Synaptic plasticity requires the production of new proteins in response to activation of synaptic receptors. NMDA receptors are also associated with synaptic plasticity. EEG reflects correlated synaptic activity caused by post-synaptic potentials of cortical neurons. Receptors on the opposite side of the synaptic gap bind neurotransmitter molecules. Retrieval of synaptic vesicles occurs by endocytosis. Additionally, endocannabinoids play an important role in regulating various forms of synaptic plasticity. This is useful to study the molecular events during the induction of synaptic plasticity. Acetylcholine then diffuses across the synaptic cleft. Every kind of synaptic plasticity has different computational uses. Peptides bind to GPCRs to induce signaling cascades that alter cellular and synaptic activity. AP180 is used in synaptic vesicle formation. This is due to depletion of synaptic vesicle contents. The serotonin transporter removes serotonin from the synaptic cleft back into the synaptic boutons. VAMP2 is targeted and cleaved by BoNT isotypes B, D, and F in synaptic neurons. This is possibly due to homeostatic synaptic scaling.