Abstract:
:NMDA receptor signaling is critical for the development of synaptic plasticity, learning, and memory, and dysregulation of NMDAR signaling is implicated in a number of neurological disorders including schizophrenia (SZ). Previous work has demonstrated that the STriatal-Enriched protein tyrosine Phosphatase 61 kDa (STEP61) is elevated in human SZ postmortem cortical samples and after administration of psychotomimetics to cultures or mice. Here, we report that activation of synaptic NMDAR by bicuculline or D-serine results in the ubiquitination and proteasomal degradation of STEP61, and increased surface localization of GluN1/GluN2B receptors. Moreover, bicuculline or D-serine treatments rescue the motor and cognitive deficits in MK-801-treated mice and reduce STEP61 in mouse frontal cortex. These results suggest that STEP61 may contribute to the therapeutic effects of D-serine.
journal_name
Mol Neurobioljournal_title
Molecular neurobiologyauthors
Xu J,Kurup P,Nairn AC,Lombroso PJdoi
10.1007/s12035-017-0555-xsubject
Has Abstractpub_date
2018-04-01 00:00:00pages
3096-3111issue
4eissn
0893-7648issn
1559-1182pii
10.1007/s12035-017-0555-xjournal_volume
55pub_type
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