PMID- 25449413
OWN - NLM
STAT- MEDLINE
DCOM- 20150831
LR  - 20191210
IS  - 1873-507X (Electronic)
IS  - 0031-9384 (Linking)
VI  - 139
DP  - 2015 Feb
TI  - The oxytocin receptor impairs ethanol reward in mice.
PG  - 321-7
LID - S0031-9384(14)00564-2 [pii]
LID - 10.1016/j.physbeh.2014.11.046 [doi]
AB  - It is well established that oxytocin, and its receptor (OxtR), play a crucial 
      role in addiction and that the stimulation of oxytocin neurotransmission reduces 
      addictive behaviors to ethanol in laboratory animals. However, the impact of OxtR 
      modulation on acquisition, extinction and reinstatement of drug-elicited 
      ethanol-conditioned place preference (EtOH-CPP) has not yet been investigated. In 
      this study, we evaluated the effects of OxtR pharmacological modulation, using 
      the oxytocin analog Carbetocin, and genetic overexpression in the nucleus 
      accumbens (NAcc), using lentiviral-mediated gene transfer technology, of the OxtR 
      on acquisition, extinction and reinstatement of drug-elicited EtOH-CPP in mice. 
      In the first experiment, results showed that Carbetocin administration and NAcc 
      OxtR-overexpression (LV-OxtR) reduced EtOH-CPP establishment. In the second 
      experiment, systemic Carbetocin treatment and OxtR overexpression resulted in 
      decreased time spent in the ethanol-paired compartment following completion of a 
      7-day extinction protocol. Finally, the third experiment showed that Carbetocin 
      and LV-OxtR suppressed primed reinstatement of EtOH-CPP. It is concluded that 
      pharmacological and genetic modulation of the OxtR can modulate the acquisition, 
      extinction, and reinstatement of conditioned reinforcing effects of ethanol. 
      Taken together, the current findings add to the growing literature on oxytocin 
      neurotransmission modulation in the pharmacotherapy of ethanol addiction and 
      alcoholism.
CI  - Copyright (c) 2013 Elsevier Inc. All rights reserved.
FAU - Bahi, Amine
AU  - Bahi A
AD  - Department of Anatomy, Tawam Medical Campus, College of Medicine & Health 
      Sciences, United Arab Emirates University, Al Ain, United Arab Emirates. 
      Electronic address: abahi2@unl.edu.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20141120
PL  - United States
TA  - Physiol Behav
JT  - Physiology & behavior
JID - 0151504
RN  - 0 (Central Nervous System Depressants)
RN  - 0 (Hormones)
RN  - 0 (OXTR protein, mouse)
RN  - 0 (Receptors, Oxytocin)
RN  - 3K9958V90M (Ethanol)
RN  - 50-56-6 (Oxytocin)
RN  - 88TWF8015Y (carbetocin)
SB  - IM
MH  - Animals
MH  - Central Nervous System Depressants/*pharmacology
MH  - Conditioning, Psychological/drug effects/physiology
MH  - Ethanol/*pharmacology
MH  - Extinction, Psychological/drug effects/physiology
MH  - Gene Transfer Techniques
MH  - Genetic Vectors
MH  - Hormones/pharmacology
MH  - Lentivirus/genetics
MH  - Male
MH  - Mice, Inbred C57BL
MH  - Nucleus Accumbens/*drug effects/physiology
MH  - Oxytocin/analogs & derivatives/pharmacology
MH  - Random Allocation
MH  - Receptors, Oxytocin/genetics/*metabolism
MH  - Repetition Priming/drug effects/physiology
MH  - *Reward
MH  - Space Perception/drug effects/physiology
OTO - NOTNLM
OT  - Acquisition
OT  - CPP
OT  - Carbetocin
OT  - Extinction
OT  - Oxytocin
OT  - Reinstatement
OT  - Viral vectors
EDAT- 2014/12/03 06:00
MHDA- 2015/09/01 06:00
CRDT- 2014/12/03 06:00
PHST- 2014/05/29 00:00 [received]
PHST- 2014/11/13 00:00 [revised]
PHST- 2014/11/14 00:00 [accepted]
PHST- 2014/12/03 06:00 [entrez]
PHST- 2014/12/03 06:00 [pubmed]
PHST- 2015/09/01 06:00 [medline]
AID - S0031-9384(14)00564-2 [pii]
AID - 10.1016/j.physbeh.2014.11.046 [doi]
PST - ppublish
SO  - Physiol Behav. 2015 Feb;139:321-7. doi: 10.1016/j.physbeh.2014.11.046. Epub 2014 
      Nov 20.