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These inducible CA1-specific or forebrain-specific NMDA knockout mice, once fed with doxycycline to disable NMDA receptor function, produced deficits in memory formation, consolidation, and storage [10], [11].
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18F-BMS PET scans were performed on control mice, rotenone-injected mice, and mice fed a MCD diet.
WT and KO mice were fed regular chow once daily in the light period (ZT 6 10) for at least 30 days and were then euthanized at 1 of 4 time points (ZT 0, 6, 12, 18) for quantification of Per2 expression by quantitative, reverse-transcriptase PCR.
C57BL/6J male mice were fed a high fat diet and were gavaged with a vehicle once or twice daily for 9 weeks.
Urine donors were from 10 B6 mice fed Diet L, 10 B6 mice fed Diet S, 10 B6-H2k mice fed Diet L and 10 B6-H2k mice fed Diet S.
When fed a HFD, mice gained significantly more weight than mice fed standard chow.
C57BL/6N mice were fed with regular diet.
C57BL/6 mice were fed normally for the same 26 weeks.
All mice were fed a normal chow diet.
Two C57BL/6 mice and two ApoE KO mice were fed a normal chow diet ad libitum.
All other mice were fed standard chow.
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