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This document is an editorial published in Frontiers in Behavioral Neuroscience titled "Improving reproducibility in behavioral neuroscience." The authors discuss the importance of reproducibility in scientific research, particularly in the field of behavioral neuroscience. They highlight the ethical implications of a lack of reproducibility and the potential waste of animal lives in research. The authors suggest that combining principles of animal welfare with experimental rigor can help combat the reproducibility crisis. They also discuss specific measures and procedures that the scientific community should adopt to improve the reliability and translational potential of pre-clinical research. [Extracted from the article]

The lizard cortex has remarkable similarities with the mammalian hippocampus. Both regions process memories, have similar cytoarchitectural properties, and are important neurogenic foci in adults. Lizards show striking levels of widespread neurogenesis in adulthood and can regenerate entire cortical areas after injury. Nitric oxide (NO) is an important regulatory factor of mammalian neurogenesis and hippocampal function. However, little is known about its role in nonmammalian neurogenesis. Here, we analyzed the distribution, morphology, and dendritic complexity (Neurolucida reconstructions) of NO-producing neurons through NADPH diaphorase (NADPHd) activity, and how they compare with the distribution of doublecortin-positive (DCX+) neurons in the hippocampal formation of the neotropical lizard Tropidurus hispidus. NADPHd-positive (NADPHd+) neurons in the dorsomedial cortex (DMC; putatively homologous to mammalian CA3) were more numerous and complex than the ones in the medial cortex (MC; putatively homologous to the dentate gyrus). We found that NADPHd+ DMC neurons send long projections into the MC. Interestingly, in the MC, NADPHd+ neurons existed in 2 patterns: small somata with low intensity of staining in the outer layer and large somata with high intensity of staining in the deep layer, a pattern similar to the mammalian cortex. Additionally, NADPHd+ neurons were absent in the granular cell layer of the MC. In contrast, DCX+ neurons were scarce in the DMC but highly numerous in the MC, particularly in the granular cell layer. We hypothesize that NO-producing neurons in the DMC provide important input to proliferating/migrating neurons in the highly neurogenic MC. [ABSTRACT FROM AUTHOR]

The article focuses on the use of cognitive reserve (CR), cognitive intervention like cognitive stimulation and cognitive rehabilitation in the treatment of Alzheimer's Disease (AD). It discusses the success of using environmental enrichment (EE), normally used in animals which can also be used for treatment of AD, although it may not halt the Brain amyloid-β (Aβ) neuronal activity.

Deposition of amyloid-β (Aβ) peptides into specific encephalic structures has been pointed as an important event related to Alzheimer's disease pathogenesis and associated with activation of glial cells, neuroinflammation, oxidative responses, and cognitive deficits. Aβ-induced pro-oxidative damage may regulate the activity of glutamate transporters, leading to reduced glutamate uptake and, as a consequence, excitotoxic events. Herein, we evaluated the effects of the pretreatment of atorvastatin, a HMG-CoA reductase inhibitor, on behavioral and biochemical alterations induced by a single intracerebroventricular (i.c.v.) injection of aggregated Aβ in mice. Atorvastatin (10 mg/kg/day, p.o.) was administered through seven consecutive days before Aβ administration. Aβ caused significant cognitive impairment in the object-place recognition task (2 weeks after the i.c.v. injection) and this phenomenon was abolished by atorvastatin pretreatment. Ex vivo evaluation of glutamate uptake into hippocampal and cerebral cortices slices showed atorvastatin, and Aβ decreased hippocampal and cortical Na-dependent glutamate uptake. However, Aβ increased Na-independent glutamate uptake and it was prevented by atorvastatin in prefrontal cortex slices. Moreover, Aβ treatment significantly increased the cerebrocortical activities of glutathione reductase and glutathione peroxidase and these events were blunted by atorvastatin pretreatment. Reduced or oxidized glutathione levels were not altered by Aβ and/or atorvastatin treatment. These results extend the notion of the protective action of atorvastatin against neuronal toxicity induced by Aβ demonstrating that a pretreatment with atorvastatin prevents the spatial learning and memory deficits induced by Aβ in rodents and promotes changes in glutamatergic and antioxidant systems mainly in prefrontal cortex. [ABSTRACT FROM AUTHOR]

