Fig. 5: NMDAR-mediated transmission and NMDAR-dependent LTP is altered in MAM pups.

a Spontaneous AMPAR and NMDAR-mediated EPSCs recorded in whole-cell configuration at −70 and +40 mV, respectively, in the CA1 of hippocampal slices from control and MAM-exposed animals. Insets show superimposed examples of spontaneous AMPAR and NMDAR-mediated responses as well as evoked NMDAR-mediated currents. b Spontaneous (n_(cont/MAM) = 14/20; p < 0.05) as well as evoked (n_(cont/MAM) = 16/16; p < 0.05) NMDAR-mediated currents are significantly larger in MAM-exposed animals. Also, the Tau decay was increased by ~25% (n_(cont/MAM) = 8/16; p < 0.05), which is consistent with an increased synaptic expression of GluN2B. c Tonic NMDA currents were recorded as the subtracted holding current at a depolarized potential of +40 mV before and after the addition of APV. These tonic NMDA currents were significantly decreased in MAM-exposed animals (n_(cont/MAM) = 10/10; p < 0.05), as revealed by a much smaller decrease in holding current with APV. d Field excitatory postsynaptic potential (fEPSP) recorded in CA1 pyramidal cell layer after stimulation of hippocampal Schaffer collaterals. Active input displays a significant postsynaptic potentiation (LTP) following high-frequency stimulation at P10 (control), not visible in non-stimulated input (n = 6; p < 0.05). e When comparing the response to high-frequency stimulation in control and MAM-exposed animals there was a clear deficit in the magnitude of the LTP in MAM-exposed rats between P8 and P12. This deficit was transient and disappeared with age such that the LTP recovered in older animals.