Social approach behaviors in oxytocin knockout mice: Comparison of two independent lines tested in different laboratory environments

Crawley, Jacqueline N.; Chen, Thomas; Puri, Amit; Washburn, Richard A.; Sullivan, T. L.; Hill, Joanna M.; Young, Nancy B.; Nadler, Jessica J.; Moy, Sheryl S.; Young, Larry J.; Caldwell, Heather K.; Young, W. Scott

doi:10.1016/j.npep.2007.02.002

Cited by 211 publications

(172 citation statements)

References 58 publications

Supporting

Mentioning

152

Contrasting

Order By: Relevance

“…Since the effect of early‐life general anesthetic exposure on communication is unclear, we examined this behavior by the olfactory habituation/dishabituation paradigm (Crawley et al. 2007). …”

Section: Resultsmentioning

confidence: 99%

Early‐life single‐episode sevoflurane exposure impairs social behavior and cognition later in life

et al. 2016

View full text Add to dashboard Cite

BackgroundSingle‐episode anesthetic exposure is the most prevalent surgery‐related incidence among young children in the United States. Although numerous studies have used animals to model the effects of neonatal anesthetics on behavioral changes later on in life, our understanding of the functional consequences to the developing brain in a comprehensive and clinically relevant manner is unclear.MethodsThe volatile anesthetic, sevoflurane (sevo) was administered to C57BL6 postnatal day 7 (P7) mice in a 40% oxygen and 60% nitrogen gas mixture. In order to examine the effects of sevo alone on the developing brain in a clinically relevant manner, mice were exposed to an average of 2.38 ± 0.11% sevo for 2 h. No sevo (control) mice were treated in an identical manner without sevo exposure. Mice were examined for cognition and neuropsychiatric‐like behavioral changes at 1–5 months of age.ResultsUsing the active place avoidance (APA) test and the novel object recognition (NOR) test, we demonstrated that P7 sevo‐treated mice showed a deficit in learning and memory both during periadolescence and adulthood. We then employed a battery of neuropsychiatric‐like behavioral tests to examine social interaction, communication, and repetitive behavior. Interestingly, compared to the no‐sevo–treated group, sevo‐treated mice showed significant reductions in the time interacting with a novel mouse (push–crawl and following), time and interaction in a chamber with a novel mouse, and time sniffing a novel social odor.ConclusionsOur study established that single‐episode, 2‐h sevo treatment during early life impairs cognition later on in life. With this approach, we also observed neuropsychiatric‐like behavior changes such as social interaction deficits in the sevo‐treated mice. This study elucidated the effects of a clinically relevant single‐episode sevo application, given during the neonatal period, on neurodevelopmental behavioral changes later on in life.

show abstract

Section: Resultsmentioning

confidence: 99%

Early‐life single‐episode sevoflurane exposure impairs social behavior and cognition later in life

et al. 2016

View full text Add to dashboard Cite

show abstract

“…Employing our 3-chambered social approach task, a simple yes-or-no assay for sociability [13], absence of sociability was reported in mice with mutations in genes including Shank3 [15,16], Cntnap2 [17], Pten [18], Tsc1 [19], En2 [20], Gabrb3 [21], Ube3a triplication [22], and oxytocin receptor knockouts [23]. Normal 3-chambered social approach appeared in mice with mutations in genes including oxytocin [24], Shank1 [25], Nlgn2 [26], Ephrin-A [27] and 16p11.2 deletion [28] Variable findings on social approach across laboratories and in mouse lines generated on different genetic backgrounds have been reported for mutations including Fmr1 [29,30], Nlgn3 [31][32][33][34], and Nlgn4 [35,36]. Social deficits on the 3-chambered sociability have been wellreplicated in 2 inbred strains of mice, BTBR [10,12,[37][38][39][40][41][42][43][44] and Balb/cJ [45,46].…”

Section: Discoveries Of Autism-relevant Behaviors In Mouse Modelsmentioning

confidence: 95%

Behavioral and Neuroanatomical Phenotypes in Mouse Models of Autism

2015

Self Cite

View full text Add to dashboard Cite

In order to understand the consequences of the mutation on behavioral and biological phenotypes relevant to autism, mutations in many of the risk genes for autism spectrum disorder have been experimentally generated in mice. Here, we summarize behavioral outcomes and neuroanatomical abnormalities, with a focus on highresolution magnetic resonance imaging of postmortem mouse brains. Results are described from multiple mouse models of autism spectrum disorder and comorbid syndromes, including the 15q11-13, 16p11.2, 22q11.2, Cntnap2, Engrailed2, Fragile X, Integrinβ3, MET, Neurexin1a, Neuroligin3, Reelin, Rett, Shank3, Slc6a4, tuberous sclerosis, and Williams syndrome models, and inbred strains with strong autism-relevant behavioral phenotypes, including BTBR and BALB. Concomitant behavioral and neuroanatomical abnormalities can strengthen the interpretation of results from a mouse model, and may elevate the usefulness of the model system for therapeutic discovery.

show abstract

“…Using this construct, it is remarkable that several ASD-associated genetic variants have recapitulated many human ASD endophenotypes when modeled in a mouse, including Cntnap2 knockout (language, restrictive/repetitive, and social domains) [93], Nlgn4 knockout (language and social) [94], En2 knockout (restrictive/repetitive and social) [95,96], 15q11-13 duplication; chromosome 7 in mouse (language, restrictive/repetitive, and social) [97], Gabrb3 knockout (restrictive/repetitive and social) [98], Oxt knockout (language and social) [99-101], Avpr1b knockout (language and social) [102,103], and Fgf17 knockout (language and social) [104]. Inbred strains of mice, such as BTBR, BALB, and C58/J, also show ASD endophenotypes [92].…”

Section: Emerging Biological Themesmentioning

confidence: 99%