https://onlinelibrary.wiley.com/doi/abs/10.1111/ejn.13959
Abstract
Neuroplasticity after ischemic injury involves both spontaneous rewiring of neural
networks and circuits as well as functional responses in neurogenic niches. These
events involve complex interactions with activated microglia, which evolve in a dynamic
manner over time. Although the exact mechanisms underlying these interactions remain
poorly understood, increasing experimental evidence suggests a determining role of
pro‐ and anti‐inflammatory microglial activation profiles in shaping both synaptogenesis
and neurogenesis. While the inflammatory response of microglia was thought to be detrimental,
a more complex profile of the role of microglia in tissue remodeling is emerging.
Experimental evidence suggests that microglia in response to injury can rapidly modify
neuronal activity and modulate synaptic function, as well as be beneficial for the
proliferation and integration of neural progenitor cells (NPCs) from endogenous neurogenic niches into functional networks thereby supporting stroke
recovery. The manner in which microglia contribute towards sculpting neural synapses
and networks, both in terms of activity‐dependent and homeostatic plasticity, suggests
that microglia‐mediated pro‐ and/or anti‐inflammatory activity may significantly contribute
towards spontaneous neuronal plasticity after ischemic lesions. In this review, we
first introduce some of the key cellular and molecular mechanisms underlying neuroplasticity
in stroke and then proceed to discuss the crosstalk between microglia and endogenous
neuroplasticity in response to brain ischemia with special focus on the engagement
of synapses and neural networks and their implications for grey matter integrity and
function in stroke repair.
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