Synaptic Plasticity During Learning
presentationposted on 20.06.2017, 00:00 by Dustin Horn
Neurons communicate at junctions called synapses, and changes (plasticity) of these synapses underlie the ability of humans to learn. Synapses are dynamic structures that can change their chemical activity within seconds. Some of these short-term changes involve the cytoskeleton (specifically actin filaments) within the dendritic spine to change only its shape. Modulation of cyclic AMP and protein kinase C pathways are also important in this process. There are also long-term changes in synapses: early and late long-term potentiation (LTP). Early LTP involves activation of calcium calmodulin dependent kinase II (CaMKII) and insertion of preexisting glutamate receptors into the cellular membrane. Late LTP requires protein synthesis. BDNF, ARC, and PSD-95 are examples of proteins required for late LTP. PSD-95 is part of the post synaptic density. The post synaptic density is correlated with the size and shape of the dendritic spine, and it organizes cellular machinery required for synaptic function. BDNF is a neurotrophin linked to the MAPK pathway. Many of the proteins required for late LTP are translated locally in the dendrites. How the neuron traffics the appropriate mRNA and cellular machinery to the correct location within dendrites is still unknown. Previous researchers hypothesized a "synaptic tag" guides molecules to their correct location, and CaMKII and actin remodeling are important for creating this tag. I have designed an experiment to uncover the molecular identity the tag. If successful, the experiment will increase our understanding of synaptic plasticity and proper neuronal function.