Radical processes following gamma-irradiation of frozen concentrated matrices of heparin and dextran sulphate.
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Biomedical subjects
Publications and source records attributed to R E Morgan.
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Long-Evans rats exposed chronically to lead (Pb) acetate (0, 75, or 300 ppm) were tested as adults on an automated, three-choice visual discrimination task as part of a larger study designed to elucidate the cognitive effects of developmental Pb exposure. Median adult BPb levels for the groups were <5, 20, and 36 microgram/dl. The pattern of results suggested a linear effect, with increasing lead dose producing progressively slower learning and an increased incidence of "impaired" individuals. This latter measure proved to be slightly more sensitive than the former, suggesting individual differences in susceptibility to Pb neurotoxicity. Additional analyses revealed that the impairing effect of Pb was seen in both the chance and post-chance learning phases, indicating that the deficit was not limited to (but could include) attentional function. Reaction time on incorrect trials was reduced in the 300-ppm group, whereas no Pb effect was seen for correct trials. The present findings suggest that chronic developmental Pb exposure produces an associative deficit as well as a tendency to respond rapidly, but does not affect information-processing speed.
The present study tested the hypothesis that early lead (Pb) exposure causes lasting attentional dysfunction. Long-Evans dams were fed Pb-adulterated water during gestation and/or lactation; the offspring were tested as adults. The results of a visual discrimination task revealed no Pb effects on learning rate or information-processing speed. However, lasting effects of the early Pb exposure were seen in the subsequent vigilance tasks, particularly in the final task in which onset of the visual cue and cue duration varied randomly across trials. Exposure during both gestation and lactation impaired response initiation. In addition, animals exposed to Pb during lactation only or lactation+gestation committed significantly more omission errors than controls under two specific conditions: (1) trials in which a delay was imposed prior to cue presentation and (2) trials that followed an incorrect response. The pattern of treatment differences indicated that early Pb exposure produced lasting impairment of sustained attention and increased reactivity to errors. Both effects may contribute to the cognitive impairment, problematic classroom behaviors, and increased delinquency associated with early Pb exposure in children. These findings also demonstrate that the developmental timing of the exposure determines the pattern of effects. Thus, conclusions regarding whether or not a particular cognitive or affective function is impaired or spared by early Pb exposure must be limited to the specific timing and intensity of exposure.
Long-Evans dams were exposed to Pb acetate in the drinking water during both gestation and lactation, or lactation only. This report presents the results of an automated, olfactory, serial reversal task administered to the adult offspring. Although overall learning rate was not significantly affected by Pb exposure, analyses of specific phases of the learning process revealed that all three exposed groups required significantly more trials than controls to reach criterion from the point at which perseverative responding to the previously correct cue ended. These in-depth analyses revealed that the reversal learning impairment of the Pb-exposed animals was not due to a deficit in inhibiting responses to the previously correct cue, the mechanism commonly assumed to underlie impaired reversal learning. Instead, the analyses revealed that two other independent Pb effects were responsible for the prolonged postperseverative learning period: a response bias and an impaired ability to associate cues and/or actions with affective consequences. The contribution of these two factors varied as a function of the timing and intensity of the Pb exposure. It is hypothesized that the Pb-induced associative deficit may reflect lasting damage to the amygdala and/or nucleus accumbens, which comprise a system thought to modulate the process by which environmental cues acquire affective significance.
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