MIT Libraries logoDSpace@MIT

MIT
View Item 
  • DSpace@MIT Home
  • MIT Libraries
  • MIT Theses
  • Doctoral Theses
  • View Item
  • DSpace@MIT Home
  • MIT Libraries
  • MIT Theses
  • Doctoral Theses
  • View Item
JavaScript is disabled for your browser. Some features of this site may not work without it.

Valence encoding and memory in the amygdala

Author(s)
Zhang, Xiangyu,Ph.D.Massachusetts Institute of Technology.
Thumbnail
Download1200350254-MIT.pdf (22.32Mb)
Other Contributors
Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences.
Advisor
Susumu Tonegawa.
Terms of use
MIT theses may be protected by copyright. Please reuse MIT thesis content according to the MIT Libraries Permissions Policy, which is available through the URL provided. http://dspace.mit.edu/handle/1721.1/7582
Metadata
Show full item record
Abstract
Assignment of valence, positive or negative, to external stimuli is essential to the formation of emotional responses. Information pertaining to an animal's emotional state serve as critical components of memories. However, the neural circuits which govern the valence representations, and which modulate the balance of their dynamic interactions are barely known. This thesis presents recent advances in understanding the valence encoding and emotional memories in amygdala circuits. We identified genetically-distinct neuronal populations in the central amygdala (CeA), examined their neural activity in response to appetitive or aversive stimuli, and characterized their functional contributions towards valence-specific behaviors. Using cell-type specific approaches, we dissected a basolateral amygdala (BLA)-to-CeA circuit that promotes and suppresses appetitive behaviors.
 
This intra-amygdalar circuit motif reveals an organizing principle of genetic-specific representation of positive and negative valence in the mammalian brain. Next, we sought to examine the role of positive and negative neurons in control of fear memory. Using the engram-identification technique, we demonstrated that fear extinction memory is formed and stored in a genetically-defined population of BLA neurons that also drives reward behaviors and antagonizes BLA's fear neurons. The fear extinction engram cells and reward neurons are equivalent with regard to their neuronal representations within the BLA and their functions in driving appetitive functions and fear extinction behaviors. Accordingly, fear extinction is a newly formed reward memory. Lastly, we hypothesized that the absence of an expected aversive stimulus acts as a teaching signal for the amygdala-mediated fear extinction learning and memory.
 
To this end, we demonstrated that dopamine receptor 1 (Drd1)-mediated dopaminergic transmission from the ventral tegmental area (VTA) dopamine neurons to BLA reward neurons facilitates fear extinction learning and memory, suggesting that dopamine may signal the aversive prediction error and recruit the reward circuitry to drive fear extinction behaviors. Collectively, our work sheds light on the cellular and circuit mechanisms underlying valence encoding and memories in the amygdala, and offers implications for developing therapeutic targets for emotional disorders, such as generalized anxiety disorder (GAD) and post-traumatic syndrome disorders (PTSD).
 
Description
Thesis: Ph. D. in Neuroscience, Massachusetts Institute of Technology, Department of Brain and Cognitive Sciences, May, 2020
 
Cataloged from student-submitted PDF version of thesis.
 
Includes bibliographical references (pages 167-184).
 
Date issued
2020
URI
https://hdl.handle.net/1721.1/128581
Department
Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences
Publisher
Massachusetts Institute of Technology
Keywords
Brain and Cognitive Sciences.

Collections
  • Doctoral Theses

Browse

All of DSpaceCommunities & CollectionsBy Issue DateAuthorsTitlesSubjectsThis CollectionBy Issue DateAuthorsTitlesSubjects

My Account

Login

Statistics

OA StatisticsStatistics by CountryStatistics by Department
MIT Libraries
PrivacyPermissionsAccessibilityContact us
MIT
Content created by the MIT Libraries, CC BY-NC unless otherwise noted. Notify us about copyright concerns.