Postsynaptic Signals Mediating Induction of Long-Term Synaptic Depression in the Entorhinal Cortex
Figure 2
The induction of long-term
depression is dependent on activation of NMDA glutamate receptors and on
increases in postsynaptic calcium. (a) Constant bath application of the
NMDA receptor antagonist APV (50M) blocked the induction of long-term
depression by 15 minutes of paired-pulse low-frequency stimulation (PP LFS). (b) Blocking increases in
postsynaptic calcium by including the calcium chelator BAPTA (10 mM) in the recording
electrode solution also blocked the induction of LTD. The transient facilitation of EPSPs immediately
following stimulation was significant for the BAPTA condition but not the APV
condition, and responses were at baseline levels at the end of the recording
periods. The block of lasting depression suggests that calcium influx via NMDA
receptors is required for induction of LTD.