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Does Early-Life Exposure to Stress Shape or Impair Cognition?
A predominant view in psychology is that early psychosocial adversity (e.g., abuse) impairs cognition, because children from stressful backgrounds (e.g., violent households) score lower on standard tests of intelligence, language, memory, inhibition, and other abilities. However, recent studies indicate that these people may exhibit improved detection, learning, and memory on tasks involving stimuli that are ecologically relevant to them (e.g., dangers), compared with safely nurtured peers. These findings contradict the view that cognition of stressed people is generally impaired; they suggest, rather, that these people's minds are developmentally specialized toward local environmental conditions. Here, we review recent research supporting this hypothesis. In addition, we propose that novel studies should examine whether stressed children show not only improved detection but also improved memory and reasoning on tasks involving stimuli that are ecologically relevant to them. Finally, we discuss clinical implications of switching from conceptualizing stressed minds as \"adapted\" rather than \"impaired.\"
Journal Article
Targeting mGlu1 Receptors in the Treatment of Motor and Cognitive Dysfunctions in Mice Modeling Type 1 Spinocerebellar Ataxia
Type 1 spinocerebellar ataxia (SCA1) is a progressive neurodegenerative disorder with no effective treatment to date. Using mice modeling SCA1, it has been demonstrated that a drug that amplifies mGlu1 receptor activation (mGlu1 receptor PAM, Ro0711401) improves motor coordination without the development of tolerance when cerebellar dysfunction manifests (i.e., in 30-week-old heterozygous ataxin-1 [154Q/2Q] transgenic mice). SCA1 is also associated with cognitive dysfunction, which may precede cerebellar motor signs. Here, we report that otherwise healthy, 8-week-old SCA1 mice showed a defect in spatial learning and memory associated with reduced protein levels of mGlu1α receptors, the GluN2B subunit of NMDA receptors, and cannabinoid CB1 receptors in the hippocampus. Systemic treatment with Ro0711401 (10 mg/kg, s.c.) partially corrected the learning deficit in the Morris water maze and restored memory retention in the SCA1 mice model. This treatment also enhanced hippocampal levels of the endocannabinoid, anandamide, without changing the levels of 2-arachidonylglycerol. These findings suggest that mGlu1 receptor PAMs may be beneficial in the treatment of motor and nonmotor signs associated with SCA1 and encourage further studies in animal models of SCA1 and other types of SCAs.
Journal Article
The mirror of the medieval : an anthropology of the Western historical imagination
\"Since its invention by Renaissance humanists, the myth of the 'Middle Ages' has held a uniquely important place in the Western historical imagination. Whether envisioned as an era of lost simplicity or a barbaric nightmare, the medieval past has always served as a mirror for modernity. This book gives an eye-opening account of the ways various political and intellectual projects--from nationalism to the discipline of anthropology--have appropriated the Middle Ages for their own ends. Deploying an interdisciplinary toolkit, author K. Patrick Fazioli grounds his analysis in contemporary struggles over power and identity in the Eastern Alps, while also considering the broader implications for scholarly research and public memory\"--Provided by publisher.
Book
The changing of α5‐GABAA receptors expression and distribution participate in sevoflurane‐induced learning and memory impairment in young mice
Background Sevoflurane is a superior agent for maintaining anesthesia during surgical procedures. However, the neurotoxic mechanisms of clinical concentration remain poorly understood. Sevoflurane can interfere with the normal function of neurons and synapses and impair cognitive function by acting on α5‐GABAAR. Methods Using MWM test, we evaluated cognitive abilities in mice following 1 h of anesthesia with 2.7%–3% sevoflurane. Based on hippocampal transcriptome analysis, we analyzed the differential genes and IL‐6 24 h post‐anesthesia. Western blot and RT‐PCR were performed to measure the levels of α5‐GABAAR, Radixin, P‐ERM, P‐Radixin, Gephyrin, IL‐6, and ROCK. The spatial distribution and expression of α5‐GABAAR on neuronal somata were analyzed using histological and three‐dimensional imaging techniques. Results MWM test indicated that partial long‐term learning and memory impairment. Combining molecular biology and histological analysis, our studies have demonstrated that sevoflurane induces immunosuppression, characterized by reduced IL‐6 expression levels, and that enhanced Radixin dephosphorylation undermines the microstructural stability of α5‐GABAAR, leading to its dissociation from synaptic exterior and resulting in a disordered distribution in α5‐GABAAR expression within neuronal cell bodies. On the synaptic cleft, the expression level of α5‐GABAAR remained unchanged, the spatial distribution became more compact, with an increased fluorescence intensity per voxel. On the extra‐synaptic space, the expression level of α5‐GABAAR decreased within unchanged spatial distribution, accompanied by an increased fluorescence intensity per voxel. Conclusion Dysregulated α5‐GABAAR expression and distribution contributes to sevoflurane‐induced partial long‐term learning and memory impairment, which lays the foundation for elucidating the underlying mechanisms in future studies. The increase in unphosphorylated Radixin causes the diffusion of α5‐GABAARs from the extra‐synaptic space to the synaptic cleft. α5‐GABAARs are localized to a smaller area at synaptic cleft but in unchanged confinement space at extra‐synaptic space, with reduced expression in the extra‐synaptic space but no change in the synaptic cleft, but all resulted in an increase in fluorescence intensity per voxel.
