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DECIPHERING NEURONAL SIGNALING WITHIN A SINGLE DENDRITIC SPINE IN LONG TERM POTENTIATION
- Date Issued:
- 2022
- Abstract/Description:
- Organization and function of neuronal circuits require not only the interaction between the intrinsic components of the individual neurons but also the synaptic interactions that incorporate them into functional entities. Dendritic spines are the major sites for excitatory synaptic transmission, and are considered as the basic unit of information transfer in nervous system. Structural plasticity of dendritic spines is highly associated with functional plasticity, playing critical roles in learning and memory. Here, we explored mechanisms underlying PKCα and structural plasticity of dendritic spines. We examined the spatiotemporal activation of actin regulators with 2pFLIM, including small GTPases Rac1, Cdc42 and Ras, in the presence or absence of PKCα during single-spine structural plasticity. Removal of PKCα expression in the postsynapse attenuated Rac1 activation during structural plasticity without affecting Ras or Cdc42 activity. Moreover, disruption of a PDZ binding domain within PKCα led to impaired Rac1 activation and deficits in structural spine remodeling. This work described that PKCα regulates the activation of Rac1, but not Ras or Cdc42, during sLTP of dendritic spines, and this modulation relies on PKCα’s PDZ-binding motif.
Title: | DECIPHERING NEURONAL SIGNALING WITHIN A SINGLE DENDRITIC SPINE IN LONG TERM POTENTIATION. |
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Name(s): |
Tu, Xun , author Yasuda, Ryohei, Thesis advisor Florida Atlantic University, Degree grantor Department of Biological Sciences Charles E. Schmidt College of Science |
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Type of Resource: | text | |
Genre: | Electronic Thesis Or Dissertation | |
Date Created: | 2022 | |
Date Issued: | 2022 | |
Publisher: | Florida Atlantic University | |
Place of Publication: | Boca Raton, Fla. | |
Physical Form: | application/pdf | |
Extent: | 149 p. | |
Language(s): | English | |
Abstract/Description: | Organization and function of neuronal circuits require not only the interaction between the intrinsic components of the individual neurons but also the synaptic interactions that incorporate them into functional entities. Dendritic spines are the major sites for excitatory synaptic transmission, and are considered as the basic unit of information transfer in nervous system. Structural plasticity of dendritic spines is highly associated with functional plasticity, playing critical roles in learning and memory. Here, we explored mechanisms underlying PKCα and structural plasticity of dendritic spines. We examined the spatiotemporal activation of actin regulators with 2pFLIM, including small GTPases Rac1, Cdc42 and Ras, in the presence or absence of PKCα during single-spine structural plasticity. Removal of PKCα expression in the postsynapse attenuated Rac1 activation during structural plasticity without affecting Ras or Cdc42 activity. Moreover, disruption of a PDZ binding domain within PKCα led to impaired Rac1 activation and deficits in structural spine remodeling. This work described that PKCα regulates the activation of Rac1, but not Ras or Cdc42, during sLTP of dendritic spines, and this modulation relies on PKCα’s PDZ-binding motif. | |
Identifier: | FA00013974 (IID) | |
Degree granted: | Dissertation (Ph.D.)--Florida Atlantic University, 2022. | |
Collection: | FAU Electronic Theses and Dissertations Collection | |
Note(s): | Includes bibliography. | |
Subject(s): |
Dendritic Spines Neuronal Plasticity Long-Term Potentiation |
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Persistent Link to This Record: | http://purl.flvc.org/fau/fd/FA00013974 | |
Use and Reproduction: | Copyright © is held by the author with permission granted to Florida Atlantic University to digitize, archive and distribute this item for non-profit research and educational purposes. Any reuse of this item in excess of fair use or other copyright exemptions requires permission of the copyright holder. | |
Use and Reproduction: | http://rightsstatements.org/vocab/InC/1.0/ | |
Host Institution: | FAU | |
Is Part of Series: | Florida Atlantic University Digital Library Collections. |