Astrocytes play a crucial role in neural circuit development, function, and disease. They regulate synapse formation, maturation, and elimination through secreted and contact-mediated signals. Recent studies show that astrocytes are involved in the pathophysiology of psychiatric and neurological disorders linked to synaptic defects. Astrocytes control synapse formation by secreting molecules like thrombospondins (TSPs) and hevin, which promote excitatory synaptogenesis. TSPs, particularly TSP1 and TSP2, are essential for normal synapse formation, while hevin supports synapse maturation. Astrocytes also regulate inhibitory synapse formation by secreting molecules that influence presynaptic and postsynaptic differentiation. Astrocyte contact with synapses can enhance synaptic activity and promote synapse formation. Astrocytes also control synapse maturation by secreting glypicans, which increase the expression of AMPA receptors, leading to functional synapse formation. Additionally, astrocytes regulate dendritic spine maturation by interacting with synapses and modulating synaptic activity. They also play a role in synapse pruning by releasing signals that induce microglial phagocytosis of synapses, which is crucial for neural circuit refinement. Astrocytes are involved in synaptic pruning through the complement system, with astrocytes inducing the expression of complement proteins that mark synapses for removal. This process is regulated by neural activity and is essential for neural circuit development. Astrocytes also contribute to synaptic pruning by phagocytosing neuronal debris and synapses, especially in conditions like glaucoma. In human diseases such as Rett syndrome, fragile X syndrome, and Down syndrome, astrocyte dysfunction is implicated in synaptic defects. For example, MECP2 deficiency in astrocytes impairs synaptogenesis, while FMRP deficiency in astrocytes leads to abnormal dendritic morphology and synapse density. TSP1 levels are reduced in astrocytes from Down syndrome patients, contributing to synaptic defects. These findings suggest that astrocytes are critical for synaptic development and that targeting astrocytes may offer new therapeutic strategies for neurodevelopmental disorders. Future research will focus on understanding astrocyte signaling pathways and their role in synaptic plasticity and disease.Astrocytes play a crucial role in neural circuit development, function, and disease. They regulate synapse formation, maturation, and elimination through secreted and contact-mediated signals. Recent studies show that astrocytes are involved in the pathophysiology of psychiatric and neurological disorders linked to synaptic defects. Astrocytes control synapse formation by secreting molecules like thrombospondins (TSPs) and hevin, which promote excitatory synaptogenesis. TSPs, particularly TSP1 and TSP2, are essential for normal synapse formation, while hevin supports synapse maturation. Astrocytes also regulate inhibitory synapse formation by secreting molecules that influence presynaptic and postsynaptic differentiation. Astrocyte contact with synapses can enhance synaptic activity and promote synapse formation. Astrocytes also control synapse maturation by secreting glypicans, which increase the expression of AMPA receptors, leading to functional synapse formation. Additionally, astrocytes regulate dendritic spine maturation by interacting with synapses and modulating synaptic activity. They also play a role in synapse pruning by releasing signals that induce microglial phagocytosis of synapses, which is crucial for neural circuit refinement. Astrocytes are involved in synaptic pruning through the complement system, with astrocytes inducing the expression of complement proteins that mark synapses for removal. This process is regulated by neural activity and is essential for neural circuit development. Astrocytes also contribute to synaptic pruning by phagocytosing neuronal debris and synapses, especially in conditions like glaucoma. In human diseases such as Rett syndrome, fragile X syndrome, and Down syndrome, astrocyte dysfunction is implicated in synaptic defects. For example, MECP2 deficiency in astrocytes impairs synaptogenesis, while FMRP deficiency in astrocytes leads to abnormal dendritic morphology and synapse density. TSP1 levels are reduced in astrocytes from Down syndrome patients, contributing to synaptic defects. These findings suggest that astrocytes are critical for synaptic development and that targeting astrocytes may offer new therapeutic strategies for neurodevelopmental disorders. Future research will focus on understanding astrocyte signaling pathways and their role in synaptic plasticity and disease.