Grant: Operating Grant

Our ability to think, learn and remember reflects our brain function. The neurons in our brain are organized in networks through which information flows, is processed and sometimes stored. The precise functioning of these networks is largely controlled by functional connections between neurons called synapses. The strength of individual synapses is dynamically regulated by experience and activity and can either be depressed or potentiated for brief or prolonged periods of time. These activity-dependent mechanisms, broadly defined as synaptic plasticity, decisively influence how information flows and are widely believed to contribute to the ability of the brain to learn and remember. Both theoretical and experimental work are showing that these activity-dependent mechanisms need to be properly fine-tuned and controlled by what is called homeostatic mechanisms to assure proper network function. Recently, it has been hypothesized that abnormal balance between these opposing mechanisms lead to malfunctioning of neural network function and thus may contribute to several neurological and psychiatric diseases, in particular Alzheimer's disease, schizophrenia and addiction. Here, we are proposing novel electrophysiological, optical and molecular approaches to study in details these homeostatic mechanisms at central synapses and determine how they interplay with other forms of synaptic plasticity to control neuronal function.