It has been proposed that metabotropic glutamate receptor-dependent long-term depression (mGluR-LTD) can reverse cocaine-evoked synaptic plasticity in the ventral tegmental area (VTA). Mameli et al. have now unraveled the expression mechanism of mGluR-LTD in the VTA of mice exposed to a single dose of cocaine. LTD in this system is not due to the simple removal of AMPA receptors (AMPARs) from the synapse. Instead, AMPARs are replaced by new ones that contain newly synthesized GluR2 subunits. The synapse thus expresses LTD not because there are fewer receptors but because the conductance of the new GluR2-containing AMPARs is reduced.
- Correcting Cocaine-Induced Plasticity
A decrease in the effectiveness of synapses in a particular brain region is caused by replacement of one glutamate receptor subtype with a less efficient one.Permalink: