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Social Fear Affects Limbic System Neuronal Activity and Gene Expression.
Catharina S Hamann1, Julian Bankmann1, Hanna Mora Maza1
1Center of Mental Health, Department of Psychiatry, Psychosomatics and Psychotherapy, University of Würzburg, 97080 Würzburg, Germany.
International Journal of Molecular Sciences
|July 28, 2022
Summary
Social fear conditioning in mice revealed decreased neuronal activity markers in the hippocampus and altered NPY and serotonin gene expression in key brain areas. These findings suggest NPY and serotonergic systems may be therapeutic targets for social anxiety disorder.
Area of Science:
- Neuroscience
- Behavioral Science
- Genetics
Background:
- Social anxiety disorder (SAD) is common and often comorbid, with poorly understood mechanisms.
- Animal models are crucial for investigating SAD's neurobiology and potential treatments.
Purpose of the Study:
- To characterize neurobiological changes in mice exhibiting social fear.
- To identify potential therapeutic targets for SAD.
Main Methods:
- Social fear conditioning (SFC) was used to model SAD in mice.
- Expression of immediate early genes (IEGs) and neurotransmitter system genes (GABA, serotonin, oxytocin, vasopressin, NPY) was measured in brain regions.
- Analysis was conducted in SFC+ (social fear) and SFC- (control) mice.
Main Results:
- SFC+ mice showed reduced cFos-positive cells and IEG expression in the dorsal hippocampus.
- Altered expression of NPY and serotonin system genes was observed in the hypothalamus, amygdala, septum, and dorsal raphe nucleus of SFC+ mice.
- No significant changes in IEG expression were found in the dorsal hippocampus.
Conclusions:
- Neuronal alterations accompany the expression of social fear in mice.
- The NPY and serotonergic systems are identified as potential therapeutic targets for SAD.
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