Topic: organotypic hippocampal slice cultures

The postsynaptic site of excitatory synapses is characterized by an electron-dense region called postsynaptic density (PSD), which is usually located at the tip of dendritic spines. The PSD has been shown to undergo morphological changes in response to behavioral and electrophysiological inputs. This process can be highly dynamic and occurs over different time scales. To bridge the observation gap between short-term plastic events (ranging from minutes to hours) and long-term effects (several hours to days), we engineered a novel on stage microscope-incubator optimized for long-term culturing

Since the first enzyme replacement therapy (ERT) for Gaucher disease was approved in 1991, ERT has become standard of care for several lysosomal storage diseases (LSD), collectively characterized by dysfunctional lysosomal enzymes leading to pathological substrate accumulation. Sanfilippo Syndrome type A (MPSIIIA) is a monogenetic disease caused by >150 different loss-of-function mutations in the lysosomal enzyme N-Sulfoglucosamine Sulfohydrolase (SGSH), resulting in accumulation of heparan sulfate (HS). This accumulation disrupts cellular homeostasis with consequences for autophagy and mit

Learning resulting in long-term memory correlates with the formation of new dendritic spines. However, are these newly grown spines only a correlate or a necessity for long-term memory storage? The most direct way to answer this fundamental question is to build a tool to selectively eliminate newly formed dendritic spines, and to then apply this tool in vivo to observe whether a recently acquired long-term memory is destabilized.To this end, we have developed a chemical-genetic selective new spine elimination tool (NSET) in organotypic hippocampal slice cultures. This tool consists of two comp

Synapse loss is a key feature of many neurodegenerative diseases involving cognitive deficits, and is also the strongest correlate of cognitive decline in Alzheimer’s disease (AD). In addition, the integrity of dendritic spines, the post-synaptic sites of excitatory synapses, have been shown to play a key role in cognitive resilience against AD. Given the critical role of synaptic loss in cognitive decline, we hypothesized that synaptic compensation and repair play a vital role in counteracting synapse loss and as a consequence, in delaying the onset of cognitive deficits. The aim of our study