Exaggerated NMDA mediated LTD in a mouse model of Down syndrome and pharmacological rescuing by memantine | Zendy

Jonah J. Scott-McKean | Zendy; Alberto C. S. Costa | Zendy

AI Assistant Blog Pricing

Home ZAIA Blog

Open Access

Exaggerated NMDA mediated LTD in a mouse model of Down syndrome and pharmacological rescuing by memantine

Author(s) -

Jonah J. Scott-McKean,

Alberto C. S. Costa

Publication year - 2011

Publication title -

learning and memory

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.228

H-Index - 136

eISSN - 1549-5485

pISSN - 1072-0502

DOI - 10.1101/lm.024182.111

Subject(s) - nmda receptor , memantine , hippocampal formation , antagonist , hippocampus , neuroscience , glutamate receptor , pharmacology , psychology , chemistry , medicine , receptor , biochemistry

The Ts65Dn mouse is the best-studied animal model for Down syndrome. In the experiments described here, NMDA-mediated or mGluR-mediated LTD was induced in the CA1 region of hippocampal slices from Ts65Dn and euploid control mice by bath application of 20 µM NMDA for 3 min and 50 µM DHPG for 5 min, respectively. We found that Ts65Dn mice display exaggerated NMDA-induced, but not mGluR-induced, LTD in the CA1 region of the hippocampus compared with euploid control animals. In addition, this abnormal level of LTD can be pharmacologically rescued by the NMDA receptor antagonist memantine.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.

Having issues? You can contact us here

Accelerating Research