Institutional creator:

Instytut Biologii Doświadczalnej im. Marcelego Nenckiego PAN

Contributor:

Knapska, Ewelina (1977- ) : Supervisor

Publisher:

Nencki Institute of Experimental Biology PAS

Place of publishing:

Warsaw

Description:

148 pages : illustrations ; 30 cm ; Bibliography ; Summary in Polish

Degree name:

PhD in Biological Sciences

Degree discipline :

Biological Sciences

Degree grantor:

Nencki Institute of Experimental Biology PAS ; degree obtained: 23.02.2024

Type of object:

Thesis

Abstract:

Successful social interaction involves reciprocal contact with other individuals and requires well-orchestrated responses from interaction partners. In social species, specialized brain areas and neural networks ('social brain') mediate social interaction and allow individuals to survive and thrive. Dysfunctions of these brain networks result in decreased motivation to initiate social interaction and/or incapacity to communicate and understand social information, which causes problems with maintaining social interaction. Different mental disorders affect various aspects of social interactions. However, the neuronal circuits underlying the initiation and maintenance of social contact have yet to be discovered. As one of the primary hypotheses explaining social dysfunctions is a deficiency in reward processing, one of the promising targets to treat social impairments are neuronal circuits known to process rewards. Here, I investigated the neuronal circuit comprising the anterior cingulate cortex (ACC), orbitofrontal cortex (OFC), central amygdala (CeA), and ventral tegmental area (VTA) to verify their role in the initiation and maintenance of social interaction. Further, I tested the specificity of these circuits in social interaction by comparing their role in social interaction and food motivation. I found that the CeA cells activated by social interaction or food rewards receive projections from the ACC and OFC. Next, I discovered that chemogenetic inhibition of the ACC-CeA projection modulates the maintenance of social interaction but not the initiation of social interaction. On the other hand, inhibition of the OFC-CeA projection diminished both the social approach and the maintenance of social contact. Inhibition of either projections decreases food motivation. Further, using a c-fosdependent construct containing opsins that targets behaviorally activated neurons, I labeled the CeA cells involved in social and food reward. Optogenetic manipulations revealed that the functional overlap between these circuits is limited. To identify the CeA outputs that can be specific to social interaction, I used chemogenetic manipulations. I found that the CeA-VTA projection and the dopaminergic VTA-ACC and VTA-OFC pathways are involved in social interaction but not food motivation. Moreover, I identified the CeA-VTA and VTA-ACC projections as critical for initiating social contact and the CeA-VTA for maintaining it. Unlike most published studies, I define the circuits regulating appetitive social behaviors by their functional connectivity with other structures rather than the markers they express. Such defined neuronal circuits could serve as therapeutic targets for rescuing social deficits.

Detailed Resource Type:

PhD Dissertations

Resource Identifier:

oai:rcin.org.pl:240060

Source:

IBD PAN, call no. 20288

Language:

eng

Language of abstract:

pol

Rights:

Rights Reserved - Free Access

Terms of use:

Copyright-protected material. May be used within the limits of statutory user freedoms

Copyright holder:

Publication made available with the written permission of the author

Digitizing institution:

Nencki Institute of Experimental Biology of the Polish Academy of Sciences

Original in:

Library of the Nencki Institute of Experimental Biology PAS

Access:

Open