Miquel Bosch graduated in Biochemistry and received his Ph.D. in Neuroscience from the University of Barcelona (Spain). He performed postdoctoral stays at the National Institute for Basic Biology (NIBB, Japan), the Massachusetts Institute of Technology (MIT, USA), the Institute for Bioengineering of Catalonia (IBEC, Spain), and the IDIBAPS Institute (Spain). In 2020 he became an Assistant Professor at the International University of Catalonia (UIC) and launched the Laboratory of Synaptic Plasticity as Group Leader. Dr. Bosch is currently an Associate Professor at the Dept. of Biomedical Sciences at UIC. His group investigates the molecular mechanisms of learning and memory and how synaptic plasticity is impaired in autism spectrum disorders, using new optical and photopharmacological techniques.

Title: The molecular mechanisms of memory persistence - the role of the structural plasticity of dendritic spines.

Abstract

Memories are stored in the brain through long-lasting modifications in the structure and function of synaptic connections. While functional plasticity has been extensively studied, the role of synaptic structural plasticity in memory formation remains largely unknown.

We combined advanced optical technologies to uncover the structural and molecular remodeling that occurs during the potentiation and growth of single dendritic spines. Using two-photon glutamate uncaging and live imaging, we observed how synaptic substructures evolve asynchronously through distinct temporal phases. We identified a unique protein that is rapidly and persistently captured at potentiated synapses, forming a macromolecular complex that may serve as a memory tag.

We also explored the opposite process—dendritic spine shrinkage during synaptic depression—and discovered that functional and structural changes in spine plasticity do not always correlate, depending on the neuronal network activity. Additionally, we found that the intracellular mechanisms regulated by glutamate receptors that govern spine plasticity are disrupted in autism spectrum disorders. These findings suggest that the structural plasticity of dendritic spines is not merely a byproduct of functional changes but may serve as a metaplasticity mechanism that integrates neuronal activity patterns, ultimately consolidating memory formation.