The mechanism of storing and losing long-term memories has been extensively studied. …show more content…
First, a specific tyrosine must be dephosphorylated on the receptor by the enzyme striatal-enriched tyrosine phosphatase (STEP). Once activated, the mGluR is able to activate a tumor-necrosis factor-α-converting enzyme (TACE). The stimulation of TACE will act to cleave the intramembrane protein, neuronal pentraxin receptor. When the protein is cleaved, the extracellular portion is able to stimulate the aggregation of AMPA receptors on the cell surface and help facilitate endocytosis (Lüscher & Huber, 2010). This decrease of AMPA receptors on the cell surface ultimately will cause a decrease in synaptic …show more content…
This form of LTD is associated with the calcium-dependent phosphatase calcineurin. This phosphatase has a higher affinity for Ca2+ than CaMKII, so calcineurin is able to respond to smaller changes in Ca2+ concentration. As stated previously, NMDA receptors allow calcium to flow into the neuron when they are activated. Decreased exposure to a stimulus will result in decreased activity of NMDA receptors and subsequently, decreased intracellular calcium. Calcineurin is capable of being activated by these smaller amounts of calcium. Active calcineurin is able to dephosphorylate many important proteins in the process of LTP, specifically proteins involved in the process of endocytosis. It is believed that this dephosphorylation is able to enhance endocytosis of AMPA receptors (Lüscher & Malenka, 2012). Like with mGluR LTD, the decrease of AMPA receptors on the cell surface results in decreased synaptic