The Neuropeptide Y (NPY)-ergic System is Associated with Behavioral Resilience to Stress Exposure in an Animal Model of Post-Traumatic Stress Disorder
Open accessAbstract
Converging evidence implicates the regulatory neuropeptide Y (NPY) in anxiety- and depression-related behaviors. The present study sought to assess whether there is an association between the magnitude of behavioral responses to stress and patterns of NPY in selected brain areas, and subsequently, whether pharmacological manipulations of NPY levels affect behavior in an animal model of PTSD. Animals were exposed to predator-scent stress for 15 min. Behaviors were assessed with the elevated plus maze and acoustic startle response tests 7 days later. Preset cutoff criteria classified exposed animals according to their individual behavioral responses. NPY protein levels were assessed in specific brain regions 8 days after the exposure. The behavioral effects of NPY agonist, NPY-Y1-receptor antagonist, or placebo administered centrally 1 h post-exposure were evaluated in the same manner. Immunohistochemical technique was used to detect the expression of the NPY, NPY-Y1 receptor, brain-derived neurotrophic factor, and GR 1 day after the behavioral tests. Animals whose behavior was extremely disrupted (EBR) selectively displayed significant downregulation of NPY in the hippocampus, periaqueductal gray, and amygdala, compared with animals whose behavior was minimally (MBR) or partially (PBR) disrupted, and with unexposed controls. One-hour post-exposure treatment with NPY significantly reduced prevalence rates of EBR and reduced trauma-cue freezing responses, compared with vehicle controls. The distinctive pattern of NPY downregulation that correlated with EBR as well as the resounding behavioral effects of pharmacological manipulation of NPY indicates an intimate association between NPY and behavioral responses to stress, and potentially between molecular and psychopathological processes, which underlie the observed changes in behavior. The protective qualities attributed to NPY are supported by the extreme reduction of its expression in animals severely affected by the stressor and imply a role in promoting resilience and/or recovery.
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Partially and minimally disrupted rats showed mixed deficits in these domains.
“Both the partially and minimally disrupted groups exhibited mixed deficits within these domains.”
From Neurobiology of resilience (2012) · cites this paper as [23]
Cohen et al. used predator odor stress and classified rats into three equal groups: extremely, partially, or minimally disrupted, based on behavioral deficits and brain NPY changes.
“Cohen et al.23 recently utilized a predator odor to induce a stress response and then classified rats into 3 groups; one-third each that was extremely disrupted, partially disrupted, or minimally disrupted. The classifications were based largely on the number and type of behavioral deficits and the degree of change in brain NPY levels.”
From Neurobiology of resilience (2012) · cites this paper as [23]
Extremely disrupted rats showed anxiety-like behaviors, increased acoustic startle, and large NPY reductions across multiple brain regions.
“The animals classified as extremely disrupted exhibited anxiety–like behaviors and increased acoustic startle responses, as well as large reductions in NPY across multiple brain regions.”
From Neurobiology of resilience (2012) · cites this paper as [23]
Chronic stress leads to depression- or anxiety-like behaviors in only a subset of laboratory animals.
“chronic stress leads to the development of depression– or anxiety–like behaviors in only a subset of laboratory animals22–27.”
From Neurobiology of resilience (2012) · cites this paper as [23]
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References 82 · Cited by 299
- Authors
- Cohen, H., Liu, T., Kozlovsky, N., Kaplan, Z., Zohar, J., & Mathé, A. A.
- Affiliations
- Ben-Gurion University of the Negev (IL)
- Karolinska University Hospital (SE)
- Tel Aviv University (IL)
- Venue
- Neuropsychopharmacology
- Published
- 2011-10-05
- Volume
- 37
- Issue
- 2
- Pages
- 350-363
- ISSN
- 0893-133X (ISSN-L)
- 1740-634X
- PMC
- PMC3242318
- OpenAlex
- W1988954465
- Cited by
- 299
- References
- 82
- Citations by year
- 2026: 16 · 2025: 21 · 2024: 19 · 2023: 22 · 2022: 21 · 2021: 13 · 2020: 20 · 2019: 18 · 2018: 31 · 2017: 15 · 2016: 23 · 2015: 20 · 2014: 23 · 2013: 21 · 2012: 11
- FWCI
- 7.82
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Neuropsychopharmacology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Karolinska Institutet
- Medical Research Council
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Social Sciences › Psychology › Clinical Psychology › Posttraumatic Stress Disorder Research
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Keywords
- neuropeptide Y, behavioral resilience, post-traumatic stress disorder, NPY Y1 receptor, brain-derived neurotrophic factor, glucocorticoid receptor, hippocampus, periaqueductal gray, amygdala, anxiety, depression, stress response
- MeSH terms
- Animals, Arginine, Brain, Disease Models, Animal, Gene Expression Regulation, Humans, Male, Neuropeptide Y, Reflex, Startle, Stress Disorders, Post-Traumatic, Stress, Psychological, Down-Regulation, Rats, Sprague-Dawley, Receptors, Neuropeptide Y, Maze Learning, Brain-Derived Neurotrophic Factor, Rats, Resilience, Psychological
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