The cortical destruction necessary to produce a transfer of a forced-practice function.

Peterson, George M.; Barnett, Patricia E.

doi:10.1037/h0047842

Cited by 21 publications

(1 citation statement)

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“…Further studies involving appropriately designed behavioural tasks suggested, however, that the role of the rat's cerebral cortex in the execution of skilled forelimb movements may not differ greatly from that of primates. Deficits in the manipulative capacity in the forepaw contralateral to a unilateral motor cortical lesion were observed in rats trained to reach for and grasp food pellets (Peterson and Barnett, 1961) or to manipulate a force transducer (Price and Fowler, 1981). Castro (1972a) further demonstrated that rats bearing bilateral motor cortical lesions were impaired in their digital motor capabilities to retrieve food pellets from narrow slots.…”

Section: Introductionmentioning

confidence: 96%

Impaired performance in a conditioned reaction time task after thermocoagulatory lesions of the fronto-parietal cortex in rats

Baunez

Salin²,

Nieoullon³

et al. 1998

Cerebral Cortex

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The present study examined whether cortical damage in rats may disrupt the integrative processes and motor control involved in the performance of a reaction time (RT) task. To investigate the nature of the deficits in the conditioned task, rats were subjected, after learning, to a coagulation of pia brain surface of varying extent, including the frontal and parietal cortical areas. They were then tested daily for over one month. The behavioural task required the rats to hold a lever down during a variable and random delay and react quickly to the onset of a visual cue by releasing the lever within a RT limit for food reinforcement. Extensive bilateral cortical lesions had no effect on spontaneous motor activity, but severely impaired RT performance. Latencies to release the lever after the cue were dramatically increased during the first postoperative sessions and gradually returned to baseline levels within 3 weeks, whereas less dramatic but long-lasting increase in premature responding (anticipatory response before the visual cue) was observed throughout the testing sessions. More restricted lesions to the frontoparietal cortex produced a similar pattern of incorrect responding with a faster recovery of delayed responses and a strong deficit in premature responding. The major effects of lesions confined to the rostral pole of the frontal cortex were observed on premature responding, however. The present results demonstrate that the impairment in movement initiation is rapidly recovered within 2-3 weeks even after extensive thermocoagulatory lesions of the frontal and parietal areas. This recovery suggests the involvement of adaptive processes developing progressively and probably reflecting the remarkable synaptic plasticity of the extrapyramidal motor output. In contrast, the long-lasting increase in premature responding, supposed to reflect some attentional deficits, may produce anatomofunctional long-term disorganization of subcortical structures such as the basal ganglia. Interestingly enough, these results show that the rat neocortex supports functions very similar to those of primates and provide a good model for studying these higher functions in operant motor procedures that require prior associative learning and appropriate motor coordination.

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Section: Introductionmentioning

confidence: 96%