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A N Bensoula

Publications and source records attributed to A N Bensoula.

5 recordsLinked to original sources

Sensorimotor learning in three cerebellar mutant mice.

Cerebellar damage occurs during developmental stages in three mutant mice (staggerer, hot-foot, and lurcher), causing disturbances in posture and equilibrium. During three tests of motor coordination, the performances of staggerer mutants was inferior to that of normal mice and did not improve with extended practice for up to 7 days of training. The sensorimotor performance of hot-foot mutants and of lurcher mutants was also lower than that of normal mice. Nevertheless, hot-foot mutants showed evidence of learning in two of the three tests and lurcher mutants in all three tests. Cerebellar atrophy in the latter two mutants did not prevent sensorimotor learning, but instead impaired their ability to reach the same level of performance as that of normal mice.

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Spontaneous alternation, motor activity, and spatial learning in hot-foot mutant mice.

Hot-foot mutant mice, characterized by defective innervation of Purkinje cells and an ataxic gait, were less active than normal mice in a T-maze. In spontaneous alternation testing with either single or multiple trials, hot-foot mutants, contrary to normal mice, did not alternate above chance. Moreover, the mutants had a higher number of errors and higher escape latencies in a water-filled Z-maze. These results indicate that in addition to motor coordination deficits, these cerebellar mutants have deficits in spatial learning and perseverate choices of maze arms.

Animals↗

Spatial learning in a Z-maze by cerebellar mutant mice.

Two types of cerebellar mutant mice (staggerer and lurcher) were evaluated during 5-day acquisition of a spatial learning task in a Z-maze filled with water. Although the number of errors and escape latencies decreased in normal mice, the acquisition of the cerebellar mutants was impaired but not abolished. These results indicate that the cerebellum has a role in spatial learning. Mice with cerebellar dysfunction take a more indirect route toward a goal during the course of swimming, when ataxic symptoms are no longer in evidence.

Animals↗

Spatial navigation of staggerer and normal mice during juvenile and adult stages.

Staggerer mutant mice were compared to normal mice of two different ages (2-6 mo) in two tasks requiring navigational skills in a circular maze visible platform condition and a T-maze. Staggerer mutants had higher latencies than normal mice in both tests. The performance of normal mice worsened with age for both tests. The aging factor interacted with the genotype factor only in the circular maze, where the mutant-nonmutant differential was wider among juvenile animals. In neither task was there evidence of a more pronounced impairment with aging in staggerer mutants. It remains to be determined in this mutant at more advanced stages of aging or in other models of chronic neural disease whether early neuropathology accelerates brain aging.

Aging↗

Rotorod sensorimotor learning in cerebellar mutant mice.

Lurcher mutant mice, characterized by degeneration of cerebellar granule and Purkinje cells, were compared to normal littermate controls in a rotorod test, consisting of a wheel turning at constant speed which required on the part of the animal postural adjustments in order to maintain equilibrium. Identical baseline rates for the two groups were assured by changing the speed and size of the rotating rod. Although both groups were able to learn the task, the fall latencies of normal mice exceeded those of lurchers. These results indicate that cerebellar cortical atrophy does not abolish this form of sensorimotor learning. However, brain-damaged animals are unable to reach the same level of performance as normal animals. In contrast to the results in lurcher mutants, no sensorimotor learning was displayed by hot-foot mutants and staggerer mutants.

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