Hippocampus specific iron deficiency alters competition and cooperation between developing memory systems

Iron deficiency (ID) is the most common gestational micronutrient deficiency in the world, targets the fetal hippocampus and striatum and results in long-term behavioral abnormalities. These structures primarily mediate spatial and procedural memory, respectively, in the rodent but have interconnections that result in competition or cooperation during cognitive tasks. We determined whether ID-induced impairment of one alters the function of the other by genetically inducing a 40% reduction of hippocampus iron content in late fetal life in mice and measuring dorsal striatal gene expression and metabolism and the behavioral balance between the two memory systems in adulthood. Slc11a2hipp/hipp mice had similar striatum iron content, but 18% lower glucose and 44% lower lactate levels, a 30% higher phosphocreatine:creatine ratio, and reduced iron transporter gene expression compared to wild type (WT) littermates, implying reduced striatal metabolic function. Slc11a2hipp/hipp mice had longer mean escape times on a cued task paradigm implying impaired procedural memory. Nevertheless, when hippocampal and striatal memory systems were placed in competition using a Morris Water Maze task that alternates spatial navigation and visual cued responses during training, and forces a choice between hippocampal and striatal strategies during probe trials, Slc11a2hipp/hipp mice used the hippocampus-dependent response less often (25%) and the visual cued response more often (75%) compared to WT littermates that used both strategies approximately equally. Hippocampal ID not only reduces spatial recognition memory performance but also affects systems that support procedural memory, suggesting an altered balance between memory systems

Identifying a Window of Vulnerability during Fetal Development in a Maternal Iron Restriction Model

It is well acknowledged from observations in humans that iron deficiency during pregnancy can be associated with a number of developmental problems in the newborn and developing child. Due to the obvious limitations of human studies, the stage during gestation at which maternal iron deficiency causes an apparent impairment in the offspring remains elusive. In order to begin to understand the time window(s) during pregnancy that is/are especially susceptible to suboptimal iron levels, which may result in negative effects on the development of the fetus, we developed a rat model in which we were able to manipulate and monitor the dietary iron intake during specific stages of pregnancy and analyzed the developing fetuses. We established four different dietary-feeding protocols that were designed to render the fetuses iron deficient at different gestational stages. Based on a functional analysis that employed Auditory Brainstem Response measurements, we found that maternal iron restriction initiated prior to conception and during the first trimester were associated with profound changes in the developing fetus compared to iron restriction initiated later in pregnancy. We also showed that the presence of iron deficiency anemia, low body weight, and changes in core body temperature were not defining factors in the establishment of neural impairment in the rodent offspring

The corallivorous invertebrate Drupella aids in transmission of brown band disease on the Great Barrier Reef

Brown band disease (BrB) is an increasingly prevalent coral disease in the Indo-Pacific, but although the macroscopic signs of BrB have been associated with the ciliate Philaster guamensis, many aspects of its ecology remain unknown, particularly how the disease is transmitted among coral colonies. The aim of this study was to assess biotic factors affecting BrB transmission, explicitly testing whether corallivorous species contribute to disease spread. Several fish species were observed feeding on diseased tissue in the field, but did not influence either the progression or transmission rates of BrB on coral colonies in situ. In aquarium-based experiments, the butterflyfish Chaetodon aureofasciatus neither aided nor hindered the transmission of BrB from infected to uninfected corals. In contrast, the coral-feeding gastropod Drupella sp. was a highly effective vector of BrB, infecting more than 40 % of experimental colonies. This study also demonstrated the importance of injury in facilitating BrB infection, supporting the hypothesis that the BrB pathogen invades compromised coral tissue. In conclusion, disturbances and corallivorous activities that injure live corals are likely to contribute to increased occurrence of BrB provided that feeding scars create entry wounds sufficiently extensive to facilitate infection. These findings increase the understanding of the ecology of BrB, enabling better predictions of the prevalence and severity of this disease, and informing strategies for managing the impact of BrB on coral reefs