Egg White Hydrolysate Mitigates Cadmium-induced Neurological Disorders and Oxidative Damage.

We aimed to investigate whether the consumption of Egg White Hydrolysate (EWH) acts on nervous system disorders induced by exposure to Cadmium (Cd) in rats. Male Wistar rats were divided into (a) Control (Ct): H2O by gavage for 28 days + H2O (i.p. - 15th - 28th day); (b) Cadmium (Cd): H2O by gavage + CdCl2 - 1 mg/kg/day (i.p. - 15th - 28th day); (c) EWH 14d: EWH 1 g/kg/day by gavage for 14 days + H2O (i.p.- 15th - 28th day); (d) Cd + EWH cotreatment (Cd + EWHco): CdCl2 + EWH for 14 days; (e) EWH 28d: EWH for 28 days; (f) EWHpre + Cd: EWH (1st - 28th day) + CdCl2 (15th - 28th day). At the beginning and the end of treatment, neuromotor performance (Neurological Deficit Scale); motor function (Rota-Rod test); ability to move and explore (Open Field test); thermal sensitivity (Hot Plate test); and state of anxiety (Elevated Maze test) were tested. The antioxidant status in the cerebral cortex and the striatum were biochemically analyzed. Cd induces anxiety, and neuromotor, and thermal sensitivity deficits. EWH consumption prevented anxiety, neuromotor deficits, and alterations in thermal sensitivity, avoiding neuromotor deficits both when the administration was performed before or during Cd exposure. Both modes of administration reduced the levels of reactive species, and the lipid peroxidation increased by Cd and improved the striatum's antioxidant capacity. Pretreatment proved to be beneficial in preventing the reduction of SOD activity in the cortex. EWH could be used as a functional food with antioxidant properties capable of preventing neurological damage induced by Cd.

Supplementation with Manihot esculenta Crantz (Cassava) leaves' extract prevents recognition memory deficits and hippocampal antioxidant dysfunction induced by Amyloid-ß.

OBJECTIVE: The Manihot esculenta Crantz (Cassava) is a typical South American plant rich in nutrients and energetic compounds. Lately, our group has shown that non-pharmacological interventions with natural antioxidants present different neuroprotective effects on oxidative balance and memory deficits in AD-like animal models. Here, our objective was to evaluate the neuroprotective effects of Cassava leaves' extract (CAS) in an AD-like model induced by amyloid-beta (Aß) 25-35 peptide. METHODS: Male Wistar rats (n = 40; 60 days old) were subjected to 10 days of CAS supplementation; then, we injected 2 µL Aß 25-35 in the hippocampus by stereotaxic surgery. Ten days later, we evaluated object recognition (OR) memory. Cassavas' total polyphenols, flavonoids, and condensed tannins content were measured, as well as hippocampal lipid peroxidation and total antioxidant capacity. RESULTS: CAS protected against Aß-induced OR memory deficits. In addition, Aß promoted antioxidant capacity decrease, while CAS was able to prevent it, in addition to diminishing lipoperoxidation compared to Aß. DISCUSSION: We show that treatment with Cassava leaves' extract before AD induction prevents recognition memory deficits related to Aß hippocampal injection. At least part of these effects can be related to the Cassava leaves' extract supplementation effects on diminishing lipid peroxidation and preventing a decrease in the hippocampal total antioxidant capacity in the hippocampus of AD-like animals without adverse effects. Once cassavais a plant of warm and dry ground that can adapt to growon various soil types and seems to resist several insects, our results enable Cassava to be considered asa potential preventive intervention to avoid or minimizeAD-induced memory deficits worldwide.

Physiology faculty and student contributions to schoolteacher training in neuroscience: innovations during the COVID-19 pandemic.

