Figure 8.

A schematic diagram of the NRG1-mediated enhancement of MGL and the consequent reduction in 2-AG effects. The chronic treatment of the hippocampus with NRG1 increases the expression of MGL, which is a degradative enzyme for 2-AG. This increase facilitates the degradation of 2-AG, resulting in the shortened duration of DSI and the impairment of iLTD. The location and biochemical cascade of ErbB-to-MGL signaling that is responsible for the NRG1-mediated 2-AG curtailment must be determined.