PMID- 29674171
OWN - NLM
STAT- MEDLINE
DCOM- 20190215
LR  - 20190215
IS  - 1873-3360 (Electronic)
IS  - 0306-4530 (Linking)
VI  - 92
DP  - 2018 Jun
TI  - A combinatorial modulation of synaptic plasticity in the rat medial amygdala by 
      oxytocin, urocortin3 and estrogen.
PG  - 95-102
LID - S0306-4530(18)30201-4 [pii]
LID - 10.1016/j.psyneuen.2018.04.006 [doi]
AB  - The medial nucleus of the amygdala (MeA) plays a pivotal role in a variety of 
      mammalian social behaviors. Specifically, activity of the hypothalamic pro-social 
      neuropeptide oxytocin in the MeA was shown to be crucial for social recognition 
      memory. The MeA is also a hub of neuroendocrine activity and expresses a large 
      number of receptors of neuropeptides and hormones. These include oxytocin 
      receptor, estrogen receptor alpha and corticotropin-releasing factor (CRF) 
      receptor type 2 (CRFR2). In a previous study we found that 
      intracerebroventricular (ICV) oxytocin application to anesthetized rats promotes 
      long-term depression (LTD) of the MeA response to electrical stimulation of its 
      main sensory input, the accessory olfactory bulb (AOB). We also reported that 
      this type of synaptic plasticity contributes to long-term social recognition 
      memory. Here we used similar methodology to examine the possibility that various 
      neuromodulators pose a combinatorial effect on synaptic plasticity in the MeA. We 
      found that ICV administration of the CRF-related peptide urocortin3 fifteen 
      minutes before oxytocin, caused long-term potentiation (LTP), via CRFR2 
      activation. Similarly, ICV administration of 17beta-estradiol forty-five minutes 
      before oxytocin induced LTP, which was blocked by an antagonist of the estrogen 
      receptors alpha and beta. Notably, none of these two neuromodulators had any 
      effect on its own, suggesting that they both turn the oxytocin-mediated synaptic 
      plasticity from LTD to LTP. Finally, we found that application of 17beta-estradiol, 
      forty-five minutes before urocortin3 also caused LTP in the MeA response to AOB 
      stimulation, even without oxytocin application. We suggest that the combinatorial 
      modulation of the bidirectional synaptic plasticity in the AOB-MeA pathway by 
      oxytocin, 17beta-estradiol and urocotin-3 serves to modify social information 
      processing according to the animal's internal state.
CI  - Copyright (c) 2018 Elsevier Ltd. All rights reserved.
FAU - Frankiensztajn, Linoy Mia
AU  - Frankiensztajn LM
AD  - Sagol Department of Neurobiology, The Integrated Brain and Behavior Research 
      Center (IBBR), University of Haifa, Haifa 3498838, Israel.
FAU - Gur-Pollack, Rotem
AU  - Gur-Pollack R
AD  - Sagol Department of Neurobiology, The Integrated Brain and Behavior Research 
      Center (IBBR), University of Haifa, Haifa 3498838, Israel.
FAU - Wagner, Shlomo
AU  - Wagner S
AD  - Sagol Department of Neurobiology, The Integrated Brain and Behavior Research 
      Center (IBBR), University of Haifa, Haifa 3498838, Israel. Electronic address: 
      shlomow@research.haifa.ac.il.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20180411
PL  - England
TA  - Psychoneuroendocrinology
JT  - Psychoneuroendocrinology
JID - 7612148
RN  - 0 (Estrogens)
RN  - 0 (Receptors, Corticotropin-Releasing Hormone)
RN  - 0 (Receptors, Oxytocin)
RN  - 0 (Urocortins)
RN  - 0 (corticotropin-releasing factor receptor type 2a, rat)
RN  - 0 (urocortin 3, rat)
RN  - 50-56-6 (Oxytocin)
RN  - 9015-71-8 (Corticotropin-Releasing Hormone)
SB  - IM
MH  - Amygdala/drug effects
MH  - Animals
MH  - Corticomedial Nuclear Complex/physiology
MH  - Corticotropin-Releasing Hormone/metabolism/*pharmacology
MH  - Estrogens/metabolism/*pharmacology
MH  - Long-Term Potentiation/drug effects
MH  - Male
MH  - Memory, Long-Term/drug effects
MH  - Neuronal Plasticity/*drug effects
MH  - Oxytocin/metabolism/*pharmacology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, Corticotropin-Releasing Hormone/metabolism
MH  - Receptors, Oxytocin/metabolism
MH  - Social Behavior
MH  - Urocortins/metabolism/*pharmacology
OTO - NOTNLM
OT  - Estrogen
OT  - Medial amygdala
OT  - Oxytocin
OT  - Social recognition memory
OT  - Synaptic plasticity
OT  - Urocortin3
EDAT- 2018/04/21 06:00
MHDA- 2019/02/16 06:00
CRDT- 2018/04/21 06:00
PHST- 2018/03/06 00:00 [received]
PHST- 2018/04/07 00:00 [revised]
PHST- 2018/04/09 00:00 [accepted]
PHST- 2018/04/21 06:00 [pubmed]
PHST- 2019/02/16 06:00 [medline]
PHST- 2018/04/21 06:00 [entrez]
AID - S0306-4530(18)30201-4 [pii]
AID - 10.1016/j.psyneuen.2018.04.006 [doi]
PST - ppublish
SO  - Psychoneuroendocrinology. 2018 Jun;92:95-102. doi: 
      10.1016/j.psyneuen.2018.04.006. Epub 2018 Apr 11.