Area:
Synapse/Circuit plasticity
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High-probability grants
According to our matching algorithm, Hyungbae Kwon is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2015 — 2019 |
Kwon, Hyungbae |
R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Long-Term Plasticity Expressed in Layer 2/3 Cortical Microcircuits @ Johns Hopkins University
? DESCRIPTION (provided by applicant): Normal brain function requires proper neuronal connections. Layer 2/3 cortical pyramidal neurons in a mammalian brain have similar morphological and functional characteristics, but they tend to form functionally distinct microcircuits by making specialized connections. The cellular and molecular mechanisms by which one neuron finds specific target neurons and eventually forms functional subnetworks are not fully understood. A growing body of evidence indicates that the functional microcircuit formation is largely influenced by the activity pattern arising in local circuits. Presumably, the exact timing of action potential firing, the degree of excitability, and the level of inhibition ar important, but how these factors are operated together and are expressed at the level of multiple neurons have not yet been precisely defined. We propose to address these questions by using electrophysiological and optical approaches to visualize and manipulate neuronal activities at individual cell level. In the Aim 1, we seek to determine how spikes generated in multiple neurons within a short time window influence circuit reorganization by varying three factors: spike timing and number, distance between neurons, and the number of neurons. In Aim 2, cellular mechanisms such as neuronal excitability and the involvement of disinhibition will be examined. Lastly, Aim 3 is designed to test whether circuit assembly can be manipulated in awake behaving animals. Completion of the proposed work will provide mechanistic insight during cortical circuit plasticity and would establish experimental evidence for non-random features of neural connectivity in the mammalian brain. Abnormal neuronal connectivity has been implicated in various neuropsychiatric diseases such as schizophrenia, epilepsy, and autism spectrum diseases, and can directly influence the symptoms of other brain disorders or injuries. Thus, understanding cellular mechanisms of activity-dependent redistribution of local circuits could also help inform the development of novel strategies for circuit dysfunction.
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1 |
2018 — 2021 |
Kwon, Hyungbae |
DP1Activity Code Description: To support individuals who have the potential to make extraordinary contributions to medical research. The NIH Director’s Pioneer Award is not renewable. |
Cracking the Neuromodulation Code At Single Cell Resolution @ Johns Hopkins University
Project Summary/Abstract One of challenges in modern Neuroscience is to understand circuit mechanisms that lead to complex behaviors. Our ability to monitor neuronal activity in vivo using genetically encoded calcium indicators and various imaging/optogenetic techniques such as two-photon imaging and channelrhodopsin have helped us define real-time changes in neuronal activity and the circuit basis of behaviors. However, learning and behaviors cannot be solely explained by electrophysiological properties of single neurons and their synaptic connectivity because they are modulated by internal brain state. Therefore, we cannot fully understand diverse emotional or behavioral reactions without understanding the internal brain state. Neuromodulators have been suggested as key molecules that control brain state, but their action to neurons has not been understood at cellular resolution. We have recently developed a novel technique (named ?iTango2?) that labels and manipulates neuromodulation-sensitive neuronal populations with high spatiotemporal resolution. Using this iTango2 methodology, we would like to dissect neuromodulator circuits at individual cell levels, and their physiological implications related to complex behavior will be explored in this study. In the first aim, we will examine how sparse dopamine projection in the premotor cortex contributes to cortical circuit assembly, which may uncover cellular mechanisms of the asymmetric principle of cortical neuronal connectivity. Second, we will dissect neuromodulation signaling at subcellular resolution. This will be accomplished by creating a synapse version of iTango2, ?Syn-iTango2?. In order to identify potential cortical layer- or dendritic branch-specific mechanisms, we will perform real-time monitoring of local dendritic activation triggered by neuromodulatory inputs in brain slices as well as awake behaving animals, and concomitant structural changes such as spine formation or enlargement will be examined. In the third aim, we would like to identify the neuronal ensemble responsible for social interaction, one of the essential complex behaviors in mammals. Since iTango2 links neuromodulation signals to gene expression, we will test the sufficiency of identified circuits to social behavior. Last, we will build a large library of iTango2, so that this approach becomes broadly useful to a variety of neuroscientists. In summary, completion of this study will demonstrate fine scale of neuromodulation action in a quantitative manner rather than a simple ?ON? or ?OFF? effect of neuromodulation. Monitoring neuromodulatory effects and manipulating populations of cells with high spatial and temporal resolution would dramatically increase our knowledge of the pathways that underlie vertebrate animal behaviors.
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1 |