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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

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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.

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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.