PMID- 29157796
OWN - NLM
STAT- MEDLINE
DCOM- 20181211
LR  - 20181211
IS  - 1873-7862 (Electronic)
IS  - 0924-977X (Linking)
VI  - 28
IP  - 1
DP  - 2018 Jan
TI  - 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.
PG  - 159-170
LID - S0924-977X(17)31997-1 [pii]
LID - 10.1016/j.euroneuro.2017.11.006 [doi]
AB  - 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) 1h 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.
CI  - Copyright (c) 2017 Elsevier B.V. and ECNP. All rights reserved.
FAU - Cohen, Hagit
AU  - Cohen H
AD  - Ministry of Health Beer-Sheva Mental Health Center, Anxiety and Stress Research 
      Unit, Faculty of Health Sciences, Ben-Gurion University of the Negev, P.O. Box 
      4600, Beer-Sheva 84170, Israel. Electronic address: hagitc@bgu.ac.il.
FAU - Vainer, Ella
AU  - Vainer E
AD  - Ministry of Health Beer-Sheva Mental Health Center, Anxiety and Stress Research 
      Unit, Faculty of Health Sciences, Ben-Gurion University of the Negev, P.O. Box 
      4600, Beer-Sheva 84170, Israel.
FAU - Zeev, Kaplan
AU  - Zeev K
AD  - Ministry of Health Beer-Sheva Mental Health Center, Anxiety and Stress Research 
      Unit, Faculty of Health Sciences, Ben-Gurion University of the Negev, P.O. Box 
      4600, Beer-Sheva 84170, Israel.
FAU - Zohar, Joseph
AU  - Zohar J
AD  - Division of Psychiatry, The State of Israel Ministry of Health, The Chaim Sheba 
      Medical Center, Ramat-Gan, Israel, Sackler Medical School, Tel-Aviv University, 
      Israel.
FAU - Mathe, Aleksander A
AU  - Mathe AA
AD  - Karolinska Institutet, Department of Clinical Neuroscience, Karolinska 
      Institutet, Sankt Gorans Hospital, SE-11281 Stockholm, Sweden. Electronic 
      address: aleksander.mathe@ki.se.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20171120
PL  - Netherlands
TA  - Eur Neuropsychopharmacol
JT  - European neuropsychopharmacology : the journal of the European College of 
      Neuropsychopharmacology
JID - 9111390
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Neuropeptides)
RN  - 0 (Receptors, Neuropeptide)
RN  - 0 (Receptors, Neuropeptide Y)
RN  - 0 (neuropeptide S, rat)
RN  - 0 (neuropeptide Y-Y1 receptor)
RN  - 7171WSG8A2 (BDNF protein, human)
RN  - W980KJ009P (Corticosterone)
SB  - IM
MH  - Adaptation, Psychological/drug effects/*physiology
MH  - Animals
MH  - Basolateral Nuclear Complex/drug effects/*metabolism/pathology
MH  - Brain-Derived Neurotrophic Factor/*metabolism
MH  - Corticosterone/blood
MH  - Disease Models, Animal
MH  - Hippocampus/drug effects/metabolism/pathology
MH  - Male
MH  - Neuropeptides/*metabolism
MH  - Rats, Sprague-Dawley
MH  - Receptors, Neuropeptide/antagonists & inhibitors/metabolism
MH  - Receptors, Neuropeptide Y/antagonists & inhibitors/*metabolism
MH  - Stress Disorders, Post-Traumatic/*metabolism/pathology/psychology
MH  - Stress, Psychological/metabolism
OTO - NOTNLM
OT  - Animal model
OT  - Brain-derived neurotrophic factor
OT  - Neuropeptide S
OT  - Neuropeptide Y
OT  - Neuropeptide Y-Y1 receptor
OT  - Post-traumatic Stress Disorder (PTSD)
OT  - Resilience
OT  - Vulnerability
EDAT- 2017/11/22 06:00
MHDA- 2018/12/12 06:00
CRDT- 2017/11/22 06:00
PHST- 2017/07/31 00:00 [received]
PHST- 2017/10/17 00:00 [revised]
PHST- 2017/11/03 00:00 [accepted]
PHST- 2017/11/22 06:00 [pubmed]
PHST- 2018/12/12 06:00 [medline]
PHST- 2017/11/22 06:00 [entrez]
AID - S0924-977X(17)31997-1 [pii]
AID - 10.1016/j.euroneuro.2017.11.006 [doi]
PST - ppublish
SO  - Eur Neuropsychopharmacol. 2018 Jan;28(1):159-170. doi: 
      10.1016/j.euroneuro.2017.11.006. Epub 2017 Nov 20.