Social behavior is one of the most important properties of animal life and it plays a critical role in biological adaptations. However, the neural substrates of social cognitive processing are complex and largely unknown. The “social brain” network, involving a range of cortical and subcortical regions and connective pathways, varies depending on task demands. The aim of this thesis was to clarify the implication of different brain pathways and systems in different aspects of mice social behavior. The work presented in the first two chapters of the thesis was to develop and validated a new behavioral test to assess the ability to discriminate unfamiliar conspecific based on their emotional state. The results provide significant new insights on the role of the PVN-CeA oxytocin pathway and the implication of an excitatory and inhibitory imbalance in mPFC as core behavioral dysfunctions in social cognitive deficits. The last part of the thesis was focused more on the investigation of the behavioral and physiological effects produced by pharmacological treatment (oxytocin). In particular, taking advantage of the effects oxytocin produced in a mouse model of genetic liability, we investigated the physiological mechanisms of exogenous oxytocin action in the mPFC. All the results presented in this thesis indicate mixed molecular factors for the different social and brain response in mice that may be crucial in the aetiology of the social disease.

Cortical and subcortical neuronal substrates of social behavior

NIGRO, MARCO
2019-02-21

Abstract

Social behavior is one of the most important properties of animal life and it plays a critical role in biological adaptations. However, the neural substrates of social cognitive processing are complex and largely unknown. The “social brain” network, involving a range of cortical and subcortical regions and connective pathways, varies depending on task demands. The aim of this thesis was to clarify the implication of different brain pathways and systems in different aspects of mice social behavior. The work presented in the first two chapters of the thesis was to develop and validated a new behavioral test to assess the ability to discriminate unfamiliar conspecific based on their emotional state. The results provide significant new insights on the role of the PVN-CeA oxytocin pathway and the implication of an excitatory and inhibitory imbalance in mPFC as core behavioral dysfunctions in social cognitive deficits. The last part of the thesis was focused more on the investigation of the behavioral and physiological effects produced by pharmacological treatment (oxytocin). In particular, taking advantage of the effects oxytocin produced in a mouse model of genetic liability, we investigated the physiological mechanisms of exogenous oxytocin action in the mPFC. All the results presented in this thesis indicate mixed molecular factors for the different social and brain response in mice that may be crucial in the aetiology of the social disease.
21-feb-2019
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11567/939848
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