Obesity has reached epidemic proportions worldwide and is stimulated by the ready availability of food rich in fat and sugar (highly palatable diet). This type of diet increases the risks of obesity-associated pathologies, such as insulin resistance and cardiovascular disease. Nitric oxide, a potent endogenous vasodilator, is decreased in these pathologies, mostly as a result of insulin resistance. Ectonucleotidases are ecto and soluble enzymes that regulate the availability of the nucleotides ATP, ADP, and AMP and the nucleoside adenosine in the vascular system, thereby affecting vasoconstriction, vasodilatation, and platelet aggregation homeostasis. The aim of this study was to evaluate the effects of a highly palatable diet on serum lipid and glucose parameters, nitric oxide, and ectonucleotidase activity. Forty male Wistar rats were fed 1 of 2 diets for either 45 days or 4 months: standard chow (SC, n = 10) or a highly palatable diet enriched with sucrose (HP, n = 10). Body mass, visceral fat mass, glucose tolerance, cholesterol (total, high-density lipoprotein (HDL) and non-HDL), serum triacylglycerol, liver triacylglycerol, and free glycerol were increased in the HP group after 45 days and after 4 months, whereas insulin levels were not different between the groups at either time. Furthermore, levels of nitric oxide metabolites and ATP, ADP, and AMP hydrolysis were significantly lower in the HP group (p < 0.05) after 4 months. In conclusion, the consumption of the HP diet for 4 months induced overall corporal and metabolic changes, and decreased nitric oxide metabolites and ectonucleotidase activity, thereby promoting an appropriate environment for the development of cardiovascular diseases, without apparent changes in insulin levels. L'obésité est maintenant de nature épidémique dans le monde entier et poursuit sa croissance en raison de l'accessibilité immédiate des aliments riches en sucres et en gras (régime grandement appétissant). Ce type de régime accroît le risque de pathologies associées à l'obésité telles l'insulinorésistance et la maladie cardiovasculaire. La concentration de l'oxyde nitrique, puissant agent de vasodilatation endogène, diminue en présence de ces pathologies surtout à cause de l'insulinorésistance. Les ectonucléotidases sont des ecto-enzymes solubles qui régularisent la disponibilité des nucléotides (ATP, ADP et AMP) et du nucléoside (adénosine) dans le système vasculaire et qui, de ce fait, conditionnent l'activité de vasodilatation, vasoconstriction et l'homéostasie de l'agrégation plaquettaire. Cette étude se propose d'évaluer les effets d'un régime hautement palatable sur le glucose et les lipides sériques, l'oxyde nitrique et l'activité des ectonucléotidases. Quarante rats Wistar mâles reçoivent 2 régimes différents sur une période de 45 jours ou 4 mois : une alimentation standard (SC, n = 10) et une alimentation hautement palatable enrichie de sucrose (HP, n = 10). Chez le groupe HP, on observe après 45 jours et après 4 mois une augmentation de la masse corporelle, de la masse viscérale des graisses, de la tolérance au glucose, du cholestérol (total, HDL et non HDL), du triacylglycérol sérique, du triacylglycérol hépatique et du glycérol libre, mais on n'observe aucune différence des taux d'insuline entre les 2 groupes à la fin des 2 périodes. De plus, les concentrations des métabolites de l'oxyde nitrique et l'hydrolyse de l'ATP, de l'ADP et de l'AMP sont significativement plus faibles (p < 0,05) chez le groupe HP après la période de 4 mois. En conclusion, la consommation d'aliments HP durant 4 mois suscite des modifications corporelles et métaboliques, la diminution des concentrations des métabolites de l'oxyde nitrique et de l'activité des ectonucléotidases provoquant ainsi un environnement propice au développement des maladies cardiovasculaires sans modifications notables des taux d'insuline. [ABSTRACT FROM AUTHOR]

The immunostaining for tyrosine hydroxylase (TH) in the substantia nigra pars compacta (SNpc) and in the ventral tegmental area (VTA) after intranigral infusion of 6-hydroxydopamine (6-OHDA, 6 μg/side) was analyzed in ovariectomized adult female Wistar rats. Estrogen replacement for 52 days (400-μg 17-β-estradiol capsules) did not prevent the loss of TH-immunoreactive cells induced by 6-OHDA in the SNpc. This result indicates that the neuroprotective effect of dopaminergic mesencephalic cells is not observed with long-term estrogen replacement. [Copyright &y& Elsevier]