Abstract: Synaptic pruning is a crucial process in synaptic refinement, eliminating unstable synaptic connections in neural circuits. This process is triggered and regulated primarily by spontaneous neural activity and experience-dependent mechanisms. The pruning process involves multiple molecular signals and a series of regulatory activities governing the “eat me” and “don’t eat me” states. Under physiological conditions, the interaction between glial cells and neurons results in the clearance of unnecessary synapses, maintaining normal neural circuit functionality via synaptic pruning. Alterations in genetic and environmental factors can lead to imbalanced synaptic pruning, thus promoting the occurrence and development of autism spectrum disorder, schizophrenia, Alzheimer’s disease, and other neurological disorders. In this review, we investigated the molecular mechanisms responsible for synaptic pruning during neural development. We focus on how synaptic pruning can regulate neural circuits and its association with neurological disorders. Furthermore, we discuss the application of emerging optical and imaging technologies to observe synaptic structure and function, as well as their potential for clinical translation. Our aim was to enhance our understanding of synaptic pruning during neural development, including the molecular basis underlying the regulation of synaptic function and the dynamic changes in synaptic density, and to investigate the potential role of these mechanisms in the pathophysiology of neurological diseases, thus providing a theoretical foundation for the treatment of neurological disorders.

Key words: chemokine, complement, experience-dependent driven synaptic pruning, imaging techniques, neuroglia, signaling pathways, synapse elimination, synaptic pruning