Figure 1.
Activation of mGluR II inhibits glutamatergic transmission but exerts no effects on GABAergic transmission in layer III pyramidal neurons. (A) Bath application of LY354740 (3 μM) inhibited AMPA EPSCs. Upper panel shows the average of 10 EPSCs recorded at different time points in the figure (same for the rest of the figures). Stimulation artifacts were deleted for clarity. Lower panel shows the time course of the inhibition induced by LY354740. AMPA EPSC amplitudes at different time points were normalized to the average of the AMPA EPSCs recorded for 5 min before application of LY354740. (B) Bath application of the specific mGluR II antagonist, LY341495 (3 μM), blocked the inhibition induced by LY354740. Upper panel shows the averaged trace of 10 EPSCs recorded at different time points in the figure. (C) Concentration–response curve of LY354740. The numbers in the parentheses are the number of cells used for each concentration. (D) Bath application of DCG-IV (3 μM), another mGluR II agonist, inhibited AMPA EPSCs but failed to inhibit AMPA EPSCs in the presence of mGluR II antagonist, LY341495. (E) IPSCs recorded from a layer III pyramidal neuron at different holding potentials in the intracellular solution containing Cs+-gluconate and extracellular solution supplemented with DNQX (10 μM) and dl-APV (50 μM). (F), Voltage–current relationship averaged from 5 neurons. (G) Bath application of LY354740 (3 μM) had no effects on IPSCs recorded at –70 mV. At the end of the experiments, application of bicuculline (10 μM) completely blocked IPSCs indicating that the recorded IPSCs were mediated by activation of GABAA receptors. (H) Bath application of LY354740 (3 μM) inhibited the slope of the evoked field potentials recorded from layer III.