Brain mechanisms in problem solving and intelligence: A replication and extension

Abstract Anderson (1993, 1995) recently reported the extraction of a general intelligence (g) factor from a battery of tests administered to laboratory rats, conflicting with historical evidence and our more recent study of rat problem-solving behavior ( Thompson, Crinella, & Yu, 1990) . Anderson's findings are most likely due to use of an outbred strain, whereas we and others used inbred rats. However, it has been suggested that these unique findings may be due to Anderson's use of a more g-loaded test battery. We tested this hypothesis by analyzing the performance of 120 adult male Sprague-Dawley rats on seven laboratory tests, selected for diversity and g saturation. At 21 to 23 days of age, 96 of the animals were bilaterally lesioned in one of 48 brain sites, and 24 remained unlesioned. Testing began at 42 to 45 days of age. Analysis of data from the 24 unlesioned animals showed no evidence of a g factor. When data from unlesioned and lesioned animals were combined, uniformly positive correlations were obtained, and an unrotated first principal component accounted for 34% of the variance. This component had psychometric properties analogous to g factors extracted from human test batteries. The results support our contention that the disparity between Anderson's findings and ours are due to strain differences, and not psychometric properties of the respective test batteries. The results also show that the g loading of a test is directly related to the number of brain structures required to mediate its performance—biological support for the view that tests with higher g loadings sample a proportionately greater number of elementary processes than tests with lower g loadings. Because the psychometric g factor is sensitive to the widest array of brain lesions, it may be the best measure for detecting neuropsychological deficit irrespective of lesion location.

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