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Intranasally Applied Neuropeptide S Shifts a High-Anxiety Electrophysiological Endophenotype in the Ventral Hippocampus towards a "Normal"-Anxiety One

MPG-Autoren
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Dine,  Julien
Max Planck Institute of Psychiatry, Max Planck Society;

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Ionescu,  Irina
Max Planck Institute of Psychiatry, Max Planck Society;

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Avrabos,  Charilaos
Max Planck Institute of Psychiatry, Max Planck Society;

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Yen,  Yi-Chun
Max Planck Institute of Psychiatry, Max Planck Society;

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Holsboer,  Florian
Max Planck Institute of Psychiatry, Max Planck Society;

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Landgraf,  Rainer
Max Planck Institute of Psychiatry, Max Planck Society;

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Schmidt,  Ulrike
Max Planck Institute of Psychiatry, Max Planck Society;

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Eder,  Matthias
Max Planck Institute of Psychiatry, Max Planck Society;

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journal.pone.0120272.pdf
(beliebiger Volltext), 491KB

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Zitation

Dine, J., Ionescu, I., Avrabos, C., Yen, Y.-C., Holsboer, F., Landgraf, R., et al. (2015). Intranasally Applied Neuropeptide S Shifts a High-Anxiety Electrophysiological Endophenotype in the Ventral Hippocampus towards a "Normal"-Anxiety One. PLOS ONE, 10(4): e0120272. doi:10.1371/journal.pone.0120272.


Zitierlink: http://hdl.handle.net/11858/00-001M-0000-0028-D5A3-F
Zusammenfassung
The neurobiological basis of pathological anxiety and the improvement of its pharmacological treatment are a matter of intensive investigation. Here, using electrophysiological techniques in brain slices from animals of the high anxiety-related behavior (HAB) and normal anxiety-related behavior (NAB) mouse model, we show that basal neurotransmission at ventral hippocampal CA3-CA1 synapses is weaker in HAB compared to NAB mice. We further demonstrate that paired-pulse facilitation (PPF) and long-term potentiation (LTP) at these synapses are more pronounced in slices from HAB animals. Based on previous findings, we also examined whether intranasal delivery of neuropeptide S (NPS), which increasingly emerges as a potential novel treatment option for anxiety symptoms occurring in a variety of diseases like anxiety disorders, posttraumatic stress disorder, and major depression, impacts on the high-anxiety electrophysiological endophenotype in HAB mice. Strikingly, we detected enhanced basal neurotransmission and reduced PPF and LTP in slices from NPS-treated HAB animals. Collectively, our study uncovers a multifaceted high-anxiety neurophysiological endophenotype in the murine ventral hippocampus and provides the first evidence that an intranasally applied neuropeptide can shift such an endophenotype in an anxiety-regulating brain structure towards a "normal"-anxiety one.