Ning Gu
University of Oslo
8 Papers
Ning Gu is an academic researcher from University of Oslo. The author has contributed to research in topics: Excitatory postsynaptic potential & Chemistry. The author has an hindex of 6, co-authored 6 publications.
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Papers
Kv7/KCNQ/M and HCN/h, but not KCa2/SK channels, contribute to the somatic medium after‐hyperpolarization and excitability control in CA1 hippocampal pyramidal cells
TL;DR: A computational model of a CA1 pyramidal cell predicted that M and h‐channels will generate mAHPs in a voltage‐dependent manner, as indicated by the experiments, and it is concluded that M‐ and h-channels generate the somatic mAHP in hippocampal pyramid cells, with little or no net contribution from SK channels.
383
Presynaptic Ca2+-Activated K+ Channels in Glutamatergic Hippocampal Terminals and Their Role in Spike Repolarization and Regulation of Transmitter Release
Hua Hu,Li-Rong Shao,Sorush Chavoshy,Ning Gu,Maria Trieb,Ralf Behrens,Petter Laake,Olaf Pongs,Hans-Günther Knaus,Ole Petter Ottersen,Johan F. Storm +10 more
TL;DR: Electrophysiology and immunogold cytochemistry are combined to demonstrate the existence of functional BK channels in presynaptic terminals in the hippocampus and compare their functional roles in somata and terminals of CA3 pyramidal cells, indicating that the functional role of Bk channels depends on their subcellular localization.
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BK potassium channels facilitate high-frequency firing and cause early spike frequency adaptation in rat CA1 hippocampal pyramidal cells.
TL;DR: The results strongly support the idea that BK channels play an important role for early high‐frequency, rapidly adapting firing in hippocampal pyramidal neurons, thus promoting the type of bursting that is characteristic of these cells in vivo, during behaviour.
307
Kv7/KCNQ/M-channels in rat glutamatergic hippocampal axons and their role in regulation of excitability and transmitter release
TL;DR: The results indicate that functional Kv7/KCNQ/M‐channels are present in unmyelinated axons in the brain, and that these channels may have contrasting effects on excitability depending on their subcellular localization.
135
SK (KCa2) Channels Do Not Control Somatic Excitability in CA1 Pyramidal Neurons But Can Be Activated by Dendritic Excitatory Synapses and Regulate Their Impact
TL;DR: It is concluded that SK channels in rat CA1 pyramidal cells can be activated by NMDAR-mediated synaptic input and cause feedback regulation of synaptic efficacy but are normally not appreciably activated by somatic Na(+) spikes in this cell type.
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