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Bong-Kiun Kaang

Researcher at UPRRP College of Natural Sciences

Publications -  255
Citations -  11510

Bong-Kiun Kaang is an academic researcher from UPRRP College of Natural Sciences. The author has contributed to research in topics: Synaptic plasticity & Long-term potentiation. The author has an hindex of 51, co-authored 236 publications receiving 9853 citations. Previous affiliations of Bong-Kiun Kaang include Yonsei University & Seoul National University.

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Autistic-like social behaviour in Shank2 -mutant mice improved by restoring NMDA receptor function

TL;DR: It is shown that Shank2-mutant (Shank2−/−) mice carrying a mutation identical to the ASD-associated microdeletion in the human SHANK2 gene exhibit ASD-like behaviours including reduced social interaction, reduced social communication by ultrasonic vocalizations, and repetitive jumping.
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Spatially resolved dynamics of cAMP and protein kinase A subunits in Aplysia sensory neurons

TL;DR: Cyclic adenosine monophosphate (cAMP)-dependent protein kinase, labeled with fluorescein and rhodamine on the catalytic and regulatory subunits, respectively, was injected into Aplysia sensory neurons either in culture or in intact cell clusters.
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Roles of NMDA NR2B Subtype Receptor in Prefrontal Long-Term Potentiation and Contextual Fear Memory

TL;DR: It is reported that the activation of the NR2B and NR2A subunits of the NMDA receptor is critical for the induction of cingulate LTP, regardless of the induction protocol.
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Synaptic plasticity in the anterior cingulate cortex in acute and chronic pain

TL;DR: Increasing evidence from rodent studies that ACC activation contributes to chronic pain states is discussed and several forms of synaptic plasticity that may underlie this effect are described.
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Synaptic protein degradation underlies destabilization of retrieved fear memory.

TL;DR: It is found that postsynaptic proteins were degraded in the hippocampus by polyubiquitination after retrieval of contextual fear memory, and the infusion of proteasome inhibitor into the CA1 region immediately after retrieval prevented anisomycin-induced memory impairment, as well as the extinction of fear memory.