Practice makes perfect, but only with the right hand: sensitivity to perceptual illusions with awkward grasps decreases with practice in the right but not the left hand.

It has been proposed that the visual mechanisms that control well-calibrated actions, such as picking up a small object with a precision grip, are neurally distinct from those that mediate our perception of the object. Thus, grip aperture in such situations has been shown to be remarkably insensitive to many size-contrast illusions. But most of us have practiced such movements hundreds, if not thousands of times. What about less familiar and unpracticed movements? Perhaps they would be less likely to be controlled by specialized visuomotor mechanisms and would therefore be more sensitive to size-contrast illusions. To test this idea, we asked right-handed subjects to pick up small objects using either a normal precision grasp (thumb and index finger) or an awkward grasp (thumb and ring finger), in the context of the Ponzo illusion. Even though this size-contrast illusion had no effect on the scaling of the precision grasp, it did have a significant effect on the scaling of the awkward grasp. Nevertheless, after three consecutive days of practice, even the awkward grasp became resistant to the illusion. In a follow-up experiment, we found that awkward grasps with the left hand (in right handers) did not benefit from practice and remained sensitive to the illusion. We conclude that the skilled target-directed movements are controlled by visual mechanisms that are quite distinct from those controlling unskilled movements, and that these specialized visuomotor mechanisms may be lateralized to the left hemisphere.

Middle cerebral artery (MCA) stroke produces dysfunction in adjacent motor cortex as detected by intracortical microstimulation in rats.

Middle cerebral artery (MCA) stroke in the rat produces impairments in skilled movements. The lesion damages lateral neocortex but spares primary motor cortex (M1), raising the question of the origin of skilled movement deficits. Here, the behavioral deficits of MCA stroke were identified and then M1 was examined neurophysiologically and neuroanatomically. Rats were trained on a food skilled reaching task then the lateral frontal cortex was damaged by unilateral MCA electrocoagulation contralateral to the reaching forelimb. Reach testing and training on two tasks was conducted over 30 post-surgical days. Later, M1 and the corticospinal tract were investigated using intracortical microstimulation (ICMS), anterograde and retrograde axon tracing. A skilled reaching impairment was observed post-surgery, which partly recovered with time and training. ICMS revealed a diminished forelimb movement representation in MCA rats, but a face representation comparable in size to sham rats. Anterograde and retrograde tract tracing suggest that M1 efferents were intact. Although M1 appears to be in the main anatomically spared after MCA stroke its function as assessed electrophysiologically and behaviorally is disrupted.

A comparison of different models of stroke on behaviour and brain morphology.

We compared the effects of three models of permanent ischemia, as well as cortical aspiration, on behaviour and brain morphology. Rats received a stroke either by devascularization or by two different procedures of medial cerebral artery occlusion (MCAO; small vs. large). Animals were trained in a reaching task, forepaw asymmetry, forepaw inhibition, sunflower seed task and tongue extension. Behaviour was assessed 1 week after the lesion and at 2-week intervals for a total of 9 weeks. One week after the surgery all animals were severely impaired on all tasks and although they improved over time they only reached preoperative base lines on tongue extension. Animals with small MCAOs performed better in reaching and sunflower tasks; no other behavioural differences were detected among the groups. Pyramidal cells in forelimb and cingulate areas as well as spiny neurons of the striatum were examined for dendritic branching and spine density using a Golgi-Cox procedure. Each lesion type had a different impact on cell morphology. Overall, different changes (atrophy or hypertrophy) were observed with each kind of lesion and these changes were specific for the region (forelimb, cingulate, striatum) and the condition (intact vs. damaged hemisphere). These results suggest that: (i) different lesions to the motor cortex produce subtle differences in behaviour, and (ii) the method used to induce the lesion produces striking differences in cortical and subcortical plasticity.

Complete sparing of spatial learning following posterior and posterior plus anterior cingulate cortex lesions at 10 days of age in the rat.

Neonatal posterior cingulate cortex lesions spare the spatial deficits that characterize adult lesions. The present experiments examined the possibility that the anterior cingulate cortex mediates the spared spatial behavior. Rats were given bilateral lesions of the posterior cingulate cortex or anterior plus posterior cingulate cortex on postnatal days 4 (P4), 10 (P10), or in adulthood (P120). All groups were tested for spatial learning on the Morris place task in adulthood. Adult animals were impaired on place learning relative to controls whereas place learning was spared in all the neonatal groups and sparing was complete in the group receiving day 10 lesions. The results are discussed in relation to neural mechanisms, including fiber rerouting, synaptic changes and generation of new neurons, that may mediate spared spatial following neonatal posterior cingulate cortex lesions. Also discussed is evidence indicating that the neonatal brain, especially the day 10, has a special ability to compensate for injury.