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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.
The synaptic mechanisms underlying cortical postnatal development are largely unexplored. Here, the authors reveal how spine calcium activity impacts turnover and organization of synaptic inputs on neurons in the mouse binocular visual cortex.
How cortical interneurons establish precise connections among intermingled populations of excitatory neurons remains unclear. Here, the authors reveal that Cadherins instruct cell type and input-specific synaptic targeting of interneurons onto different pyramidal cell populations.
LRFN2 in cone photoreceptors is vital for building the OFF pathway. Here authors report this cell-adhesion molecule stabilizes contacts with OFF bipolar cells, clusters their ionotropic receptors, and is required for negative-contrast vision and predator-detection behaviors.
Through circuit dissection in juvenile, adolescent and adult mice, Klune, Goodpaster and colleagues reveal multiple developmental switches in mPFC–NAc and mPFC–BLA pathways that underlie developmental transitions in threat avoidance behavior.
The development of translaminar cortical circuits remains incompletely understood. Here authors show cortical layer 5 provides translaminar inputs to layer 2/3 during development, strengthening layer 4-layer 2/3 connections and supporting the formation of the canonical cortical organization in mouse barrel cortex.
Caspases are known to mediate neuronal apoptosis during brain development. Here authors demonstrate a role for nonapoptotic caspase-3 activation in neurons with elevated activity, in the promotion of C1q deposition and synaptic phagocytosis by microglia.
In Caenorhabditis elegans, loss of the transcription factors FOS-1 and EGL-43 — orthologs of human FOS and MECOM, respectively — severely reduces presynaptic gene expression in dopaminergic neurons. These transcription factors form an activity-regulated positive feedback loop, which modulates the expression of synaptic genes and genetic programs to promote synapse formation.
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.
