ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008
Presynaptic release probability and readily releasable pool size are regulated by two independent mechanisms during posttetanic potentiation at the calyx of Held synapse.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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50 citing papers in PubMed, 80 citations in OpenAlex.
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- Apparent calcium dependence of vesicle recruitment.The Journal of physiology · 2018Article
- Prion acute synaptotoxicity is largely driven by protease-resistant PrPSc species.PLoS pathogens · 2018Article
- High glucose upregulates myosin light chain kinase to induce microfilament cytoskeleton rearrangement in hippocampal neurons.Molecular medicine reports · 2018Article
- Molecular Mechanisms of Short-Term Plasticity: Role of Synapsin Phosphorylation in Augmentation and Potentiation of Spontaneous Glutamate Release.Frontiers in synaptic neuroscience · 2018Article
- A single episode of high intensity sound inhibits long-term potentiation in the hippocampus of rats.Scientific reports · 2017Article
- Presenilins regulate synaptic plasticity and mitochondrial calcium homeostasis in the hippocampal mossy fiber pathway.Molecular neurodegeneration · 2017Article
- Dynamin-1 deletion enhances post-tetanic potentiation and quantal size after tetanic stimulation at the calyx of Held.The Journal of physiology · 2017Article
- Myosin accelerates synaptic vesicle recycling in the motor nerve endings.Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections · 2016Article
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4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
At the immature calyx of Held, the fast decay phase of a Ca(2+) transient induced by tetanic stimulation (TS) was followed by a period of elevated [Ca(2+)](i) for tens of seconds, referred to as posttetanic residual calcium (Ca(res)). We investigated the source of Ca(res) and its contribution to posttetanic potentiation (PTP). After TS (100 Hz for 4 s), posttetanic Ca(res) at the calyx of Held was largely abolished by tetraphenylphosphonium (TPP(+)) or Ru360, which inhibit mitochondrial Na(+)-dependent Ca(2+) efflux and Ca(2+) uniporter, respectively. Whereas the control PTP lasted longer than Ca(res), inhibition of Ca(res) by TPP(+) resulted in preferential suppression of the early phase of PTP, the decay time course of which well matched with that of Ca(res). TS induced significant increases in release probability (P(r)) and the size of the readily releasable pool (RRP), which were estimated from plots of cumulative EPSC amplitudes. TPP(+) or Ru360 suppressed the posttetanic increase in P(r), whereas it had little effect on the increase in RRP size. Moreover, the posttetanic increase in P(r), but not in RRP size, showed a linear correlation with the amount of Ca(res). In contrast, myosin light chain kinase (MLCK) inhibitors and blebbistatin reduced the posttetanic increase in RRP size with no effect on the increase in P(r). Application of TPP(+) in the presence of MLCK inhibitor peptide caused further suppression of PTP. These findings suggest that Ca(res) released from mitochondria and activation of MLCK are primarily responsible for the increase in P(r) and that in the RRP size, respectively.
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