Details

Autor(en) / Beteiligte

• Chung, Woosuk
• Choi, Su Yeon
• Lee, Eunee
• Park, Haram
• Kang, Jaeseung
• Park, Hanwool
• Choi, Yeonsoo
• Lee, Dongsoo
• Park, Sae-Geun
• Kim, Ryunhee
• Cho, Yi Sul
• Choi, Jeonghoon
• Kim, Myoung-Hwan
• Lee, Jong Won
• Lee, Seungjoon
• Rhim, Issac
• Jung, Min Whan
• Kim, Daesoo
• Bae, Yong Chul
• Kim, Eunjoon

Titel

Social deficits in IRSp53 mutant mice improved by NMDAR and mGluR5 suppression

Ist Teil von

• Nature neuroscience, 2015-03, Vol.18 (3), p.435-443

Ort / Verlag

United States: Nature Publishing Group

Erscheinungsjahr

2015

Link zum Volltext

Quelle

PBSC : Psychology and Behavioral Sciences Collection - Journals

Beschreibungen/Notizen

• Social deficits are observed in diverse psychiatric disorders, including autism spectrum disorders and schizophrenia. We found that mice lacking the excitatory synaptic signaling scaffold IRSp53 (also known as BAIAP2) showed impaired social interaction and communication. Treatment of IRSp53(-/-) mice, which display enhanced NMDA receptor (NMDAR) function in the hippocampus, with memantine, an NMDAR antagonist, or MPEP, a metabotropic glutamate receptor 5 antagonist that indirectly inhibits NMDAR function, normalized social interaction. This social rescue was accompanied by normalization of NMDAR function and plasticity in the hippocampus and neuronal firing in the medial prefrontal cortex. These results, together with the reduced NMDAR function implicated in social impairments, suggest that deviation of NMDAR function in either direction leads to social deficits and that correcting the deviation has beneficial effects.