Research investigating how the brain develops and learns profoundly impacts education. Understanding the brain mechanisms responsible for learning and memory and the factors that influence them, such as age, environment, emotions, and motivation, can transform educational strategies by contributing to the development of programs that optimize learning. Including neuroscience education in teachers' training requires teaching them a multidisciplinary approach to science, which presents a challenge. Furthermore, the potential educational advances from the incorporation of neuroscience into teachers' training are hindered by significant obstacles such as translating research into the classroom; this includes the spread of neuromyths and the products, practices, and programs based on them. Our group has 9 years of experience in developing courses for training teachers. However, in 2020 the world faced the COVID-19 pandemic, which imposed on society a new way of carrying out its daily activities, including teaching. This study reports the experiences of our group as we developed the ninth edition of the Neuroscience Applied to Education teachers' training in an online format that included synchronous and asynchronous activities. Sixty teachers participated in the course. The synchronous meetings lasted 1.5 h/wk and addressed different themes: neuroscience and education, neuroanatomy, neurophysiology, neurobiology of learning and memory, factors that interfere with learning, and pedagogical innovation. According to the teachers' perceptions, the course was fundamental for them in terms of acquiring new knowledge about neuroscience. Everyone agreed on the possible applicability of the concepts covered to improve their pedagogical practice and teaching environment.NEW & NOTEWORTHY This study reports the experience of developing the ninth edition of the Neuroscience Applied to Education course in an online format that included synchronous and asynchronous activities. Here we show that schoolteachers consider the course important for acquiring new knowledge about neuroscience and the applicability of the concepts covered to improve their pedagogical practice and teaching environment. The online format did not prejudice the experience, and the technologies used were well evaluated.

On the role of the dopaminergic system in the memory deficits induced by maternal deprivation.

Previous researches showed that maternal deprivation (MD) leads to memory deficits that persist until adulthood. The hippocampus, an important brain structure involved in memory processes, receives dopaminergic afferents from other brain areas that modulate memory. Here we demonstrated that MD results in object recognition memory deficits that are reverted by intra-hippocampal stimulation of D1-dopaminergic receptor and peripheral administration of a dopamine precursor. The D1-dopaminergic receptor and peripheral administration of a dopamine precursor also promoted memory persistence in control rats.

Maternal Deprivation Induces Memory Deficits That Are Reduced by One Aerobic Exercise Shot Performed after the Learning Session.

During the neonatal period, the brain is susceptible to external influences. Exposure to stressful events during this phase of life influences brain development and impacts adult life. In animals, the maternal deprivation (MD) model is effective in mimicking stress in the early stages of development. In contrast, physical exercise seems to be able to prevent deficits in memory consolidation. Although the effects of chronic exercise in cognition are already well established, little is known about the effects of acute aerobic exercise. Here, male Wistar rats divided into deprived (MD) and nondeprived (NMD) rats were submitted to the object recognition (OR) memory test. Immediately after OR training, some of the rats were submitted to a single aerobic exercise session for 30 minutes. Memory consolidation and persistence were evaluated by retention tests performed 24 h and 7, 14, and 21 days after OR training. We show that a single physical exercise session is able to modulate learning by promoting memory consolidation and persistence in rats with cognitive deficits induced by MD. Hippocampal dopamine levels, measured by HPLC, were not altered after OR training in rats that performed and in rats that did not perform an exercise session; on the other hand, while OR training promoted increase of hippocampal norepinephrine in NMD rats, the MD rats did not present this increase, regardless of the practice or not of exercise.

Green Tea and Red Tea from Camellia sinensis Partially Prevented the Motor Deficits and Striatal Oxidative Damage Induced by Hemorrhagic Stroke in Rats.

Green tea from Camellia sinensis plays a well-established neuroprotective role in several neurodegenerative diseases, including intracerebral hemorrhage (ICH). However, the other teas of the same plant do not have their properties well understood; but they can be as effective as green tea as an alternative therapy. In this study, we investigated the effects of supplementation with green tea and red tea from Camellia sinensis on motor deficits and striatum oxidative damage in rats submitted to hemorrhagic stroke (ICH). Male Wistar rats were supplemented with green tea, red tea, or vehicle for 10 days prior to ICH induction. After injury, the rats were submitted to motor tests (open field for locomotion, rotarod for balance, and neurological deficit scale (NDS)) 1, 3, and 7 days after ICH induction, while the tea supplementation was maintained. Subsequently, the rats were euthanized to striatal tissue dissection for biochemical analyzes (lipid peroxidation, reactive oxygen species, glutathione levels, and total antioxidant capacity). ICH caused locomotor and balance deficits, as well as increased the neurological deficit (NDS). Only red tea prevented locomotor deficits after injury. Green tea and red tea prevented balance deficits on the seventh day after ICH. On NDS evaluation, green tea presented a better neuroprotection than red tea (until day 3 after ICH injury). In addition, ICH increased reactive oxygen species and lipid peroxidation levels, without altering antioxidant markers. Green and red teas were effective in decreasing the lipid peroxidation levels. Therefore, green and red teas partially prevented the motor deficits and striatal oxidative damage induced by ICH. Based on our results, we can consider that the two teas seem to be equally effective to prevent motor deficits and striatal oxidative damage induced by hemorrhagic stroke in rats.