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EN
On postnatal days (PND) 12 and 13, 90 male Swiss CD-l mice were tested for orientation to 3 intensities of recorded ultrasounds while climbing an inclined wire grid surface. Motor responses and vocalization to replayed ultrasounds (55-75 kHz) of 20-, 40-, and 60-dB SPL indicated an intensity dependence. In Experiment 2, 138 pups were exposed to either contingent or noncontingent pairings of recorded ultrasounds of 55-75 kHz, averaging 40 dB, and mild inescapable footshocks, or taped vocalizations or footshocks only on PND 12, 14, or 16. At PND 18, subjects were tested for passive avoidance following exposure to the taped ultrasounds only upon entry into the dark side of a black-white compartment. Results suggested only overall, nonspecific effects of pretreatment to elicit responses antagonistic to motor activity. In Experiment 3, 36 pups at PND 15 were tested for passive avoidance with the ultrasound recordings of 40- or 80-dB onset upon entry to the dark compartment; a third group had no ultrasound exposure. A significant intensity effect confirmed that the ultrasounds had prepotent properties.
EN
The aim of this study was to investigate how the processing of auditory stimuli is affected by the simultaneous presentation of visual stimuli. This was approached in an active and passive condition, during which a P3 was elicited in the human EEG by single auditory stimuli. Subjects were presented tones, either alone or accompanied by the simultaneous exposition of pictures. There were two different sessions. In the first, the presented tones demanded no further cognitive activity from the subjects (passive or 'ignore' session), while in the second session subjects were instructed to count the tones (active or 'count' session). The central question was whether inter-modal influences of visual stimulation in the active condition would modulate the auditory P3 in the same way as in the passive condition. Brain responses in the ignore session revealed only a small P3-like component over the parietal and frontal cortex, however, when the auditory stimuli co-occurred with the visual stimuli, an increased frontal activity in the window of 300-500 ms was observed. This could be interpreted as the reflection of a more intensive involuntary attention shift, provoked by the preceding visual stimulation. Moreover, it was found that cognitive load caused by the count instruction, resulted in an evident P3, with maximal amplitude over parietal locations. This effect was smaller when auditory stimuli were presented on the visual background. These findings might support the thesis that available resources were assigned to the analysis of visual stimulus, and thus were not available to analyze the subsequent auditory stimuli. This reduction in allocation of resources for attention was restricted to the active condition only, when the matching of a template with incoming information results in a distinct P3 component. It is discussed whether the putative source of this effect is a change in the activity of the frontal cortex.
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Cognitive subtypes of dyslexia

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EN
Different theories conceptualise dyslexia as either a phonological, attentional, auditory, magnocellular, or automatisation deficit. Such heterogeneity suggests the existence of yet unrecognised subtypes of dyslexics suffering from distinguishable deficits. The purpose of the study was to identify cognitive subtypes of dyslexia. Out of 642 children screened for reading ability 49 dyslexics and 48 controls were tested for phonological awareness, auditory discrimination, motion detection, visual attention, and rhythm imitation. A combined cluster and discriminant analysis approach revealed three clusters of dyslexics with different cognitive deficits. Compared to reading-unimpaired children cluster no. 1 had worse phonological awareness; cluster no. 2 had higher attentional costs; cluster no. 3 performed worse in the phonological, auditory, and magnocellular tasks. These results indicate that dyslexia may result from distinct cognitive impairments. As a consequence, prevention and remediation programmes should be specifically targeted for the individual child's deficit pattern.
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