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

Cited 72 time in webofscience Cited 0 time in scopus
  • Hit : 485
  • Download : 0
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(-1-) 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.
Publisher
NATURE PUBLISHING GROUP
Issue Date
2015-03
Language
English
Article Type
Article
Keywords

INSULIN-RECEPTOR SUBSTRATE; LONG-TERM POTENTIATION; RARE DE-NOVO; SYNAPTIC PLASTICITY; SPECTRUM DISORDERS; AUTISM; ACTIN; HIPPOCAMPAL; ASSOCIATION; MUTATIONS

Citation

NATURE NEUROSCIENCE, v.18, no.3, pp.435 - 443

ISSN
1097-6256
DOI
10.1038/n.3927
URI
http://hdl.handle.net/10203/195843
Appears in Collection
BS-Journal Papers(저널논문)
Files in This Item
There are no files associated with this item.
This item is cited by other documents in WoS
⊙ Detail Information in WoSⓡ Click to see webofscience_button
⊙ Cited 72 items in WoS Click to see citing articles in records_button

qr_code

  • mendeley

    citeulike


rss_1.0 rss_2.0 atom_1.0