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Figure 3 | Molecular Brain

Figure 3

From: Dependence of NMDA/GSK-3β Mediated Metaplasticity on TRPM2 Channels at Hippocampal CA3-CA1 Synapses

Figure 3

Inhibition of GSK-3β phosphorylation and reduced PSD95 and AMPAR expression contributes to impaired LTD in TRPM2-/- mice. (a) The ratio of AMPAR- to NMDAR-mediated EPSCs is reduced in TRPM2-/- neurons. (b,c) The amplitude, but not the frequency, of mEPSCs is reduced in slices from TRPM2-/- mice. Representative traces of mEPSCs recordings from slices derived from WT and TRPM2-/- mice are shown. The expression of (d) PSD-95 (normalized to β-actin loading control) and (e) of the AMPAR subunit, GluR1, is depressed in slices from TRPM2-/- mice. (f) Knockout of TRPM2 causes increased phosphorylation of GSK-3β, at its inhibitory site (Ser9, n = 3). (g) Insulin application to hippocampal slices depresses AMPAR-mediated fEPSPs in slices from TRPM2-/-, but not WT, slices. (h) Simulation of dopamine D2 receptors by quinpirole (10 μM) reduces GSK-3β phosphorylation at Ser9 (n = 3). (i) D2 receptor stimulation by quinpirole rescues LTD in slices from TRPM2-/- mice.

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