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Voltage-independent GluN2A-type NMDA receptor Ca2+ signaling promotes audiogenic seizures, attentional and cognitive deficits in mice

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Academic year: 2021

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Fig. 2 Hippocampal synaptic transmission and plasticity in Grin2a S/S and Grin2a +/S mice with the GluN2A(N615S) mutation
Fig. 3 Grin2a S/S mice are viable and show no signs of neurodegeneration or altered brain structure
Fig. 4 Grin2a S/S mice are susceptible to brainstem-derived AGS that can be rescued by NMDAR antagonists
Fig. 5 MK-801-induced c-Fos expression is reduced in DG granular and CA3 pyramidal cells of Grin2a S/S mice
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