Influence of anti-Nogo-A antibody treatment on the reorganization of callosal connectivity of the premotor cortical areas following unilateral lesion of primary motor cortex (M1) in adult macaque monkeys

Abstract

Following unilateral lesion of the primary motor cortex, the reorganization of callosal projections from the intact hemisphere to the ipsilesional premotor cortex (PM) was investigated in 7 adult macaque monkeys, in absence of treatment (control; n = 4) or treated with function blocking antibodies against the neurite growth inhibitory protein Nogo-A (n = 3). After functional recovery, though incomplete, the tracer biotinylated dextran amine (BDA) was injected in the ipsilesional PM. Retrogradely labelled neurons were plotted in the intact hemisphere and their number was normalized with respect to the volume of the core of BDA injection sites. (1) The callosal projections to PM in the controls originate mainly from homotypic PM areas and, but to a somewhat lesser extent, from the mesial cortex (cingulate and supplementary motor areas). (2) In the lesioned anti-Nogo-A antibody-treated monkeys, the normalized number of callosal retrogradely labelled neurons was up to several folds higher than in controls, especially in the homotypic PM areas. (3) Except one control with a small lesion and a limited, transient deficit, the anti-Nogo-A antibody-treated monkeys recovered to nearly baseline levels of performance (73–90 %), in contrast to persistent deficits in the control monkeys. These results are consistent with a sprouting and/or sparing of callosal axons promoted by the anti-Nogo-A antibody treatment after lesion of the primary motor cortex, as compared to untreated monkeys.

Distant heterotopic callosal connections to premotor cortex in non-human primates

“…premotor cortex, Frost et al, 2003;Dancause et al, 2005) may play a role. Furthermore, when the monkeys were treated with antiNogo-A antibody (neutralizing axon growth inhibitors), the callosal connectivity of the premotor cortex was reorganized (Hamadjida et al, 2012). Our anatomical findings support the notion that post-lesional plasticity taking place in one hemisphere might trigger some adaptive changes of the callosal connectivity in case of a unilateral lesion of the premotor area (e.g.…”

Role of primary motor cortex in the control of manual dexterity assessed via sequential bilateral lesion in the adult macaque monkey: A case study

“…A plastic reorganization of neural circuits, involving non-primary motor areas, has been shown to take place (Dancause et al, 2005;McNeal et al, 2010;Hamadjida et al, 2012). There is recent evidence for a cortical somatosensory influence on the mechanisms of functional recovery after frontal lobe lesion including M1 (Morecraft et al, 2015(Morecraft et al, , 2016.…”

Rethinking Stimulation of the Brain in Stroke Rehabilitation

“…As an example, Dancause and others (2005) show rewiring between ipsilesional PMv and S1 in primate models. Similarly, Hamadjida and others (2012) illustrate structural callossal plasticity in primate models of stroke, while James and others (2009) discuss functional connectivity between ipsilesional PMC and homologue with behavioral recovery in primates and human models of stroke respectively.…”