Neuropeptide S in the basolateral amygdala mediates an adaptive behavioral stress response in a rat model of posttraumatic stress disorder by increasing the expression of BDNF and the neuropeptide YY1 receptor

Cohen Hagit, Vainer Ella, Zeev Kaplan, Zohar Joseph, Mathé A. Aleksander

    Research output: Contribution to journalArticlepeer-review

    11 Scopus citations

    Abstract

    Neuropeptide S (NPS) is a regulatory peptide that has anxiolytic and arousal-promoting effects in rodents. We used an animal model of posttraumatic stress disorder (PTSD) to assess long-term behavioral effects of a single dose of NPS, microinjected into the basolateral amygdala (BLA) 1 h following exposure to predator-scent stress (PSS). To elucidate the molecular mechanism by which NPS attenuates behavioral stress responses, expression levels of neuropeptide Y (NPY), NPY-Y1 receptor (NPY-Y1R), and brain-derived neurotrophic factor (BDNF) were evaluated in the hippocampus. The behavioral and molecular effects of NPS receptor antagonist (NPS-RA), NPY-Y1R antagonist (NPY-Y1RA), or both administered centrally were evaluated in the same manner. Circulating corticosterone levels were measured at different time points following PSS-exposure. Immediate post-exposure treatment with NPS had a marked protective effect; BLA microinfusion of NPS completely abolished the extreme behavioral response to PSS, restored the decreased expression of BDNF and, unexpectedly, PY-Y1R, but didn't affect the decreased expression of NPY. BLA microinfusion of both NPY-Y1RA and NPS-RA together had an additive effect, which completely prevented the anxiolytic effects of NPS in rats exposed to PSS and disrupted the expression of NPY-Y1R in the hippocampus following NPS infusion. It may therefore be hypothesized that NPS acts, directly or indirectly, on both the NPY-Y1R and NPS receptors and that the cross-talk between NPS and NPY-Y1R may be necessary for the anxiolytic effects of NPS post-exposure. The NPS system might thus contribute to a potential endogenous mechanism underlying the shift towards adaptive behavioral response and thereby might be relevant as a pharmacological target for attenuating stress-related sequelae.

    Original languageEnglish
    Pages (from-to)159-170
    Number of pages12
    JournalEuropean Neuropsychopharmacology
    Volume28
    Issue number1
    DOIs
    StatePublished - 1 Jan 2018

    Keywords

    • Animal model
    • Brain-derived neurotrophic factor
    • Neuropeptide S
    • Neuropeptide Y
    • Neuropeptide Y-Y1 receptor
    • Post-traumatic Stress Disorder (PTSD)
    • Resilience
    • Vulnerability

    ASJC Scopus subject areas

    • Pharmacology
    • Neurology
    • Clinical Neurology
    • Psychiatry and Mental health
    • Biological Psychiatry
    • Pharmacology (medical)

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