Abstract
The postsynaptic density (PSD) is a compact disk-shaped structure located beneath the postsynaptic plasma membrane of synapses of the central nervous system, and is thought to play a role in neurotransmission and synaptic plasticity. It lies at the top of the spine head, and based on its location and protein composition, its functions are proposed to control neurotransmitter receptor clustering, regulate receptor function, and to mediate intracellular signaling. Past studies of PSD have shown that a substantial amount of actin is present within the PSD complex, as well as several actin-binding proteins, suggesting that PSD serves as a link between the actin cytoskeleton and neurotransmitter receptors and other signaling molecules. In this study, it was observed that addition of actin to PSD resulted in structural changes of PSD. This effect caused by actin was shown by an increase in PSD turbidity, as indicated by higher absorbance at 340nm, and by an increase in the amount of fragmented PSD particles indicated by sedimentation assays and transmission electron microscopy studies. Also, addition of salt and ATP to PSD produced similar effects, but to a lesser extent compared to that caused by the addition of actin. In conclusion, actin is able to promote PSD fragmentation.