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Sudhir Sivakumaran

Researcher at Critical Path Institute

Publications -  24
Citations -  927

Sudhir Sivakumaran is an academic researcher from Critical Path Institute. The author has contributed to research in topics: Excitatory postsynaptic potential & Postsynaptic potential. The author has an hindex of 14, co-authored 19 publications receiving 802 citations. Previous affiliations of Sudhir Sivakumaran include University of Tokyo & National Centre for Biological Sciences.

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The Database of Quantitative Cellular Signaling: management and analysis of chemical kinetic models of signaling networks

TL;DR: The Database of Quantitative Cellular Signaling is a repository of models of signaling pathways intended both to serve the growing field of chemical-reaction level simulation of signaling networks, and to anticipate issues in large-scale data management for signaling chemistry.
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Control of GABA Release at Mossy Fiber-CA3 Connections in the Developing Hippocampus.

TL;DR: Combining calcium transients associated with network-driven giant depolarizing potentials or GDPs generated by the synergistic action of glutamate and GABA with MF activation increased the probability of GABA release and caused the conversion of silent synapses into conductive ones suggesting that GDPs act as coincident detector signals for enhancing synaptic efficacy.
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Correlated network activity enhances synaptic efficacy via BDNF and the ERK pathway at immature CA3–CA1 connections in the hippocampus

TL;DR: The hypothesis that, during a critical period of postnatal development, GABAA-mediated GDPs are instrumental in tuning excitatory synaptic connections is supported and insights into the molecular mechanisms involved in this process are provided.
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At immature mossy-fiber-CA3 synapses, correlated presynaptic and postsynaptic activity persistently enhances GABA release and network excitability via BDNF and cAMP-dependent PKA.

TL;DR: STD-LTP of GPSPs provides a reliable way to convey information from granule cells to the CA3 associative network at a time when glutamatergic synapses are still poorly developed, and may exert a critical control on synaptic efficacy.