The BDNF Val66Met polymorphism impairs NMDA receptor-dependent synaptic plasticity in the hippocampus

Ipe Ninan, Kevin G. Bath, Karishma Dagar, Rosalia Perez-Castro, Mark Plummer, Francis S. Lee, Moses V. Chao

Research output: Contribution to journalArticlepeer-review

116 Scopus citations

Abstract

The Val66Met polymorphism in the brain-derived neurotrophic factor (BDNF) gene results in a defect in regulated release of BDNF and affects episodic memory and affective behaviors. However, the precise role of the BDNF Val66Met polymorphism in hippocampal synaptic transmission and plasticity has not yet been studied. Therefore, we examined synaptic properties in the hippocampal CA3-CA1 synapses of BDNFMet/Met mice and matched wild-type mice. Although basal glutamatergic neurotransmission was normal, both young and adult mice showed a significant reduction in NMDA receptor-dependent long-term potentiation. We also found that NMDA receptor dependent long-term depression was decreased in BDNFMet/Met mice. However, mGluR-dependent long-term depression was not affected by the BDNF Val66Met polymorphism. Consistent with the NMDA receptor-dependent synaptic plasticity impairment, we observed a significant decrease in NMDA receptor neurotransmission in the CA1 pyramidal neurons of BDNFMet/Met mice. Thus, these results show that the BDNF Val66Met polymorphism has a direct effect on NMDA receptor transmission, which may account for changes in synaptic plasticity in the hippocampus. Copyright

Original languageEnglish (US)
Pages (from-to)8866-8870
Number of pages5
JournalJournal of Neuroscience
Volume30
Issue number26
DOIs
StatePublished - Jun 30 2010

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)

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