The hippocampus is especially sensitive to the effects of gestational and neonatal iron deficiency, even after iron repletion. This study compared the effects of iron deficiency, maintained from gestational day 2 to postnatal day (P)7, on "delay" and "trace" fear conditioning. Only the latter paradigm is critically dependent on the dorsal hippocampus. In different groups of rats, fear conditioning commenced either prior to puberty (P28 or P35) or after puberty (P56). Fear conditioning was measured using fear-potentiated startle. Both delay and trace fear conditioning were diminished by iron deficiency at P28 and P35. Hippocampal expression of the plasticity-related protein PKC-gamma was increased through trace fear conditioning, but reduced at P35 in the iron deficient group. Trace fear conditioning was enhanced by prior iron deficiency in the P56 group. This unanticipated finding in iron-repleted adults is consistent with the effects of developmental iron deficiency on inhibitory avoidance learning, but contrasts with the persistent deleterious long-term effects of a more severe iron deficiency protocol, suggesting that degree and duration of iron deficiency affects the possibility of recovery from its deleterious effects.
Chronic hypoxia (CH) present in infants with cyanotic congenital heart disease may be responsible for subsequent cognitive deficits seen in these children. In a rat model of CH [10% O(2) between postnatal day (P) 3 and 28], we have demonstrated significant alterations in energy metabolism and excitatory neurotransmission in the developing hippocampus. These alterations may adversely affect dendritic morphology, which is a highly energy-dependent and excitatory neurotransmitter-mediated event, and hippocampus-mediated behaviors. We measured the apical segment length of dendrites in pyramidal neurons of the CA1 region of the hippocampus using microtubule-associated protein-2 (MAP-2) histochemistry on P28 while the animals were hypoxic (n=8 in CH and n=6 in control), and on P56 after the animals had been normoxic for 4 weeks (n=8/group). We also compared dorsal hippocampus-dependent trace fear conditioning and dorsal hippocampus-independent delay fear conditioning on P56. Developmental trajectory of the apical segment length was similar in CH and controls, decreasing between P28 and P56. However, when compared with the controls, the apical segment length was longer in the CH group on both P28 [55.11+/-2.30 microm (CH) vs. 40.52+/-1.20 microm (control), p<0.001] and P56 [44.01+/-1.56 microm (CH) vs. 31.75+/-1.31 microm (control), p<0.001], suggesting the persistence of an immature dendritic architecture. Both trace and delay fear conditioning were decreased in the CH group, suggesting functional abnormality beyond the dorsal hippocampus. These structural and functional alterations may contribute to the cognitive deficits seen in infants at risk for CH.
The current study compared student reactions toward 3 game-like exam review activities: Jeopardy, Kahoot!, and the Immediate Feedback Assessment Technique. Across 3 semester-long sessions, 60 psychological research methods students engaged in each of these review activities in preparation for an exam in teams of 3 to 4. Subsequently, students completed a survey regarding their motivation and team process and completed another survey to indicate whether their study habits had changed. Consistent with related research, the findings showed that students rated their motivation for the activities highly and perceived minimal relationship conflict during the exercises. Study habits and exam scores were similar for all 3 review activities. The only significant difference was found for task conflict, F(2, 48) ϭ 3.87, p ϭ .028, p 2 ϭ .14, but task conflict was still low. Thus, the results suggest that all three review activities are enjoyable and do appear to have value for students.
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