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. 2016 Oct 31;113(46):13209–13214. doi: 10.1073/pnas.1616206113

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Fig. 4. — IM-AA mutation induces increases in NMDAR currents in response to 100-Hz tetanus in SC-CA1 synapses. (A) Example EPSCs recorded at −60 mV in response to a single stimulus in control solution from WT (Top, black) and IM-AA (Bottom, red) and after NMDAR block by 100 μM d-AP5 WT (Top, gray) and IM-AA (Bottom, pink) (Left). Stimulus artifacts were erased for clarity. Average EPSCs were recorded at −60 mV in response to 100-Hz tetanus in control solution from WT (Top, black) and IM-AA (Bottom, red) and after NMDAR block by 100 μM d-AP5 WT (Top, gray) and IM-AA (Bottom, pink) (Left). Example EPSCs were recorded at −60 mV in control solution from WT (Top, black) and IM-AA (Bottom, red) and after NMDAR block by 100 μM d-AP5 WT (Top, gray) and IM-AA (Bottom, pink) (Right). (B) Average peak amplitude of evoked NMDAR-mediated EPSCs during a 100-Hz train from WT (black, n = 4) and IM-AA (red, n = 4) in the presence of 1 μM ω-Ctx, 50 μM picrotoxin, and 10 μM CGP55845 hydrochloride.