ArticleThe Journal of physiology1999
Sr2+-dependent asynchronous evoked transmission at rat striatal inhibitory synapses in vitro.
Article in The Journal of physiology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 35 citations in OpenAlex.
- ICER-Controlled inhibitory plasticity of amygdala engram neurons regulates fear memory precision.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Impact of distinct neurotransmitter release modes on neuronal signaling.Molecular psychiatry · 2026Review
- Activation of Metabotropic Glutamate Receptor 3 Modulates Thalamo-accumbal Transmission and Rescues Schizophrenia-Like Physiological and Behavioral Deficits.Biological psychiatry · 2024Article
- Two forms of asynchronous release with distinctive spatiotemporal dynamics in central synapses.eLife · 2023Article
- Enhanced GABAergic Inhibition of Cholinergic Interneurons in the zQ175Frontiers in systems neuroscience · 2020Article
- Selective molecular impairment of spontaneous neurotransmission modulates synaptic efficacy.Nature communications · 2017Article
- Desensitization-resistant and -sensitive GPCR-mediated inhibition of GABA release occurs by Ca2+-dependent and -independent mechanisms at a hypothalamic synapse.Journal of neurophysiology · 2016Article
- An Engineered Metal Sensor Tunes the Kinetics of Synaptic Transmission.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- PGC-1α provides a transcriptional framework for synchronous neurotransmitter release from parvalbumin-positive interneurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- An alien divalent ion reveals a major role for Ca²⁺ buffering in controlling slow transmitter release.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Synapsin II desynchronizes neurotransmitter release at inhibitory synapses by interacting with presynaptic calcium channels.Nature communications · 2013Article
- Two GABAA responses with distinct kinetics in a sound localization circuit.The Journal of physiology · 2012Article
- Altered localization of GABA(A) receptor subunits on dentate granule cell dendrites influences tonic and phasic inhibition in a mouse model of epilepsy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
- beta-Adrenoceptor-mediated long-term up-regulation of the release machinery at rat cerebellar GABAergic synapses.The Journal of physiology · 2005Article
- Altered synaptic and electrical properties of lumbar motoneurons in the neurological glial mutant taiep rat.Experimental brain research · 2004Article
- Intraterminal Ca2+ concentration and asynchronous transmitter release at single GABAergic boutons in rat collicular cultures.The Journal of physiology · 2003Article
- Ionic dependence of Ca2+ channel modulation by syntaxin 1A.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- Retrograde modulation of transmitter release by postsynaptic subtype 1 metabotropic glutamate receptors in the rat cerebellum.The Journal of physiology · 2001Article
- Analysis and implications of equivalent uniform approximations of nonuniform unitary synaptic systems.Biophysical journal · 2000Article
- Probing fundamental aspects of synaptic transmission with strontium.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. At striatal inhibitory synapses in cell culture, replacement of extracellular Ca2+ with Sr2+ desynchronized inhibitory postynaptic currents (IPSCs), reducing their peak amplitude and producing a succession of late, asynchronous synaptic events (late release). In the averaged IPSC waveform this resulted in an increase in both the fast and the slow decay time constant as well as in the time to peak. 2. Rapid removal of extracellular Sr2+ during late release was without effect on the time course of the averaged IPSC. Thus, late release is not dependent on continuous Sr2+ influx, but must be related to the way in which Sr2+, as opposed to Ca2+, interacts with constituents of the intracellular space. 3. After application of the membrane-permeant acetoxymethyl ester (AM) form of the Ca2+-chelator BAPTA, Sr2+-induced late release was greatly reduced and the kinetics of the Sr2+-dependent IPSC approached those of the Ca2+-dependent response. EGTA AM had a similar but less pronounced effect. 4. Using rapid solution exchange, we stimulated synapses first in Sr2+- or Ca2+- and 100-300 ms afterwards in Ca2+-containing solution. Paired-pulse facilitation of late release was the same whether the conditioning pulse induced a presynaptic influx of Sr2+ or of Ca2+. 5. It is concluded that Sr2+-mediated asynchrony is probably due to a less efficient intraterminal buffering of Sr2+ as opposed to Ca2+, allowing for Sr2+ ions to activate release in an area less confined to the immediate vicinity of the presynaptic Ca2+ channel. This hypothesis explains both the action of endogenous buffers and the apparent lack of specific facilitatory interaction between Ca2+-mediated and Sr2+-induced late release.
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