Journal Article
Possible mechanisms of lycopene amelioration of learning and memory impairment in rats with vascular dementia
Oxidative stress is involved in the pathogenesis of vascular dementia. Studies have shown that lycopene can significantly inhibit oxidative stress; therefore, we hypothesized that lycopene can reduce the level of oxidative stress in vascular dementia. A vascular dementia model was established by permanent bilateral ligation of common carotid arteries. The dosage groups were treated with lycopene (50, 100 and 200 mg/kg) every other day for 2 months. Rats without bilateral carotid artery ligation were prepared as a sham group. To test the ability of learning and memory, the Morris water maze was used to detect the average escape latency and the change of search strategy. Hematoxylin-eosin staining was used to observe changes of hippocampal neurons. The levels of oxidative stress factors, superoxide dismutase and malondialdehyde, were measured in the hippocampus by biochemical detection. The levels of reactive oxygen species in the hippocampus were observed by dihydroethidium staining. The distribution and expression of oxidative stress related protein, neuron-restrictive silencer factor, in hippocampal neurons were detected by immunofluorescence histochemistry and western blot assays. After 2 months of drug administration, (1) in the model group, the average escape latency was longer than that of the sham group, and the proportion of straight and tend tactics was lower than that of the sham group, and the hippocampal neurons were irregularly arranged and the cytoplasm was hyperchromatic. (2) The levels of reactive oxygen species and malondialdehyde in the hippocampus of the model group rats were increased, and the activity of superoxide dismutase was decreased. (3) Lycopene (50, 100 and 200 mg/kg) intervention improved the above changes, and the lycopene 100 mg/kg group showed the most significant improvement effect. (4) Neuron-restrictive silencer factor expression in the hippocampus was lower in the sham group and the lycopene 100 mg/kg group than in the model group. (5) The above data indicate that lycopene 100 mg/kg could protect against the learning-memory ability impairment of vascular dementia rats. The protective mechanism was achieved by inhibiting oxidative stress in the hippocampus. The experiment was approved by the Animal Ethics Committee of Fujian Medical University, China (approval No. 2014-025) in June 2014.
Journal Article
Retrieval practice facilitates learning by strengthening processing in both the anterior and posterior hippocampus
Introduction and Methods A large number of behavioral studies show that retrieval practice is a powerful way of strengthening learning of new information. Repeated retrieval might support long‐term retention in a quantitative sense by inducing stronger episodic representations or in a qualitative sense by contributing to the formation of more gist‐like representations. Here we used fMRI to examine the brain bases related to the learning effects following retrieval practice and provide imaging support for both views by showing increased activation of anterior and posterior hippocampus regions during a delayed memory test. Results Brain activity in the posterior hippocampus increased linearly as a function of number of successful retrievals during initial learning, whereas anterior hippocampus activity was restricted to items retrieved many but not few times during the learning phase. Conclusion Taken together, these findings indicate that retrieval practice strengthens subsequent retention via “dual action” in the anterior and posterior hippocampus, possibly reflecting coding of individual experiences as well as integration and generalization across multiple experiences. Our findings are of educational significance by providing insight into the brain bases of a learning method of applied relevance. The hippocampus (HC) and the “testing effect” have each been studied extensively for their potential in memory and learning. Here we provide novel evidence related to the well‐established “testing effect” by highlighting that retrieval practice facilitates learning by strengthening processing in both the anterior and posterior HC. These findings are of educational significance by providing unique insights into the brain bases of a learning method of applied relevance and emphasize the important role of hippocampus for durable learning in school.
Journal Article
Dietary Polyphenol Supplementation Prevents Alterations of Spatial Navigation in Middle-Aged Mice
Spatial learning and memory deficits associated with hippocampal synaptic plasticity impairments are commonly observed during aging. Besides, the beneficial role of dietary polyphenols has been suggested as potential functional food candidates to prevent this memory decline. Indeed, polyphenols could potentiate the signaling pathways of synaptic plasticity underlying learning and memory. In this study, spatial learning deficits of middle-aged mice were first highlighted and characterized according to their navigation patterns in the Morris water maze task. An eight-week polyphenol-enriched diet, containing a polyphenol-rich extract from grape and blueberry (PEGB; from the Neurophenols Consortium) with high contents of flavonoids, stilbenes and phenolic acids, was then successful in reversing these age-induced effects. The use of spatial strategies was indeed delayed with aging whereas a polyphenol supplementation could promote the occurrence of spatial strategies. These behavioral results were associated with neurobiological changes: while the expression of hippocampal calmodulin kinase II (CaMKII) mRNA levels was reduced in middle-aged animals, the polyphenol-enriched diet could rescue them. Besides, an increased expression of nerve growth neurotrophic factor (NGF) mRNA levels was also observed in supplemented adult and middle-aged mice. Thus these data suggest that supplementation with polyphenols could be an efficient nutritional way to prevent age-induced cognitive decline.
Journal Article
Utilizing zebrafish and okadaic acid to study Alzheimer's disease
Despite the many years of extensive research using rodent models to study Alzheimer's disease (AD), no cure or disease halting drug exists. An increasing number of people are suffering from the disease and a therapeutic intervention is needed. Therefore, it is necessary to have complementary models to aid in the drug discovery. The zebrafish animal model is emerging as a valuable model for the investigation of AD and neurodegenerative drug discovery. The main genes involved in human AD have homologous counterparts in zebrafish and have conserved function. The basic brain structure of the zebrafish is also conserved when compared to the mammalian brain. Recently an AD model was established by administering okadaic acid to zebrafish. It was used to test the efficacy of a novel drug, lanthionine ketimine-5-ethyl ester, and to elucidate its mechanism of action. This demonstrated the ability of the okadaic acid-induced AD zebrafish model to be implemented in the drug discovery process for therapeutics against AD.
Journal Article