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Abstract:
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.
