Seen in Fragile X Syndrome is highly enhanced LTD. This is because FMRP acts as a negative feedback regulator in the process which couples metabotropic glutamate receptor (mGluR5) with activity-dependent glutamate release with changes in the translation of proteins by suppressing protein biosynthesis at polyribosomes. When FMRP is absent, protein production goes awry and LTD is enhanced as a result of this dysregulation. To go into further detail regarding the pathways that lead to this:

• mGluR5 couples to phospholipase C (PLC) via Gq (a G protein) and signals via extracellular-regulated kinase and mammalian target of rapamycin (mTOR) to regulate protein translation at polyribosomes
• Additionally, since mGluR-mediated LTD is insensitive to changes in intracellular calcium, another pathway is as follows: Homer → Pike-L → phosphoinositide 3-kinase (PI3K)
• PI3K then activates the mTOR extracellular signal-regulated kinase pathway: PI3K→ PIP3 → AKT → mTOR → FMRP