Distributed disruption and remodelling of synaptome architecture following traumatic brain injury

Abstract

A single cortical impact in mice altered the number and molecular composition of excitatory synapses across 222 brain regions. Early effects targeted synapses with rapid protein turnover, followed by changes in slow-turnover synapses. This injury-induced remodelling of synaptome architecture mirrors responses to genetic mutation, ageing, sleep deprivation and experience, suggesting that reorganisation of excitatory synapse populations is a shared mechanism underlying brain plasticity across diverse conditions.