Figure 4: Schematic summary of the use of interference peptides to study the physiological functions of LTD.

The figure shows brain regions that have been targeted for infusion or viral expression of interference peptides in studies that focused on the physiological role of long-term depression (LTD). All peptides are introduced in Box 3 except the mGluR-ct peptide, which prevents binding of mGluR1 with Homer1b/c (see Ref. 172 for details). In the hippocampus GluA2_3Y was found to block the stress-induced disruption of spatial memory retrieval when administered systemically¹² and to prevent the disruptive effects of protein kinase M ζ (PKMζ) inhibition on object location memory¹²⁵. In layer IV of the visual cortex, G2CT was found to block the effects of monocular deprivation on ocular dominance and the depression of deprived-eye responses¹⁴⁸. G2CT was found to disrupt object recognition memory in the perirhinal cortex¹³¹. In the ventral tegmental area, mGluR-ct was found to block the reversal of acute cocaine synaptic potentiation¹⁷². In the amygdala, GluA2_3Y was found to impair conditioned fear extinction^123,124 and to prevent the disruptive effects of PKMζ inhibition on long-term memory for conditioned fear¹²⁵. In the nucleus accumbens, GluA2_3Y was found to block the expression of behavioural sensitization to amphetamine¹⁵⁵ and Pep2-EVKI was found to block drug-induced cocaine reinstatement¹⁸⁰. In the medial prefrontal cortex, GluA2_3Y was found to reduce the cue-induced reinstatement of heroin-seeking behaviour¹⁵⁶.