ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1998
Use-dependent decline of paired-pulse facilitation at Aplysia sensory neuron synapses suggests a distinct vesicle pool or release mechanism.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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Who cites it
18 citing papers in PubMed, 57 citations in OpenAlex.
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- Enhancing GABAergic signaling ameliorates aberrant gamma oscillations of olfactory bulb in AD mouse models.Molecular neurodegeneration · 2021Article
- Contribution of PKC to the maintenance of 5-HT-induced short-term facilitation at sensorimotor synapses of Aplysia.Journal of neurophysiology · 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
- State-, timing-, and pattern-dependent neuromodulation of synaptic strength by a serotonergic interneuron.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Long-term sensitization training produces spike narrowing in Aplysia sensory neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
- Neurosteroid-induced enhancement of short-term facilitation involves a component downstream from presynaptic calcium in hippocampal slices.The Journal of physiology · 2006Article
- Burst-induced synaptic depression and its modulation contribute to information transfer at Aplysia sensorimotor synapses: empirical and computational analyses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003Article
- Modulation of spike-mediated synaptic transmission by presynaptic background Ca2+ in leech heart interneurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003Article
- Persistent, exocytosis-independent silencing of release sites underlies homosynaptic depression at sensory synapses in Aplysia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002Article
- Brain-derived neurotrophic factor modulates cerebellar plasticity and synaptic ultrastructure.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002Article
- Contribution of postsynaptic Ca2+ to the induction of post-tetanic potentiation in the neural circuit for siphon withdrawal in Aplysia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001Article
- Phosphorylation regulates spontaneous and evoked transmitter release at a giant terminal in the rat auditory brainstem.The Journal of physiology · 2000Article
- Long-term enhancement of central synaptic transmission by chronic brain-derived neurotrophic factor treatment.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1999Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
We have characterized paired-pulse facilitation at Aplysia sensory neuron-to-motoneuron synapses. This simple form of very short-term synaptic plasticity displayed an unusual feature: it decreased dramatically with repeated testing. Synaptic depression at these synapses and this use-dependent decrease in paired-pulse facilitation occurred independently of each other. Paired-pulse facilitation was inversely correlated with the size of the initial synaptic connection and was absent at stronger synapses. The use-dependent decrease in paired-pulse facilitation occurred at the same rate at large synapses as at small synapses, although the initial paired-pulse facilitation at large synapses was substantially smaller. Rates of synaptic depression were also independent of initial synaptic strength. Paired-pulse facilitation was blocked by presynaptic EGTA injection, but not by postsynaptic EGTA or BAPTA injection. These results indicate that presynaptic Ca2+ influx plays a critical role in paired-pulse facilitation. However, the persistence of the decrease in paired-pulse facilitation for longer than 15 min suggests that Ca2+ from the first paired action potential produces facilitation via a modulatory mechanism rather than by summating with Ca2+ influx during the second paired action potential in activating the Ca2+ binding sites that initiate exocytosis. This modulatory mechanism may not involve protein phosphorylation because paired-pulse facilitation was unaffected by the protein kinase inhibitors H7 and KN-62. These findings further suggest that release by the second paired action potential occurs at sites distinct from those that mediate release by the first action potential.
Indexed as
Identifiers
9852569PMC6793359W1501752630What 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.