Emerging concepts and functions of autophagy as a regulator of synaptic components and plasticity
Protein homeostasis (proteostasis) is crucial to the maintenance of neuronal integrity and function. As the contact sites between neurons, synapses rely heavily on precisely regulatedprotein-protein interactions to support synaptic transmission and plasticity processes. Autophagyis an effective degradative pathway that can digest cellular components and maintain cellularproteostasis. Perturbations of autophagy have been implicated in aging and neurodegenerationdue to a failure to remove damaged proteins and defective organelles. Recent evidence hasdemonstrated that autophagosome formation is prominent at synaptic terminals and neuronalautophagy is regulated in a compartment-specific fashion. Moreover, synaptic components includingsynaptic proteins and vesicles, postsynaptic receptors and synaptic mitochondria are known to bedegraded by autophagy, thereby contributing to the remodeling of synapses. Indeed, emergingstudies indicate that modulation of autophagy may be required for different forms of synapticplasticity and memory formation. In this review, I will discuss our current understanding of theimportant role of neuronal/synaptic autophagy in maintaining neuronal function by degradingsynaptic components and try to propose a conceptual framework of how the degradation of synapticcomponents via autophagy might impact synaptic function and contribute to synaptic plasticity.