Chunk #34 — Results — Pharmacologically suppressing Kir3.2 channels restores synaptic plasticity in DG of Ts65Dn mice

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Evidence that increased Kcnj6 gene dose is necessary for deficits in behavior and dentate gyrus synaptic plasticity in the Ts65Dn mouse model of Down syndrome.

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2N slices (p = 0.28 and 0.20 for STP and LTP respectively). Interestingly, fluoxetine affected neither STP (Veh: 111.1 ± 2.9%, n = 13; Flx: 113.7 ± 5.2%, n = 7; p = 0.64) nor LTP (Veh: 110.5 ± 2.4%, n = 13; Flx: 112.8 ± 4.5%, n = 7; p = 0.61) in 2N mice (Fig. 7, dark green). Together with the findings for Kcnj6 dose reduction reported above, these data are evidence that Kir3.2 subunit-containing potassium channels contribute to defects in synaptic plasticity in Ts65Dn mice.