Frontal-temporal disconnection abolishes object discrimination learning set in macaque monkeys

Two previous studies have shown that frontal–temporal disconnection in monkeys, produced by unilateral ablation of frontal cortex in one hemisphere and of visual inferior temporal cortex in the opposite hemisphere is entirely without effect on visual object–reward association learning in concurrent discrimination tasks. This is a surprising finding in light of the severe impairments that follow frontal–temporal disconnection in many other tests of visual learning and memory, including delayed matching-to-sample and several conditional learning tasks. To explore the limits of this preserved object-reward association learning, we trained monkeys on visual object discrimination learning set (DLS) prior to frontal–temporal disconnection. As a result of training with single object–reward associations, the monkeys acquired a proficient learning set, evidenced by the rapid learning of new single object–reward association problems. This rapid learning was not affected by unilateral ablations of either inferior temporal cortex alone or frontal cortex alone but was severely impaired after final surgery to complete the disconnection. Moreover, each individual monkey now learned single object–reward association problems at the slow rate at which that individual had learned such problems before the formation of learning set. This result shows that frontal–temporal disconnection abolishes visual learning set

The role of prefrontal cortex in object-in-place learning in monkeys

Previous ablation studies in monkeys suggest that prefrontal cortex is involved in a wide range of learning and memory tasks. However, monkeys with crossed unilateral lesions of frontal and temporal cortex are unimpaired at concurrent object-reward association learning but are impaired at conditional learning and the implementation of memory-based performance rules. We trained seven monkeys preoperatively on an associative learning task that required them to associate objects embedded in unique complex scenes with reward. Three monkeys then had crossed unilateral lesions of frontal and inferior temporal cortex and the remaining monkeys had bilateral prefrontal cortex ablation. Both groups were severely impaired postoperatively. These results show that both bilateral prefrontal cortex ablation and frontal-temporal disconnection impair associative learning for objects embedded in scenes. The results provide evidence that the function of frontal-temporal interactions in memory is not limited to conditional learning tasks and memory-dependent performance rules. We propose that rapid object-in-place learning requires the interaction of frontal cortex with inferotemporal cortex because visual object and contextual information which is captured over multiple saccades must be processed as a unique complex event that is extended in time. The present results suggest a role for frontal-temporal interaction in the integration of visual information over time.

Macro-connectomics and microstructure predict dynamic plasticity patterns in the non-human primate brain

The brain displays a remarkable ability to adapt following injury by altering its connections through neural plasticity. Many of the biological mechanisms that underlie plasticity are known, but there is little knowledge as to when, or where in the brain plasticity will occur following injury. This knowledge could guide plasticity-promoting interventions and create a more accurate roadmap of the recovery process following injury. We causally investigated the timecourse of plasticity after hippocampal lesions using multi-modal MRI in monkeys. We show that post-injury plasticity is highly dynamic, but also largely predictable on the basis of the functional connectivity of the lesioned region, gradients of cell densities across the cortex and the pre-lesion network structure of the brain. The ability to predict which brain areas will plastically adapt their functional connectivity following injury may allow us to decipher why some brain lesions lead to permanent loss of cognitive function, while others do not