Immunolocalization of glutathione reductase in the murine brain.

Free radical species arise from the univalent reduction of oxygen. The cytosolic agent H2O2, produced during enzymatic scavenging of the superoxide radical (O2-) is in turn removed predominantly via the oxidation of reduced glutathione (GSH) to the oxidized form (GSSG) by glutathione peroxidase. Subsequently GSSG is recycled back to GSH by glutathione reductase (GSH-red). Little is known about the distribution of this enzyme in the brain. The aim of this study was to determine the distribution of this enzyme in the brain of different murine species by means of immunocytochemical techniques, although most attention was given to the distribution of GSH-red in the forebrain. In most brain areas GSH-red positive neurons were detected, but the regional intracellular staining intensity differed markedly. The pre-piriform and piriform cortices, the pyramidal cell layers of the hippocampus, and the dentate gyrus were heavily stained. The caudate nucleus displayed a progressive increase in the intracellular staining intensity from the rostral to the caudolateral parts. Furthermore, in the thalamus, there was a gradual decrease in GSH-red staining from the medial to the lateral parts. The mesencephalon was poor in immunopositive cells, and in the substantia nigra pars reticulata, almost no labeling was detected. However, the substantia nigra pars compacta showed an intense GSH-red immunoreactivity. The results show a specific localization of glutathione reductase in distinct brain regions, suggesting a variable potency of different brain areas in dealing with the damaging oxidative actions of free radicals. Also, differential GSH-red expression patterns were found in the various murine species. Some species showed a pronounced GSH-red immunoreactivity in glial cells, specifically in regions that lacked neuronal GSH-red immunoreactivity.

Delay of gratification: mothers' predictions about four attentional techniques.

Mothers' predictions about the ability of their own children to delay gratification using different techniques were investigated. Fifty-one mothers of children 4 to 6 years old were asked to evaluate distraction, thinking about the incentive, tasting the incentive, and a control. These conditions were derived from the research of Mischel and his associates (1974), who demonstrated the effectiveness of distraction in aiding children's delay behavior. Parents were predicted to expect delay to be enhanced by the distraction technique and hampered by the thinking about the incentive and tasting the incentive techniques, with the latter being the least effective. Contrary to our predictions, mothers failed to predict effectiveness of distraction compared with the two incentive-focused techniques. Reasons are advanced for more research on parents' knowledge and valuing of metacognitive strategies appropriate for their children.

L-deprenyl reduces brain damage in rats exposed to transient hypoxia-ischemia.

BACKGROUND AND PURPOSE: L-Deprenyl (Selegiline) protects animal brains against toxic substances such as 1-methyl-1,2,3,6-tetrahydropyridine and 6-hydroxydopamine. Experiments were conducted to test whether L-deprenyl prevents or reduces cerebral damage in a transient hypoxia/ischemia rat model. METHODS: Rats were treated for 14 days with 2 mg/kg and 10 mg/kg L-deprenyl or saline. After surgery a 20-minute hypoxia/ischemia period was induced by simultaneous occlusion of the left common carotid artery and reduction of the percentage of oxygen in the gas mixture to 10%. Rats were killed 24 hours later. Silver staining was used to reveal damage in several brain regions. RESULTS: In the brain, both L-deprenyl dosages reduced damage up to 78% compared with the controls. Total brain damage was decreased from 23%-31% to 5%-9% with the L-deprenyl treatment (2 mg/kg: F1.13 = 6.956, P < .05; 10 mg/kg: F1.13 = 5.731, P < .05). In the striatum, significant treatment effects were found between both the L-deprenyl groups (2 mg/kg and 10 mg/kg, respectively) and the saline group (F1.13 = 14.870, P < .005; and F1.13 = 8.937, P = .01; respectively). In the thalamus, significant treatment effects were seen in the 2-mg/kg L-deprenyl group (F1.13 = 11.638, P < .005) and the 10-mg/kg group (F1.13 = 8.347, P < .05) compared with the control group. No significant damage decrease was seen in the hippocampus and the cortex. CONCLUSIONS: The results show that L-deprenyl is effective as a prophylactic treatment for brain tissue when it is administered before hypoxia/ischemia. Mechanisms responsible for the observed protection remain unclear. The regional differences in damage, however, are in accordance with the reported regional increase in superoxide dismutase and catalase activities after L-deprenyl treatment, suggesting the involvement of free radicals and scavenger enzymes.

The effects of cooperative and individualistic reward on intrinsic motivation.

The effects of cooperative versus individualistic reward on students' intrinsic motivation were investigated. The controlling aspects of extrinsic reward may be heightened or produce greater ego threat in the individualistic situation when compared with a group situation. We predicted that students in the cooperative social situation would show higher levels of intrinsic motivation. Fifth-grade students from existing cooperative groups were assigned randomly to receive a tangible reward based on either cooperative or individualistic achievement for completing pattern block designs. Cooperation affected intrinsic motivation positively. Students in the cooperative dyad solved the block designs more quickly, interacted positively, and viewed the task as easier than did those in the individualistic situation, and they reported that their peers were helpful. There was little evidence that the controlling functions of reward or ego-threat were factors in producing the outcome. Some evidence supporting the importance of the social nature of cooperation was provided.