Synapses are plastic - their strength adapts according to dynamic changes in the level or in the type of stimulation. Synaptic plasticity occurs, for example, during periods of increased/decreased neuronal activity, in response to particular stimuli, or during behavior, and it serves as a mechanism for short- or long-term storage of experience. Plasticity can sharply change synaptic function – and that change can last milliseconds, days, or throughout the lifetime of an organism. This plasticity is necessary for an array of functions, from the processing and integration of sensory information, to cognitive functions such as learning and memory.
Our group studies presynaptic mechanisms of plasticity formation. We previously identified Ca2+/calmodulin signaling (Lipstein et al., Neuron 2013) and Ca2+-phospholipids signaling (Lipstein et al., Neuron 2021) as major pathways that operate at the presynaptic active zone during periods of strong neuronal activity to enhance synaptic strength and the accuracy of information encoding. Current studies are focused on understanding how synaptic plasticity is changed by inborn synaptic disorders (see below), and how plasticity manifests in diverse synapse subtypes. We use slice electrophysiology, proteomics and structural methods to characterize changes that accompany short- and long-term synaptic plasticity events.