Long-term depression requiring tACPD-receptor activation and NMDA-receptor blockade.

In slices from the rat visual cortex, application of the metabotropic glutamate receptor (mGluR) agonist trans-1-aminocyclo-pentane-1,3-dicarboxylic acid (tACPD), whether combined with tetanization or not, produced only a reversible depression but not long-term depression (LTD) of synaptic transmission. In the presence of both tACPD and the NMDA receptor antagonist D-(-)-2-amino-5-phosphonopentanoate, tetanization induced LTD. These findings suggest requirement of tACPD-sensitive mGluR subtypes for inducing a form of LTD in the visual cortex.