Designing a facile low cost synthesis strategy for the Na-V-S-O systems, NaV(SO4)2, Na3V(SO4)3 and Na2VO(SO4)2.

Alkali metal transition metal sulfates have attracted considerable interest as potential electrodes for Na ion battery materials. While there has been significant research on Fe based systems, research on V based systems has been lacking, apart from a recent report on Na2VO(SO4)2. This can be related to the complex synthetic routes previously reported to make sodium vanadium sulfate systems. In this paper, we report a simple route towards the synthesis of three such sodium vanadium sulfate systems, NaV(SO4)2, Na2VO(SO4)2, and Na3V(SO4)3. We analyse the resulting products through X-ray diffraction and Raman spectroscopy to highlight the formation of high quality samples via this simple solution route, with subsequent low temperature (<400 °C) heat treatment. This facile new route will allow these materials to be considered for future applications rather than as simply chemical curiosities.

Chronic postnatal DE-71 exposure: effects on learning, attention and thyroxine levels.

Polybrominated diphenyl ethers (PBDEs) are ubiquitous, bioaccumulative flame retardants. Much remains to be learned about their developmental toxicological properties, particularly with regards to chronic exposure. In two experiments, male Long-Evans rats ingested the commercial pentaBDE mixture DE-71 from birth onward, first through the milk of lactating dams (who ingested 5 or 7.5 mg DE-71/day in a custom-mixed chow), then directly via chow consumption (at a dose of 3 or 4.5 mg/day). Control rats consumed the same brand of chow without DE-71. As adults, the rats were assessed for learning and attention using a series of five-choice serial reaction time tasks. A challenge with the muscarinic cholinergic antagonist scopolamine (0, 0.01, 0.03, or 0.05 mg/kg injected s.c.) was conducted on the final attention task. Serum total thyroxine (T4) levels were obtained at the end of testing. Total T4 was significantly lower in both DE-71 groups than in controls. Visual discrimination learning was unaffected by DE-71, but rats ingesting 4.5 mg/day DE-71 demonstrated significant impairments in sustained attention and inhibitory control, as evidenced by increased premature responding and decreased accuracy of responding in Attention Task 1. However, the DE-71-exposed rats did not respond differentially to the effects of scopolamine on attention compared to controls. These effects of chronic developmental DE-71 exposure differ from effects seen with brief postnatal exposure, suggesting that more research needs to be done on the more environmentally relevant chronic exposure model.

A mouse model of fragile X syndrome exhibits heightened arousal and/or emotion following errors or reversal of contingencies.

This study was designed to further assess cognitive and affective functioning in a mouse model of Fragile X syndrome (FXS), the Fmr1(tm1Cgr) or Fmr1 "knockout" (KO) mouse. Male KO mice and wild-type littermate controls were tested on learning set and reversal learning tasks. The KO mice were not impaired in associative learning, transfer of learning, or reversal learning, based on measures of learning rate. Analyses of videotapes of the reversal learning task revealed that both groups of mice exhibited higher levels of activity and wall-climbing during the initial sessions of the task than during the final sessions, a pattern also seen for trials following an error relative to those following a correct response. Notably, the increase in both behavioral measures seen early in the task was significantly more pronounced for the KO mice than for controls, as was the error-induced increase in activity level. This pattern of effects suggests that the KO mice reacted more strongly than controls to the reversal of contingencies and pronounced drop in reinforcement rate, and to errors in general. This pattern of effects is consistent with the heightened emotional reactivity frequently described for humans with FXS.

Attentional dysfunction, impulsivity, and resistance to change in a mouse model of fragile X syndrome.

On a series of attention tasks, male mice with a mutation targeted to the fragile X mental retardation 1 (Fmrl) gene (Fmrl knockout [KO] mice) committed a higher rate of premature responses than wild-type littermates, with the largest differences seen when task contingencies changed. This finding indicates impaired inhibitory control, particularly during times of stress or arousal. The KO mice also committed a higher rate of inaccurate responses than controls, particularly during the final third of each daily test session, indicating impaired sustained attention. In the selective attention task, the unpredictable presentation of potent olfactory distractors produced a generalized disruption in the performance of the KO mice, whereas for controls, the disruption produced by the distractors was temporally limited. Finally, the attentional disruption seen following an error was more pronounced for the KO mice than for controls, further implicating impaired regulation of arousal and/or negative affect. The present study provides the first evidence that the Fmrl KO mouse is impaired in inhibitory control, attention, and arousal regulation, hallmark areas of dysfunction in fragile X syndrome. The resistance to change also seen in these mice provides a behavioral index for studying the autistic features of this disorder.

Early lead exposure produces lasting changes in sustained attention, response initiation, and reactivity to errors.

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.