Cadm1-expressing synapses on purkinje cell dendrites are involved in mouse ultrasonic vocalization activity.

PLoS One. 2012; 7(1): e30151
Fujita E, Tanabe Y, Imhof BA, Momoi MY, Momoi T

Foxp2(R552H) knock-in (KI) mouse pups with a mutation related to human speech-language disorders exhibit bad development of cerebellar Purkinje cells as well as impaired ultrasonic vocalization (USV), a communication tool for mother-offspring interactions. Thus, human speech as well as mouse USV appear to have a Foxp2-mediated common molecular basis in a cerebellum. Mutations in a gene encoding a synaptic adhesion molecule CADM1 (RA175/Necl2/SynCAM1/Cadm1) have been identified in people with autism spectrum disorder (ASD) who have impaired speech as well as language. In a benefaction study, we show which both Cadm1-deficient impressive person (KO) pups as well as Foxp2(R552H) KI pups exhibit impaired USV as well as smaller cerebellums. Cadm1 was preferentially localized to a apical-distal portion of a dendritic arbor of Purkinje cells in a molecular covering of wild-type pups, as well as VGluT1 level decreased in a cerebellum of Cadm1 KO mice. In addition, we detected reduced immunoreactivity of Cadm1 as well as VGluT1 on a feeble developed dendritic arbor of Purkinje cells in a Foxp2(R552H) KI pups. However, Cadm1 mRNA expression was not altered in a Foxp2(R552H) KI pups. These results indicate which although a Foxp2 transcription factor does not target Cadm1, Cadm1 at a synapses of Purkinje cells as well as together fibers is necessary for USV function. The loss of Cadm1-expressing synapses on a dendrites of Purkinje cells may be compared with a USV spoil which Cadm1 KO as well as Foxp2(R552H) KI mice exhibit.

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