OpenQuestion holds
Registered trials
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.