Seoul National University · Neuroscience
Professor Bong-Kiun Kaang's research lab focuses on the cellular and molecular mechanisms underlying learning, memory, and neurodevelopmental disorders. The lab investigates synaptic plasticity, engram cell connectivity, and the role of specific ion channels and cytoskeletal proteins in memory formation and stability. Using innovative techniques such as dual-eGRASP and gene transfer in model systems like Aplysia, the lab explores how neuronal circuits encode and maintain memories, with a particular emphasis on the synaptic engram and its dysfunction in conditions like autism and Parkinson’s disease.
Figures are computed from collected data and may differ slightly.
Memory resides in engram cells distributed across the brain. However, the site-specific substrate within these engram cells remains theoretical, even though it is generally accepted that synaptic plasticity encodes memories. We developed the dual-eGRASP (green fluorescent protein reconstitution across synaptic partners) technique to examine synapses between engram cells to identify the specific neuronal site for memory storage. We found an increased number and size of spines on CA1 engram cells
Although potassium channels play a variety of roles in shaping the electrical properties of neurons, little is known about how these channels are constituted in neurons. To examine the assembly and physiological function of A-type K+ channels in mature differentiated neurons, we have developed a highly efficient gene transfer method for Aplysia neurons that has allowed us to express about 10(7) copies of the cloned Aplysia Shaker (Sh) K+ channel (AK01a) in single identified cells. We find that e
Cofilin-actin rods are inclusion-like structures that are induced by certain chemical or physical stresses in cultured cells, and the rods formed in neurons are thought to be associated with neurodegeneration. Here, we cloned an Aplysia cofilin homolog and overexpressed it in cultured neurons. Overexpressed cofilin formed rod-like structures that included actin. The overall neuronal morphology was unaffected by cofilin overexpression; however, a decrease in number of synaptic varicosities was ob
In this review, we focus on the role of the Shank family of proteins in autism. In recent years, autism research has been flourishing. With genetic, molecular, imaging and electrophysiological studies being supported by behavioural studies using animal models, there is real hope that we may soon understand the fundamental pathology of autism. There is also genuine potential to develop a molecular-level pharmacological treatment that may be able to deal with the most severe symptoms of autism, an
These results suggest that the dopaminergic nigrostriatal pathway may have a role in inhibiting noxious stimuli, and that abnormal inflammatory responses and neural activity in basal ganglia is correlated to pain processing in PD induced by MPTP treatment.
Memory is composed of various phases including cellular consolidation, systems consolidation, reconsolidation, and extinction. In the last few years it has been shown that simple association memories can be encoded by a subset of the neuronal population called engram cells. Activity of these cells is necessary and sufficient for the recall of association memory. However, it is unclear which molecular mechanisms allow cellular engrams to encode the diverse phases of memory. Further research is ne
Autism spectrum disorder is a debilitating mental illness and social issue. Autism spectrum disorder patients suffer from social isolation, cognitive deficits, compulsive behavior, and sensory deficits, including hyposensitivity to pain. However, recent studies argued that autism spectrum disorder patients show physiological pain response and, in some cases, even extremely intense pain response to harmless stimulation. Recently, Shank gene family was reported as one of the genetic risk factors o
Our daily experiences and learnings are stored in the form of memories. These experiences trigger synaptic plasticity and persistent structural and functional changes in neuronal synapses. Recently, cellular studies of memory storage and engrams have emerged over the last decade. Engram cells reflect interconnected neurons via modified synapses. However, we were unable to observe the structural changes arising from synaptic plasticity in the past, because it was not possible to distinguish the s
These findings suggest that the T185 variant functions as a risk factor in neurodegeneration with endolysosomal defects. This study provides a better understanding of pathogenic functions of TMEM106B, which is a risk factor for the progression of neurodegenerative diseases that are associated with endosomal defects in the aged brain.
The primary motor cortex, a dynamic center for overall motion control and decision making, undergoes significant alterations upon neural stimulation. Over the last few decades, data from numerous studies using rodent models have improved our understanding of the morphological and functional plasticity of the primary motor cortex. In particular, spatially specific formation of dendritic spines and their maintenance during distinct behaviors is considered crucial for motor learning. However, wheth
Calcium-calmodulin-dependent protein kinase IV (CaMKIV) phosphorylates the major transcription factor cyclic AMP-response element binding protein (CREB), which plays a role in emotional behavior. Here, CaMKIV knockout mice (CaMKIV(-/-)) were tested in a battery of stress and anxiety-related behavioral tests, to determine if CaMKIV plays a role in emotional behavior. CaMKIV(-/-) exhibited a decrease in anxiety-like behavior in both the elevated plus maze and dark-light emergence tests when compar
An accumulating body of evidence shows that reactivated long-term memory undergoes a dynamic process called reconsolidation, in which de novo protein synthesis is required to maintain the memory. These findings open up a new dimension in the field of memory research. However, few studies have shown how once-consolidated memory becomes labile. The authors' recent findings have demonstrated that pre-existing long-term memory becomes unstable via the ubiquitin/ proteasome-dependent protein degradat
The cAMP-dependent signaling pathway is critically involved in memory-related synaptic plasticity. cAMP-specific type 4 phosphodiesterases (PDE4) play a role in this process by regulating the cAMP concentration. However, it is unclear how PDE4 is involved in regulating synaptic plasticity. To address this issue in Aplysia sensory-to-motor synapses, we identified a long isoform of the PDE4 homolog in Aplysia kurodai (apPDE), with genetic and biochemical properties similar to those of mammalian PD
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