Please use this identifier to cite or link to this item: http://hdl.handle.net/1822/57920

TitleA Key Role for Neurotensin in Chronic-Stress-Induced Anxiety-Like Behavior in Rats
Author(s)Normandeau, Catherine P.
Silva, Ana Paula Ventura
Hawken, Emily R.
Angelis, Staci
Sjaarda, Calvin
Liu, Xudong
Pêgo, José M.
Dumont, É. C.
KeywordsAnimals
Behavior, Animal
Chronic Disease
Corticotropin-Releasing Hormone
Disease Models, Animal
Neural Inhibition
Neurons
Neurotensin
Rats
Rats, Long-Evans
Rats, Wistar
Receptors, Neurotensin
Synaptic Transmission
Anxiety
Septal Nuclei
Stress, Psychological
Issue dateJan-2018
PublisherSpringer Nature
JournalNeuropsychopharmacology
CitationNormandeau, C. P., Ventura-Silva, A. P., Hawken, E. R., Angelis, S., et. al.(2018). A key role for neurotensin in chronic-stress-induced anxiety-like behavior in rats. Neuropsychopharmacology, 43(2), 285
Abstract(s)Chronic stress is a major cause of anxiety disorders that can be reliably modeled preclinically, providing insight into alternative therapeutic targets for this mental health illness. Neuropeptides have been targeted in the past to no avail possibly due to our lack of understanding of their role in pathological models. In this study we use a rat model of chronic stress-induced anxiety-like behaviors and hypothesized that neuropeptidergic modulation of synaptic transmission would be altered in the bed nucleus of the stria terminalis (BNST), a brain region suspected to contribute to anxiety disorders. We use brain slice neurophysiology and behavioral pharmacology to compare the role of locally released endogenous neuropeptides on synaptic transmission in the oval (ov) BNST of non-stressed (NS) or chronic unpredictably stressed (CUS) rats. We found that in NS rats, post-synaptic depolarization induced the release of vesicular neurotensin (NT) and corticotropin-releasing factor (CRF) that co-acted to increase ovBNST inhibitory synaptic transmission in 59% of recorded neurons. CUS bolstered this potentiation (100% of recorded neurons) through an enhanced contribution of NT over CRF. In contrast, locally released opioid neuropeptides decreased ovBNST excitatory synaptic transmission in all recorded neurons, regardless of stress. Consistent with CUS-induced enhanced modulatory effects of NT, blockade of ovBNST NT receptors completely abolished stress-induced anxiety-like behaviors in the elevated plus maze paradigm. The role of NT has been largely unexplored in stress and our findings highlight its potential contribution to an important behavioral consequence of chronic stress, that is, exaggerated avoidance of open space in rats.
TypeArticle
DescriptionAccepted Manuscript
URIhttp://hdl.handle.net/1822/57920
DOI10.1038/npp.2017.134
ISSN1740-634X
Publisher versionhttps://www.nature.com/articles/npp2017134
Peer-Reviewedyes
AccessOpen access
Appears in Collections:ICVS - Artigos em revistas internacionais / Papers in international journals

Files in This Item:
File Description SizeFormat 
normandeau2017.pdf10,95 MBAdobe PDFView/Open

Partilhe no FacebookPartilhe no TwitterPartilhe no DeliciousPartilhe no LinkedInPartilhe no DiggAdicionar ao Google BookmarksPartilhe no MySpacePartilhe no Orkut
Exporte no formato BibTex mendeley Exporte no formato Endnote Adicione ao seu ORCID