ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2000
Release-independent short-term synaptic depression in cultured hippocampal neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
What it found
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Who cites it
60 citing papers in PubMed, 130 citations in OpenAlex.
- Short-term plasticity of human spinal inhibitory circuits after isometric and isotonic ankle training.European journal of applied physiology · 2013Trial
- Spinal use-dependent plasticity of synaptic transmission in humans after a single cycling session.The Journal of physiology · 2007Trial
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- Microglial deficiency in the ATRX chromatin remodeler elicits a viral mimicry immune response that impacts neuronal function and behavior.PLoS biology · 2025Article
- The computational power of the human brain.Frontiers in cellular neuroscience · 2023Review
- Physiological effects of cathodal electrode configuration for transspinal stimulation in humans.Journal of neurophysiology · 2022Article
- Analog transmission of action potential fine structure in spiral ganglion axons.Journal of neurophysiology · 2021Article
- Communication consumes 35 times more energy than computation in the human cortex, but both costs are needed to predict synapse number.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- The control of release probability at nerve terminals.Nature reviews. Neuroscience · 2019Review
- Past and Future of Analog-Digital Modulation of Synaptic Transmission.Frontiers in cellular neuroscience · 2019Review
- Dynamic Factors for Transmitter Release at Small Presynaptic Boutons Revealed by Direct Patch-Clamp Recordings.Frontiers in cellular neuroscience · 2019Review
- Kinetics of transmitter release at the calyx of Held synapse.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2018Review
- Article
- Simulation of synaptic short-term plasticity using Ba(CF3SO3)2-doped polyethylene oxide electrolyte film.Scientific reports · 2016Article
- Modulation of Synaptic Plasticity by Glutamatergic Gliotransmission: A Modeling Study.Neural plasticity · 2016Article
- A Review on Locomotor Training after Spinal Cord Injury: Reorganization of Spinal Neuronal Circuits and Recovery of Motor Function.Neural plasticity · 2016Review
- Fidelity of frequency and phase entrainment of circuit-level spike activity during DBS.Journal of neurophysiology · 2015Article
- The active-zone protein Munc13 controls the use-dependence of presynaptic voltage-gated calcium channels.eLife · 2015Article
- Controlling Ion Conductance and Channels to Achieve Synaptic-like Frequency Selectivity.Nano-micro letters · 2015Article
- Abnormal cortical synaptic transmission in CaV2.1 knockin mice with the S218L missense mutation which causes a severe familial hemiplegic migraine syndrome in humans.Frontiers in cellular neuroscience · 2015Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Short-term synaptic plasticity may dramatically influence neuronal information transfer, yet the underlying mechanisms remain incompletely understood. In autapses (self-synapses) formed by cultured hippocampal neurons, short-term synaptic depression (STD) had several unusual features. (1) Reduction of neurotransmitter release probability with Cd(2+), a blocker of voltage-gated calcium channels, did not change depression. (2) Lowering [Ca(2+)](o) and/or raising [Mg(2+)](o) had little effect on STD in cells with strong baseline depression, but in cells with more modest baseline depression, it reduced the depression. (3) Random variations in the size of initial EPSCs did not influence successive EPSC sizes. These findings were inconsistent with release-dependent mechanisms, such as vesicle depletion, post-synaptic receptor desensitization, and autoreceptor inhibition. Instead, other results suggested that changes in action potentials (APs) contributed to depression. The somatic APs declined in amplitude with repetitive stimulation, and modest reduction of AP amplitudes with tetrodotoxin inhibited EPSCs. Notably, tetrodotoxin also increased depression. Similar changes in axonal APs could produce STD in at least two ways. First, decreasing presynaptic spike amplitudes could reduce calcium entry and release probability. Alternatively, APs could fail to propagate through some axonal branches, reducing the number of active synapses. To explore these possibilities, we derived the expected variance of EPSCs for the two scenarios. Experimentally, the variance increased and then decreased on average with successive responses during trains of APs, confirming a unique prediction from the conduction failure scenario. Thus, STD had surprising properties, incompatible with commonly postulated mechanisms but consistent with AP conduction failure at axonal branches.
Indexed as
Identifiers
10729328PMC6772230W1567391514What 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.