Stability of the memory trace
Our research in reconsolidation of memory trace is focused protein synthesis because inhibiting such synthesis following training results in amnesia for the task. Proteins synthesised during training must be transported to the synapse, and disrupting microtubules with colchicine and hence blocking transport results in transient amnesia. Reactivating memory for a previously learned avoidance triggers a biochemical cascade analogous to that following the initial training, and renders the memory labile once more to protein synthesis inhibitors. However, the reminder-induced cascade differs in certain key features from that following training, does not require synaptic access to somatically synthesised proteins but instead engage local protein synthesis at the synapse, rather than in the soma.
Cell adhesion molecules
Long-term memory is generally believed to be stored in the brain in the form of altered patterns of neuronal connectivity. Modifying these patterns requires the remodelling of synapses, by changing their number, dimensions or morphology. Our research is focused on the specificity of cell-cell adhesion which results from the integration of a number of different adhesion systems. As even a single cell type uses multiple molecular mechanisms in adhering to the other cells and to the extracellular matrix, we focused our attention to NCAM, L1 and APP.
