Fig. 4: NMDAR surface dynamics and synaptic plasticity are developmentally impaired in the MAM model.
From: Alteration of NMDA receptor trafficking as a cellular hallmark of psychosis
a Schematic description of the experimental workflow. Cultured hippocampal networks were made from rat pups. Examples of immuncytochemical staining of neurons (NeuN, green), nucleus (DAPI, blue), and glial cells (GFAP, red) in cultured network at 10 days in vitro from control or MAM-exposed pups. b Representative trajectories (50 ms acquisition) of surface GluN2B-NMDAR-QD complexes on neurons from control or MAM-exposed pups at three developmental stages: days in vitro 6–10 (D8), days in vitro 10–15 (D12), days in vitro 15–22 (D20). Scale bars = 5 µm/300 nm (left/right). Right, Comparison of GluN2B-NMDAR diffusion coefficient control or MAM-exposed conditions (D8 cont, n = 1916 trajectories; D8 MAM, n = 1220; D12 cont, n = 2055; D12 MAM, n = 946; D20 cont, n = 1288; D20 MAM, n = 1317; **p < 0.01, Mann–Whitney test). Data are represented as mean ± sem. c Surface immunostaining of GluN2B-NMDAR onto neurons from control or MAM-exposed pups (synapses were detected with Homer1c-GFP). Scale bars = 5/1 µm (left/right). d Comparison of the GluN2B, GluN2A, GluN3A-NMDAR cluster areas between conditions (GluN2B synaptic cont, n = 2144 clusters; GluN2B synaptic MAM, n = 2468, ***p < 0.001, Student’s t-test; GluN2B extrasynaptic cont, n = 1733; GluN2B extrasynaptic MAM, n = 1421, **p < 0.01, Student’s t-test; GluN2A cont, n = 56; GluN2A MAM, n = 41; GluN3A cont, n = 59; GluN3A MAM, n = 48).
