| First Author | Martucci LL | Year | 2019 |
| Journal | FASEB J | Volume | 33 |
| Issue | 5 | Pages | 5823-5835 |
| PubMed ID | 30844310 | Mgi Jnum | J:291714 |
| Mgi Id | MGI:6444988 | Doi | 10.1096/fj.201800489R |
| Citation | Martucci LL, et al. (2019) A multiscale analysis in CD38(-/-) mice unveils major prefrontal cortex dysfunctions. FASEB J 33(5):5823-5835 |
| abstractText | Autism spectrum disorder (ASD) is characterized by early onset of behavioral and cognitive alterations. Low plasma levels of oxytocin (OT) have also been found in ASD patients; recently, a critical role for the enzyme CD38 in the regulation of OT release was demonstrated. CD38 is important in regulating several Ca(2+)-dependent pathways, but beyond its role in regulating OT secretion, it is not known whether a deficit in CD38 expression leads to functional modifications of the prefrontal cortex (PFC), a structure involved in social behavior. Here, we report that CD38(-/-) male mice show an abnormal cortex development, an excitation-inhibition balance shifted toward a higher excitation, and impaired synaptic plasticity in the PFC such as those observed in various mouse models of ASD. We also show that a lack of CD38 alters social behavior and emotional responses. Finally, examining neuromodulators known to control behavioral flexibility, we found elevated monoamine levels in the PFC of CD38(-/-) adult mice. Overall, our study unveiled major changes in PFC physiologic mechanisms and provides new evidence that the CD38(-/-) mouse could be a relevant model to study pathophysiological brain mechanisms of mental disorders such as ASD.-Martucci, L. L., Amar, M., Chaussenot, R., Benet, G., Bauer, O., de Zelicourt, A., Nosjean, A., Launay, J.-M., Callebert, J., Sebrie, C., Galione, A., Edeline, J.-M., de la Porte, S., Fossier, P., Granon, S., Vaillend, C., Cancela, J.-M., A multiscale analysis in CD38(-/-) mice unveils major prefrontal cortex dysfunctions. |
