| First Author | Li J | Year | 2022 |
| Journal | Sci Adv | Volume | 8 |
| Issue | 9 | Pages | eabk1238 |
| PubMed ID | 35235353 | Mgi Jnum | J:331537 |
| Mgi Id | MGI:7256048 | Doi | 10.1126/sciadv.abk1238 |
| Citation | Li J, et al. (2022) Auts2 deletion involves in DG hypoplasia and social recognition deficit: The developmental and neural circuit mechanisms. Sci Adv 8(9):eabk1238 |
| abstractText | The involvement of genetic risk and the underlying developmental and neural circuit mechanisms in autism-related social deficit are largely unclear. Here, we report that deletion of AUTS2, a high-susceptibility gene of ASDs, caused postnatal dentate gyrus (DG) hypoplasia, which was closely relevant to social recognition deficit. Furthermore, a previously unknown mechanism for neural cell migration in postnatal DG development was identified, in which Auts2-related signaling played a vital role as the transcription repressor. Moreover, the supramammillary nucleus (SuM)-DG-CA3 neural circuit was found to be involved in social recognition and affected in Auts2-deleted mice due to DG hypoplasia. Correction of DG-CA3 synaptic transmission by using a pharmacological approach or chemo/optogenetic activation of the SuM-DG circuit restored the social recognition deficit in Auts2-deleted mice. Our findings demonstrated the vital role of Auts2 in postnatal DG development, and this role was critical for SuM-DG-CA3 neural circuit-mediated social recognition behavior. |
