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Author

Chuljung Kwak

Other affiliations: Seoul National University
Bio: Chuljung Kwak is an academic researcher from UPRRP College of Natural Sciences. The author has contributed to research in topics: Long-term potentiation & Memory consolidation. The author has an hindex of 11, co-authored 20 publications receiving 1228 citations. Previous affiliations of Chuljung Kwak include Seoul National University.

Papers
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Journal ArticleDOI
03 Dec 2010-Science
TL;DR: It is found that protein kinase M zeta (PKMζ) maintains pain-induced persistent changes in the mouse anterior cingulate cortex (ACC) and could be a new therapeutic target for treating chronic pain.
Abstract: Synaptic plasticity is a key mechanism for chronic pain It occurs at different levels of the central nervous system, including spinal cord and cortex Studies have mainly focused on signaling proteins that trigger these plastic changes, whereas few have addressed the maintenance of plastic changes related to chronic pain We found that protein kinase M zeta (PKMζ) maintains pain-induced persistent changes in the mouse anterior cingulate cortex (ACC) Peripheral nerve injury caused activation of PKMζ in the ACC, and inhibiting PKMζ by a selective inhibitor, ζ-pseudosubstrate inhibitory peptide (ZIP), erased synaptic potentiation Microinjection of ZIP into the ACC blocked behavioral sensitization These results suggest that PKMζ in the ACC acts to maintain neuropathic pain PKMζ could thus be a new therapeutic target for treating chronic pain

352 citations

Journal ArticleDOI
21 Jan 2015-Neuron
TL;DR: This work characterized two forms of long-term potentiation in the anterior cingulate cortex (ACC) that require kainate receptors and a postsynaptic form (post-LTP) that requires N-methyl-D-aspartate receptors, providing a mechanism by which two form of LTP in the ACC may converge to mediate the interaction between anxiety and chronic pain.

257 citations

Journal ArticleDOI
TL;DR: The results suggest that although adult newborn neurons contribute to contextual fear memory, they may not be involved in the extinction or erasure of hippocampus-dependent contextual fearMemory extinction is not affected, and hippocampal neurogenesis is impaired.
Abstract: Newborn neurons in the subgranular zone (SGZ) of the hippocampus incorporate into the dentate gyrus and mature. Numerous studies have focused on hippocampal neurogenesis because of its importance in learning and memory. However, it is largely unknown whether hippocampal neurogenesis is involved in memory extinction per se. Here, we sought to examine the possibility that hippocampal neurogenesis may play a critical role in the formation and extinction of hippocampus-dependent contextual fear memory. By methylazoxymethanol acetate (MAM) or gamma-ray irradiation, hippocampal neurogenesis was impaired in adult mice. Under our experimental conditions, only a severe impairment of hippocampal neurogenesis inhibited the formation of contextual fear memory. However, the extinction of contextual fear memory was not affected. These results suggest that although adult newborn neurons contribute to contextual fear memory, they may not be involved in the extinction or erasure of hippocampus-dependent contextual fear memory.

145 citations

Journal ArticleDOI
TL;DR: It is found that PI3Kγ has a crucial and specific role in NMDA receptor (NMDAR)-mediated synaptic plasticity at mouse Schaffer collateral–commissural synapses and the impairment of NMDAR LTD by PI3kγ blockade was specifically correlated with deficits in behavioral flexibility.
Abstract: Phosphatidylinositol 3-kinase (PI3K) has been implicated in synaptic plasticity and other neural functions in the brain. However, the role of individual PI3K isoforms in the brain is unclear. We investigated the role of PI3Kγ in hippocampal-dependent synaptic plasticity and cognitive functions. We found that PI3Kγ has a crucial and specific role in NMDA receptor (NMDAR)-mediated synaptic plasticity at mouse Schaffer collateral-commissural synapses. Both genetic deletion and pharmacological inhibition of PI3Kγ disrupted NMDAR long-term depression (LTD) while leaving other forms of synaptic plasticity intact. Accompanying this physiological deficit, the impairment of NMDAR LTD by PI3Kγ blockade was specifically correlated with deficits in behavioral flexibility. These findings suggest that a specific PI3K isoform, PI3Kγ, is critical for NMDAR LTD and some forms of cognitive function. Thus, individual isoforms of PI3Ks may have distinct roles in different types of synaptic plasticity and may therefore influence various kinds of behavior.

133 citations

Journal ArticleDOI
TL;DR: It is demonstrated that increased basal Erk activity and corresponding baseline increases in excitatory synaptic function are responsible for the LTP impairments and, consequently, the learning deficits in mouse models of NS.
Abstract: In Noonan syndrome (NS) 30-50% of subjects show cognitive deficits of unknown etiology and with no known treatment. Here, we report that knock-in mice expressing either of two NS-associated mutations in Ptpn11, which encodes the nonreceptor protein tyrosine phosphatase Shp2, show hippocampal-dependent impairments in spatial learning and deficits in hippocampal long-term potentiation (LTP). In addition, viral overexpression of an NS-associated allele PTPN11(D61G) in adult mouse hippocampus results in increased baseline excitatory synaptic function and deficits in LTP and spatial learning, which can be reversed by a mitogen-activated protein kinase kinase (MEK) inhibitor. Furthermore, brief treatment with lovastatin reduces activation of the GTPase Ras-extracellular signal-related kinase (Erk) pathway in the brain and normalizes deficits in LTP and learning in adult Ptpn11(D61G/+) mice. Our results demonstrate that increased basal Erk activity and corresponding baseline increases in excitatory synaptic function are responsible for the LTP impairments and, consequently, the learning deficits in mouse models of NS. These data also suggest that lovastatin or MEK inhibitors may be useful for treating the cognitive deficits in NS.

120 citations


Cited by
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Journal ArticleDOI
TL;DR: Recent progress in the integration of adult-born neurons into the circuitry of the adult hippocampus suggests an important role for adult hippocampal neurogenesis in learning and memory, but its specific function in these processes has remained elusive.
Abstract: The integration of adult-born neurons into the circuitry of the adult hippocampus suggests an important role for adult hippocampal neurogenesis in learning and memory, but its specific function in these processes has remained elusive. In this article, we summarize recent progress in this area, including advances based on behavioural studies and insights provided by computational modelling. Increasingly, evidence suggests that newborn neurons might be involved in hippocampal functions that are particularly dependent on the dentate gyrus, such as pattern separation. Furthermore, newborn neurons at different maturation stages may make distinct contributions to learning and memory. In particular, computational studies suggest that, before newborn neurons are fully mature, they might function as a pattern integrator by introducing a degree of similarity to the encoding of events that occur closely in time.

1,951 citations

Journal ArticleDOI
27 Mar 2014-Cell
TL;DR: In this Review, the molecular, cellular, and circuit mechanisms that underlie how memories are made, stored, retrieved, and lost are examined.

795 citations

Journal ArticleDOI
03 Nov 2016-Cell
TL;DR: The molecular machinery involved in the generation of new neurons from a pool of adult neural stem cells and their integration into functional hippocampal circuits is discussed.

793 citations

Journal ArticleDOI
30 Oct 2013-Neuron
TL;DR: The progress over the last two and a half decades is reviewed, the future challenges in the field are discussed and a large number of proteins have been identified that regulate this complex process.

783 citations

Journal ArticleDOI
23 Feb 2012-Neuron
TL;DR: The pain phenotype can serve as a window on underlying pathophysiological neural mechanisms and as a guide for developing personalized pain medicine.

680 citations