Compensatory Relearning Following Stroke: Cellular and Plasticity Mechanisms in Rodents

Abstract

von Monakow’s theory of diaschisis states the functional ‘standstill’ of intact brain regions that are remote from a damaged area, often implied in recovery of function. Accordingly, neural plasticity and activity patterns related to recovery are also occurring at the same regions. Recovery relies on plasticity in the periinfarct and homotopic contralesional regions and involves relearning to perform movements. Seeking evidence for a relearning mechanism following stroke, we found that rodents display many features that resemble classical learning and memory mechanisms. Compensatory relearning is likely to be accompanied by gradual shaping of these regions and pathways, with participating neurons progressively adapting cortico-striato-thalamic activity and synaptic strengths at different cortico-thalamic loops – adapting function relayed by the striatum. Motor cortex functional maps are progressively reinforced and shaped by these loops as the striatum searches for different functional actions. Several cortical and striatal cellular mechanisms that influence motor learning may also influence post-stroke compensatory relearning. Future research should focus on how different neuromodulatory systems could act before, during or after rehabilitation to improve stroke recovery.

Operationalization of the learned non-use phenomenon - A Delphi study

“…These observations are corroborated by later studies in rodents [e.g. (Jones and Schallert, 1994; Kerr et al, 2016; Balbinot and Schuch, 2018)] and monkeys [e.g. (Friel and Nudo, 1998; Kaeser et al, 2010; Murata et al, 2015)] employing cortical lesion models giving rise to some possible explanations for the underlying neural mechanisms [reviewed in (Jones, 2017; Buetefisch, 2015)].…”

Lesion Size- and Location-Dependent Recruitment of Contralesional Thalamus and Motor Cortex Facilitates Recovery after Stroke in Mice

“…Post-stroke reorganization of motor representation is related to thalamo-cortical loops, a redundant system to integrate sensory and motor signals [ 34 ]. In the acute phase after stroke, rapid changes in sensory processing occur within the peri-infarct zone, which extend to somatotopic regions of the unaffected hemisphere related to enhanced sensory responses [ 35 ].…”

Experimental cortical stroke induces aberrant increase of sharp-wave-associated ripples in the hippocampus and disrupts cortico-hippocampal communication

“…13,41 Yet little is known about the dynamics of hippocampal oscillations in the course of brain ischemia and how they respond to critical dip of CBF that causes irreversible neuronal damage in the cortex, leading to the disruption of connectivity between cortex and the other brain networks including the hippocampal formation. 11 Changes in the inhibitory and excitatory neurotransmitter systems have been well documented in the motor cortex after stroke 42,43 ; however, little is known regarding how they change other remote brain regions such as the hippocampus and their effects on neuronal activity. The current study sought to determine how distal MCA stroke affected cortical and hippocampal oscillatory activity.…”