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If knowing BBB status could potentially help us guide acute stroke care decisions, understanding the exact mechanisms behind the BBB dysregulation and the pathophysiology leading to HT is key to come up with a direct therapeutic strategy to modulate BBB

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The requirement for the homeostatic mechanism to be robust means that it must successfully prevent runaway synaptic dynamics across a broad range of input patterns and postsynaptic firing of electrophysiologically heterogeneous inhibitory neurons equipped with diverse plasticity mechanisms

Research is ongoing and not definitive