LTD involves multiple cellular and molecular mechanisms. One key player is the NMDA receptor, which allows calcium ions to enter the neuron. The influx of calcium activates a cascade of intracellular signals, including protein phosphatases such as PP1 and calcineurin. These phosphatases dephosphorylate synaptic proteins, leading to the internalization of AMPA receptors from the postsynaptic membrane. The removal of AMPA receptors reduces the synaptic response, thereby inducing LTD.