Abstract
The brain has the ability to reconstruct neural structures and functions to compensate for the brain lesions caused by stroke, although it is highly limited in primates including humans. Animal studies in which experimental lesions were induced in the brain have contributed to the current understanding of the neural mechanisms underlying functional recovery. Here, I have highlighted recent advances in non-human primate models using primate species such as macaques and marmosets, most of which have been developed to study the mechanisms underlying the recovery of motor functions after stroke. Cortical lesion models have been used to investigate motor recovery after lesions to the cortical areas involved in movements of specific body parts. Models of a focal stroke at the posterior internal capsule have also been developed to bridge the gap between the knowledge obtained by cortical lesion models and the development of intervention strategies because the severity and outcome of motor deficits depend on the degree of lesions to the region. This review will also introduce other stroke models designed to study the plastic changes associated with development and recovery from cognitive and sensory impairments. Although further validation and careful interpretation are required, considering the differences between non-human primate brains and human brains, studies using brain-lesioned non-human primates offer promise for improving translational outcomes.
Highlights
The regeneration of lost neural circuitry after stroke, the most frequent cause of brain lesions, is poor because mature neurons do not divide to replace the lost neurons and because the presence of inhibitory factors prevents functional and structural recovery of the lesioned neuronal tissue (Buchli and Schwab, 2005; Galtrey and Fawcett, 2007)
Plastic changes of the nervous system and functional compensation in the remaining intact brain areas are thought to underlie the functional recovery after brain lesions, and the concept of neurorehabilitation, which focuses on enhancing plasticity following brain lesions, has Primate Stroke Models and Recovery received considerable attention over the past decades
Using the macaque central post-stroke pain (CPSP) model, a recent study indicated that a significant reduction in synaptic terminals in pain-related cortical areas is associated with the development of CPSP (Nagasaka et al, 2021). Another recent study using the macaque CPSP model showed that functional connectivity is inappropriately strengthened between the mediodorsal nucleus of the thalamus and the amygdala, which are thought to be involved in the emotional aspects of pain, and that repetitive transcranial magnetic stimulation over the primary motor cortex normalizes this strengthened connectivity (Kadono et al, 2021)
Summary
The regeneration of lost neural circuitry after stroke, the most frequent cause of brain lesions, is poor because mature neurons do not divide to replace the lost neurons and because the presence of inhibitory factors prevents functional and structural recovery of the lesioned neuronal tissue (Buchli and Schwab, 2005; Galtrey and Fawcett, 2007). The neuronal structures of the motor cortex and corticospinal tract of these monkeys are especially more compatible with humans than the other experimental primate species described below (Kuypers, 1982; Alstermark et al, 2004; Courtine et al, 2007; Isa et al, 2007; Lemon, 2008) The combination of this homology of the motor system with the relatively large brains enables acquisition of imaging data on par with those evaluated in clinical research. Squirrel monkeys (Saimiri sciureus) and capuchin monkeys (Cebus apella) are New World monkey species classified as lissencephalic and gyrencephalic primates, respectively (Table 1) Their body sizes are larger than those of common marmosets and smaller than those of macaques. Induction of controlled focal lesions to a specific brain region will enable the comparison among different species
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
