A potential mechanism for the expression of DHPG-induced LTD, based on the mobilization of AMPA receptors. A. Baseline: Synapses have a wide distribution of Pr skewed in favour of low probabilities of release. In this scheme Pr does not alter. There is also a wide range of quantal amplitudes (q), which are shown simplified here as giving rise to strong (2 AMPA receptors) and weak (1 AMPA receptor) synapses. B. Induction: Stimulation of mGluRs (mGluR5) by DHPG transiently activates PTPs to dephosphorylate and mobilize AMPA receptors. At high Pr synapses, AMPA receptors are internalized (and degraded) to either result in silencing (in a minority of very high Pr synapses) or a decrease in q. At a proportion of low Pr synapses AMPA receptors are inserted to maintain a constant level of AMPA receptors available to respond to synaptic release. These could be delivered from extrasynaptic sites by lateral diffusion, thereby leading to the decrease in this AMPA receptor population. C. Expression: In the simplified scheme shown here there would be a large decrease in the mean synaptic current (due to the silencing of a high Pr, strong synapse), no change in sensitivity to L-glutamate (localized to synapses by uncaging), no change in mEPSC amplitude or its quantal distribution but a decrease in average Pr (due to the functional elimination of a high Pr synapse - i.e., a reduction in n), a corresponding decrease in mEPSC frequency and an increase in PPF (due to the selective silencing of a high Pr synapse).