Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
Synaptic development is the biological process by which a synapse between two neurons forms. The membranes of the two neurons become closely apposed and this is accompanied by presynaptic differentiation, during which synaptic vesicles gather close to the active zone, and postsynaptic differentiation, including the clustering of neurotransmitter receptors.
Connecting cerebral organoids with an axon bundle models inter-regional projections and enhances neural activity. Optogenetic stimulation induces short-term plasticity, offering insights into macroscopic circuit development and functionality.
The proteomic changes that occur during synapse development are not fully understood. In this work, the authors characterise the postsynaptic proteome changes that occur during development in male mice and marmosets.
This paper identifies the evolutionarily conserved liprin-α protein family as key mediators of presynaptic assembly in human neurons. Their recruitment to sites formed by contacting neurons is the critical initial step that triggers presynaptic differentiation.
The glutamate transporter GLAST in astrocyte regulates synapse function by glutamate clearance. Here, the authors show that Down syndrome cell adhesion molecule (DSCAM) in Purkinje cells controls synaptogenesis through the intercellular association with GLAST in the developing cerebellum.
Latrophilin-3 organizes synapses through a convergent dual-pathway mechanism in which Gαs signalling is activated and phase-separated postsynaptic protein scaffolds are recruited.
A study analyses the nanotopography of presynaptic calcium channels and release sensors and the degree of their coupling during maturation of an inhibitory synapse.
Cytoplasmic mislocalization of TDP-43 in neurodegenerative disease affects mRNA maturation and protein levels of stathmin-2, leading to a reduction in axon diameter and tearing of outer myelin layers and thereby disrupting neuronal function.
The stress associated with early-life social deprivation in mice results in corticosterone-driven overstimulation of cortical synapse removal by astrocytes and behavioural abnormalities in mature animals.
