ArticleJournal of neurophysiology2010
Dynamic modulation of phasic and asynchronous glutamate release in hippocampal synapses.
Article in Journal of neurophysiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- Nanomolar Cadmium Disrupts Neurotransmitter Release Timing via a ROS-dependent Mechanism at the Mouse Neuromuscular Junction: Modulation by Nanomolar ZnNeurochemical research · 2026Article
- SNAP-25 disease variants affect synaptic transmission by destabilizing SNARE complexes within a multimeric SNARE ring.Cell reports · 2026Article
- Number and relative abundance of synaptic vesicles in functionally distinct priming states determine synaptic strength and short-term plasticity.The Journal of physiology · 2025Article
- Article
- Autaptic Cultures: Methods and Applications.Frontiers in synaptic neuroscience · 2020Article
- Bayesian analysis of the kinetics of quantal transmitter secretion at the neuromuscular junction.Journal of computational neuroscience · 2015Article
- Loss of Local Astrocyte Support Disrupts Action Potential Propagation and Glutamate Release Synchrony from Unmyelinated Hippocampal Axon Terminals In Vitro.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Actin-dependent rapid recruitment of reluctant synaptic vesicles into a fast-releasing vesicle pool.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Independent vesicle pools underlie different modes of release during neuronal development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Downregulation of parvalbumin at cortical GABA synapses reduces network gamma oscillatory activity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Modelling vesicular release at hippocampal synapses.PLoS computational biology · 2010Article
- Shunting inhibition controls the gain modulation mediated by asynchronous neurotransmitter release in early development.PLoS computational biology · 2010Article
- Rapid activation of dormant presynaptic terminals by phorbol esters.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Although frequency-dependent short-term presynaptic plasticity has been of long-standing interest, most studies have emphasized modulation of the synchronous, phasic component of transmitter release, most evident with a single or a few presynaptic stimuli. Asynchronous transmitter release, vesicle fusion not closely time locked to presynaptic action potentials, can also be prominent under certain conditions, including repetitive stimulation. Asynchrony has often been attributed to residual Ca(2+) buildup in the presynaptic terminal. We verified that a number of manipulations of Ca(2+) handling and influx selectively alter asynchronous release relative to phasic transmitter release during action potential trains in cultured excitatory autaptic hippocampal neurons. To determine whether other manipulations of vesicle release probability also selectively modulate asynchrony, we probed the actions of one thoroughly studied modulator class whose actions on phasic versus asynchronous release have not been investigated. We examined the effects of the phorbol ester PDBu, which has protein kinase C (PKC) dependent and independent actions on presynaptic transmitter release. PDBu increased phasic and asynchronous release in parallel. However, while PKC inhibition had relatively minor inhibitory effects on PDBu potentiation of phasic and total release during action potential trains, PKC inhibition strongly reduced phorbol-potentiated asynchrony, through actions most evident late during stimulus trains. These results lend new insight into PKC-dependent and -independent effects on transmitter release and suggest the possibility of differential control of synchronous versus asynchronous vesicle release.
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