The present study was designed to examine the relationship between localization of function in the brain and representation of the basic factors of intelligence and to investigate the effect of the occasion of brain lesions on change of intellectual structures. The quantitative findings reported in this study were based upon the test results from a battery of seventeen intelligencepsychological indicators applied individually to twenty-eight subjects, including patients with various types of brain damage, and to eighty normal control individuals. The experimental subjects were divided by age into the Low Group (7:6-10:0), the Middle Group (13:6-17:10), the High Group (20:4-28:6), the Frontal Group, the Temporal Group, the Occipital Group on lobe lesions, and the Left Group and the Right Group on hemisphere lesions. The centroid method of factor analysis and orthogonal rotation of axes were applied to the original correlation matrix based on those seventeen variables, and two factors were extracted in three age groups. The nature of these factors might be summarized as the basic capacity of reasoning (Factor I) and the ability of reproducing knowledge in a practical situation (Factor II). When applied to subjects of each age group, the test showed no differences between early and late brain injury, but when applied to patients with left- and right-hemisphere lesions, it was found that those whose left hemisphere had damage made poor records in variables positively loaded with Factor I and Factor II. And subjects with frontal lobe damage had losses in variables positively loaded with Factor I. From these facts the inferences are drawn that the left hemisphere is relevant to the verbal abilities and frontal lobe lesions are associated with losses of the basic capacity of reasoning.
In Exp. I, 80 rats were trained to discriminate vertical vs. horizontal stripe cues to a criterion of 9 successive correct trials on a single day. They could escape or avoid electric shock (0.5mA, 700V. A. C.) when the correct cue was chosen (Fig. 1). Animals were injected p. o. 5cc/kg of a solution involving either saline, 200mg/kg or 400mg/kg of OP 519 (OP), or 200mg/kg of meprobamate (MPB) before trials. Two days after reaching the criterion, rats were required to relearn the same problem; half of each group (saline, OP 200, OP 400 and MPB) were given the same drug treatment, while the rest were not injected at all. The results (Table 1) indicate an inhibitory effect upon discrimination learning only for the MPB-treated rats. However, when drug condition was shifted from MPB to no injection in relearning (Croup IVB), trials to criterion reduced to the level of the saline conditions. Correlation in trials to criterion between learning and relearning was positive for all groups with a mean of. 38 (p<.01). That is, slow learners in original learning were more likely to be slow in relearning, too. Thus superior results of Group IVB to Group IVA would indicate that the inhibitory effect of MPB is only temporary or drug-state dependent. Neither OP or MPB was found to retard running speed and only a small or no correlation was observed between running speed and trials to criterion (Table 2). Exp. II was a replication of Exp. I except that both learning and relearning were motivated by hunger drive rather than by electric shock, and rats (n=32) were given six trials per day. Results showed a suppressive effect of MPB and, to less degree, of OP upon discrimination learning. In addition this effect of MPB remained in relearning even though no injection was given (Table 3). Again a significant positive correlation was found between trials to criterion in learning and in relearning. Running time was retarded by MPB in learning but not in relearning. However, the obtained inhibitory effect of MPB could not be attributed to the drug's ataxic effect since correlation between trials to criterion and running speed was slightly positive (Table 4). In Exp. III, hungry rats were given further trials after reaching the learning criterion on the same discrimination problem as in Exp. I and II. Rats (n=14) were shifted their drug conditions, either from saline to drug, saline to saline, drug to saline or drug to drug after they attained perfect trials on three successive days. Another group of rats (n=8) were similarly shifted their drug conditions every three days. Results were summarized in Tables 5 and 6. Drug-learning dissociation was found only by MPB; correct responses decreased suddenly when drug condition was changed from saline to MPB, while they increased when the condition was reversed. Running time was almost identical under saline, OP and MPB. In summary MPB at 200mg/kg, p. o. retarded discrimination learning in rats whether they were motivated by electric shock or by food deprivation. OP had a similar but less effect for hungry rats. The obtained inhibitory effect of MPB and OP could not be explained in terms of the drug's ataxic effect. MPB was found to produce state-dependent or to dissociate, learning especially after over-learning.