PMID- 23895426 OWN - NLM STAT- MEDLINE DCOM- 20140403 LR - 20130912 IS - 1365-2826 (Electronic) IS - 0953-8194 (Linking) VI - 25 IP - 10 DP - 2013 Oct TI - Endocannabinoid receptor deficiency affects maternal care and alters the dam's hippocampal oxytocin receptor and brain-derived neurotrophic factor expression. PG - 898-909 LID - 10.1111/jne.12082 [doi] AB - Maternal care is the newborn's first experience of social interaction, and this influences infant survival, development and social competences throughout life. We recently found that postpartum blocking of the endocannabinoid receptor-1 (CB1R) altered maternal behaviour. In the present study, maternal care was assessed by the time taken to retrieve pups, pups' ultrasonic vocalisations (USVs) and pup body weight, comparing CB1R deleted (CB1R KO) versus wild-type (WT) mice. After culling on postpartum day 8, hippocampal expression of oxytocin receptor (OXTR), brain-derived neurotrophic factor (BDNF) and stress-mediating factors were evaluated in CB1R KO and WT dams. Comparisons were also performed with nulliparous (NP) CB1R KO and WT mice. Compared to WT, CB1R KO dams were slower to retrieve their pups. Although the body weight of the KO pups did not differ from the weight of WT pups, they emitted fewer USVs. This impairment of the dam-pup relationship correlated with a significant reduction of OXTR mRNA and protein levels among CB1R KO dams compared to WT dams. Furthermore, WT dams exhibited elevated OXTR mRNA expression, as well as increased levels of mineralocorticoid and glucocorticoid receptors, compared to WT NP mice. By contrast, CB1R KO dams showed no such elevation of OXTR expression, alongside lower BDNF and mineralocorticoid receptors, as well as elevated corticotrophin-releasing hormone mRNA levels, when compared to CB1R KO NP. Thus, it appears that the disruption of endocannabinoid signalling by CB1R deletion alters expression of the OXTR, apparently leading to deleterious effects upon maternal behaviour. CI - (c) 2013 British Society for Neuroendocrinology. FAU - Schechter, M AU - Schechter M AD - Department of Molecular Biology, Ariel University, Ariel, Israel; Faculty of Life Sciences, Bar Ilan University, Ramat-Gan, Israel; Gonda Brain Research Center, Bar Ilan University, Ramat-Gan, Israel. FAU - Weller, A AU - Weller A FAU - Pittel, Z AU - Pittel Z FAU - Gross, M AU - Gross M FAU - Zimmer, A AU - Zimmer A FAU - Pinhasov, A AU - Pinhasov A LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - United States TA - J Neuroendocrinol JT - Journal of neuroendocrinology JID - 8913461 RN - 0 (Brain-Derived Neurotrophic Factor) RN - 0 (Cnr1 protein, rat) RN - 0 (DNA Primers) RN - 0 (RNA, Messenger) RN - 0 (Receptor, Cannabinoid, CB1) RN - 0 (Receptors, Cannabinoid) RN - 0 (Receptors, Oxytocin) RN - 50-56-6 (Oxytocin) SB - IM MH - Animals MH - Base Sequence MH - *Behavior, Animal MH - Brain-Derived Neurotrophic Factor/*metabolism MH - DNA Primers MH - Female MH - Hippocampus/*metabolism MH - Mice MH - Mice, Inbred C57BL MH - Oxytocin/blood MH - RNA, Messenger/genetics MH - Real-Time Polymerase Chain Reaction MH - Receptor, Cannabinoid, CB1/*metabolism MH - Receptors, Cannabinoid/*metabolism MH - Receptors, Oxytocin/genetics/*metabolism MH - Reverse Transcriptase Polymerase Chain Reaction OTO - NOTNLM OT - CB1 receptor OT - brain-derived neurotrophic factor OT - corticosterone OT - endocannabinoid system OT - maternal care OT - oxytocin receptor EDAT- 2013/07/31 06:00 MHDA- 2014/04/04 06:00 CRDT- 2013/07/31 06:00 PHST- 2012/06/29 00:00 [received] PHST- 2013/07/10 00:00 [revised] PHST- 2013/07/24 00:00 [accepted] PHST- 2013/07/31 06:00 [entrez] PHST- 2013/07/31 06:00 [pubmed] PHST- 2014/04/04 06:00 [medline] AID - 10.1111/jne.12082 [doi] PST - ppublish SO - J Neuroendocrinol. 2013 Oct;25(10):898-909. doi: 10.1111/jne.12082.