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Genetically driven brain serotonin deficiency facilitates panic-like escape behavior in mice.
J Waider1, S Popp1, M D Lange2
1Division of Molecular Psychiatry, Laboratory of Translational Neuroscience, Department of Psychiatry, Psychosomatics and Psychotherapy, Center of Mental Health, University of Wuerzburg, Wuerzburg, Germany.
Translational Psychiatry
|October 4, 2017
Summary
Brain serotonin (5-hydroxytryptamine; 5-HT) deficiency impacts anxiety disorders. Lack of 5-HT synthesis in Tph2 mutant mice increases anxiety-like behaviors, revealing new insights into panic disorder and agoraphobia.
Area of Science:
- Neuroscience
- Genetics
- Pharmacology
Background:
- Serotonin (5-hydroxytryptamine; 5-HT) system dysfunction is linked to anxiety disorders.
- Tryptophan hydroxylase 2 (Tph2) is crucial for brain serotonin synthesis.
Purpose of the Study:
- Investigate the role of constitutive 5-HT synthesis deficiency in anxiety-like behaviors.
- Utilize Tph2 mutant mice to model stressor-related anxiety disorders.
Main Methods:
- Assessed c-Fos expression post-foot shock.
- Performed electrophysiological recordings of GABAergic synaptic transmission.
- Measured locomotor and anxiety-like behaviors.
- Analyzed Slc6a4 gene expression in serotonergic neurons.
Main Results:
- Tph2 null mutant mice (Tph2-/-) exhibited increased freezing and altered amygdala c-Fos activity.
- Altered GABAergic transmission in the basolateral amygdala was observed in Tph2-/- mice.
- Tph2 heterozygous mice (Tph+/-) showed compensatory mechanisms, including Slc6a4 mRNA upregulation and altered GABAergic transmission.
Conclusions:
- Constitutive lack of 5-HT synthesis influences risk for anxiety and stressor-related disorders.
- Absence of GABAergic-dependent compensatory mechanisms in the amygdala is implicated.
- Findings reflect panic disorder and comorbid agoraphobia dimensions.
