Figure 2
From: Dependence of NMDA/GSK-3β Mediated Metaplasticity on TRPM2 Channels at Hippocampal CA3-CA1 Synapses
NMDAR function is unaffected by disruption of TRPM2 channel expression. Neither peak (a) nor steady-state/peak (b) currents, generated in response to rapid applications of NMDA to cultured hippocampal neurons, are affected by loss of TRPM2 expression. Similarly, the sensitivity of NMDA-evoked responses (peak amplitude (c), total charge transfer (d) and representative traces (e) recorded from cultured hippocampal neurons, to inhibition by the GluN2B specific antagonist, Ro 25-6981, is unaltered in neurons from TRPM2-/-. (f) Inhibition of pharmacologically isolated NMDAR-mediated synaptic currents, recorded from CA1 pyramidal neurons in response to Schaffer-collateral stimulation, by Ro 25-6981 is unaltered in slices from TRPM2-/-. For all results presented in panels a-d, n = 5; for panel f, WT: n = 6; TRPM2-/-: n = 5)