Fig. 1.

Group I and group I/II mGluR agonists directly excite granule cells (GCs). A: bath application of the group I/II mGluR agonist (±)-1-aminocyclopentane-trans-1,3-dicarboxylic acid (ACPD; 50 μM, at lower bars) resulted in membrane potential depolarization and increased action potential firing in this rat GC. Similar responses were produced by re-application of ACPD, indicating minimal desensitization to the agonist. ACPD-evoked responses were reversible, and the membrane potential typically returned to control levels within 5 min after washout. B: response of the cell in A is shown at an extended time scale. Traces 1–3 correspond to the similarly labeled time points in A. C: application of blockers of fast synaptic transmission [synaptic blockers; 6-cyano-7-nitroquinoxalene-2,3-dione (CNQX), 10 μM; 2-amino-5-phosphonovaleric acid (APV), 50 μM; gabazine, 5 μM] to the same cell shown in A reduced the baseline spontaneous synaptic activity. The depolarizing response to ACPD under these conditions was smaller than that without synaptic blockers and did not reach spike threshold. D: group I mGluR agonist (RS)-3,5-dihydroxyphenylglycine (DHPG; 50 μM) depolarized and increased the firing rate of this typical mouse GC. E: in the same cell shown in D, blockers of fast synaptic transmission reduced baseline spontaneous synaptic activity [spontaneous excitatory postsynaptic potentials (EPSPs)] and DHPG evoked a more moderate depolarization. F: bar graph summarizing the effects of ACPD on rat and mouse GCs with or without synaptic blockers (SB). Data are expressed as changes in membrane voltage compared with control; see text for numbers of GCs tested. DHPG group data are included in Fig. 4. *, significantly different from control, P < 0.05, paired t-test. #, significantly different from non-SB group, P < 0.05, independent t-test, see text for specific P values.