ArticleFrontiers in cellular neuroscience2015
A use-dependent increase in release sites drives facilitation at calretinin-deficient cerebellar parallel-fiber synapses.
Article in Frontiers in cellular neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- Estimates of quantal synaptic parameters in light of more complex vesicle pool models.Frontiers in cellular neuroscience · 2025Article
- The role of the vesicular monoamine transporter 2 in the inhibitory effect of tetrabenazine and valbenazine compared to reserpine on the vesicular release of monoamine transmitters.Frontiers in cellular neuroscience · 2025Article
- CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- A synaptic amplifier of hunger for regaining body weight in the hypothalamus.Cell metabolism · 2023Article
- Calretinin-Expressing Synapses Show Improved Synaptic Efficacy with Reduced Asynchronous Release during High-Rate Activity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Cytosolic CaCold Spring Harbor perspectives in biology · 2020Review
- Article
- Control of Presynaptic Parallel Fiber Efficacy by Activity-Dependent Regulation of the Number of Occupied Release Sites.Frontiers in systems neuroscience · 2019Article
- What We Can Learn From Cumulative Numbers of Vesicular Release Events.Frontiers in cellular neuroscience · 2019Article
- Developmental Increase of Neocortical Presynaptic EfficacyFrontiers in synaptic neuroscience · 2019Article
- Synaptotagmin CaFrontiers in molecular neuroscience · 2018Review
- Frequency-dependent mobilization of heterogeneous pools of synaptic vesicles shapes presynaptic plasticity.eLife · 2017Article
- Molecular Machines Regulating the Release Probability of Synaptic Vesicles at the Active Zone.Frontiers in synaptic neuroscience · 2016Review
- Ca(2+) current facilitation determines short-term facilitation at inhibitory synapses between cerebellar Purkinje cells.The Journal of physiology · 2015Article
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3 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Endogenous Ca(2+)-binding proteins affect synaptic transmitter release and short-term plasticity (STP) by buffering presynaptic Ca(2+) signals. At parallel-fiber (PF)-to-Purkinje neuron (PN) synapses in the cerebellar cortex loss of calretinin (CR), the major buffer at PF terminals, results in increased presynaptic Ca(2+) transients and an almost doubling of the initial vesicular releases probability (p r). Surprisingly, however, it has been reported that loss of CR from PF synapses does not alter paired-pulse facilitation (PPF), while it affects presynaptic Ca(2+) signals as well as p r. Here, we addressed this puzzling observation by analyzing the frequency- and Ca(2+)-dependence of PPF at unitary PF-to-PN synapses of wild-type (WT) and CR-deficient (CR(-/-)) mice using paired recordings and computer simulations. Our analysis revealed that PPF in CR(-/-) is indeed smaller than in the WT, to a degree, however, that indicates that rapid vesicle replenishment and recruitment of additional release sites dominate the synaptic efficacy of the second response. These Ca(2+)-driven processes operate more effectively in the absence of CR, thereby, explaining the preservation of robust PPF in the mutants.
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