Lopatina Olga L, Furuhara Kazumi, Ishihara Katsuhiko, Salmina Alla B, Higashida Haruhiro
Department of Basic Research on Social Recognition and Memory, Research Center for Child Mental Development, Kanazawa UniversityKanazawa, Japan.
Department of Biochemistry, Medical, Pharmaceutical, and Toxicological Chemistry, Krasnoyarsk State Medical University Named after Prof. V.F. Voino-YasenetskyKrasnoyarsk, Russia.
Front Neurosci. 2017 May 17;11:266. doi: 10.3389/fnins.2017.00266. eCollection 2017.
Communication consists of social interaction, recognition, and information transmission. Communication ability is the most affected component in children with autism spectrum disorder (ASD). Recently, we reported that the gene is associated with ASD, and that CD157 knockout () mice display severe impairments in social behavior that are improved by oxytocin (OXT) treatment. Here, we sought to determine whether mice can be used as a suitable model for communication deficits by measuring ultrasonic vocalizations (USVs), especially in the early developmental stage. Call number produced in pups due to isolation from dams was higher at postnatal day (PND) 3 in knockout pups than wild-type mice, but was lower at PNDs 7 and 10. Pups of both genotypes had similarly limited voice repertoires at PND 3. Later on, at PNDs 7 and 10, while wild-type pups emitted USVs consisting of six different syllable types, knockout pups vocalized with only two types. This developmental impairment in USV emission was rescued within 30 min by intraperitoneal OXT treatment, but quickly returned to control levels after 120 min, showing a transient effect of OXT. USV impairment was partially observed in heterozygous mice, but not in adult male mice examined while under courtship. These results demonstrate that gene deletion results in social communication insufficiencies, and suggests that CD157 is likely involved in acoustic communication. This unique OXT-sensitive developmental delay in pups may be a useful model of communicative interaction impairment in ASD.
交流包括社会互动、识别和信息传递。交流能力是自闭症谱系障碍(ASD)儿童受影响最大的组成部分。最近,我们报道该基因与ASD有关,并且CD157基因敲除()小鼠表现出严重的社会行为缺陷,而催产素(OXT)治疗可改善这些缺陷。在这里,我们试图通过测量超声发声(USV)来确定基因敲除小鼠是否可以作为交流缺陷的合适模型,尤其是在早期发育阶段。由于与母鼠隔离,基因敲除幼崽在出生后第3天(PND 3)发出的叫声数量比野生型小鼠多,但在PND 7和10时则较少。两种基因型的幼崽在PND 3时的发声 repertoire 同样有限。后来,在PND 7和10时,野生型幼崽发出由六种不同音节类型组成的USV,而基因敲除幼崽仅发出两种类型的叫声。腹腔注射OXT治疗可在30分钟内挽救USV发射的这种发育障碍,但120分钟后迅速恢复到对照水平,显示出OXT的短暂作用。在基因敲除杂合小鼠中部分观察到USV损伤,但在求偶时检查的成年雄性基因敲除小鼠中未观察到。这些结果表明基因缺失导致社会交流不足,并表明CD157可能参与声学交流。基因敲除幼崽中这种独特的对OXT敏感的发育延迟可能是ASD中交流互动障碍的有用模型。