Matrix metalloproteinases play a crucial role in adult visual plasticity in the brains of healthy and stroke-affected mice and their activity has to be within a narrow window for experience-induced plasticity to occur.

A combined rehabitative protocol after stroke in the mouse normalizes transcallosal inhibition and promotes "true recovery" of forelimb motor function.

The number of inflows and outflows at the occluded capillary governs the local flow reduction, and the different topological configurations are probably designed for distinct functional tasks.

Excitation of contralesional cortex after stroke suppresses the expression of genes related to plastic neuronal reintegration and accordingly modulates perilesional remodeling and functional network communication at local and global scales.

Mice with aquaporin-4 channel deletion exhibit larger interstitial spaces, brain volume and water content, alongside reduced CSF space volume, which may increased resistance towards brain fluid efflux and suppress glymphatic flow.

A critical re-evaluation of some of the quintessential examples given as evidence for cortical reorganisation argues that, contrary to the prevalent view, any opportunities for functional change in cortical organisation are incremental and constrained by the underlying structural ‘blueprint'.

Longitudinal calcium imaging in awake mice after stroke suggests impairments in neuronal activity, functional connectivity, and neural assembly architecture is transient and limited to cortex immediately adjacent to the stroke.

Neuronal activity modulates blood–brain barrier permeability, influencing synaptic plasticity and local network reorganization in the healthy brain.