Fig. 5

Treatment with T₃ 1 μM for 48 h inhibits iGluRs evoked currents in cultured cortical glutamatergic neurons and downregulates synaptotagmin levels after oxygen and glucose deprivation (OGD). a In an in vitro model of acute cerebral ischemia, levels of synaptotagmin are decreased in cells pre-treated with T₃ 1 μM for 48 h but no difference was observed in the control conditions (Vh, n = 5; T₃ 1 μM, n = 5). b Human brains of stroke and non-stroke control cases have been analyzed for levels of synaptotagmin 1&2. Levels of synaptotagmin are decreased in the infarct core (IC) in comparison with control (Ctrl) and peri-infarct (PI) regions (n = 3 for each brain region). For uncropped images of western blots see Additional file 1: Figure S7 c Representative images of expression of Thyroid hormone receptors TRα1 and TRβ1 (AF488, green) in cultured cortical glutamatergic neurons. TRα1 was mainly localized in the cytoplasm and TRβ1 was expressed in the cytoplasm and nucleus. Scale bar 20 μm. d Representative traces obtained during voltage ramps from − 110 to + 20 mV after application of glutamate 50 μM and glycine 3 μM, held at − 80 mV. After application of AMPA and NMDA antagonists, CNQX and MK-801 respectively, currents were almost fully reverted. e I-V relationship of glutamate 50 μM and glycine 3 μM induced current in cortical neurons under voltage clamp condition under the membrane potential of − 80 mV. Each trace is the result of the average of three ramps for each 10 mV (Vh, n = 3; T₃ 1 μM, n = 4). Results are displayed as means ± SEM. Statistical analysis was performed with two-tailed unpaired Student’s t test to compare glutamate induced currents in cells pre-treated with T₃ 1 μM for 48 h, *p < 0.05, ** p < 0.01, *** p < 0.001