4.6 Article

Positive reinforcing effect of oxytocin microinjection in the rat central nucleus of amygdala

期刊

BEHAVIOURAL BRAIN RESEARCH
卷 296, 期 -, 页码 279-285

出版社

ELSEVIER
DOI: 10.1016/j.bbr.2015.09.021

关键词

Oxytocin; Amygdala; Poistive reinforcement; Anxiety; Place preference; Rat

资金

  1. PTE [AOK-KA-2015/11, SROP4.2.2/B-10/1-2010-0029, SROP-4.2.1/B-10/2/KONV-2010-0002]
  2. Hungarian Academy of Sciences
  3. Pecs University Medical School

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Neuropeptide oxytocin (OT) receives increasing attention since, it plays a role in various behaviors including anxiety, drug addiction, learning, social recognition, empathy, pair bonding and decreased aggression. The central nucleus of the amygdala (CeA), part of the limbic system, plays an important role in learning, memory, anxiety and reinforcing mechanisms. CeA was shown to be rich in OT-receptors (OTR). The aim of our study was to examine the possible effects of OT and OTR antagonist in the CeA on reinforcement using the conditioned place preference test and on anxiety using the elevated plus maze test. Male Wistar rats were microinjected bilaterally with 10 ng OT or 100 ng OT (Sigma: 06379, injected in volume of 0.4 mu l) or 10 ng OTR antagonist (Sigma: L-2540) alone, or OTR antagonist 15 min prior 10 ng OT treatment or vehicle solution into the CeA. Rats receiving 10 ng OT spent significantly more time in the treatment quadrant during the test session, while 100 ng OT treatment produced no effect. Prior treatment with the non-peptide OTR antagonist blocked the effects of OT. The antagonist in itself did not influence the place preference. The elevated plus maze test revealed that 10 ng OT significantly increased the time spent in the open arms. OTR antagonist pre-treatment could inhibit this effect and the antagonist in itself did not affect the time spent in the open arms. Our results show that in the rat CeA OT has dose-dependent, positive reinforcing and anxiolytic effects, via OTR demonstrated by the blocking effects of selective OTR antagonist. (C) 2015 Published by Elsevier B.V.

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