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Reflex-ontogeny and intestinal morphometrics were evaluated in Wistar rats whose mothers were fed on a high-fat diet during the perinatal period. Male pups (n=52) formed four experimental groups: NN (pups from mothers with lab chow diet during gestation and lactation); NH (pups from mothers with lab chow diet during pregnancy and high-fat in lactation); HH (pups from mothers with high-fat diet during gestation and lactation); HN (pups from mothers with high-fat diet during pregnancy and lab chow in lactation). The reflex ontogeny, the maturation of physical characteristics and parameters of somatic growth were evaluated during lactation. In addition, the body mass index (BMI), the specific rate of weight gain (SRWG), the Lee index, the weight of the brain and intestinal parameters were analyzed after weaning. High-fat diet during pregnancy (HH and HN groups) delayed the maturation of reflexes and physical characteristics. The high-fat diet affected somatic growth differently, reducing somatic growth parameters in the groups NH and HH and increasing in the HN group. The highest SRWG was found in group HN. SRWG and BMI were reduced in the groups NH and HH. The relative intestinal weight was reduced in the groups NH, HH and HN. The relative length of small intestine was longer in group HN than in group NN. The total height of the mucosa and size of the villous were lower in group HH than in group NN. In conclusion, high-fat diet promoted negative consequences for the development of the nervous and enteric systems of the offspring(AU)

Ontogenia refleja y morfometría intestinal fueron evaluados en crías de ratas Wistar que fueron alimentadas con una dieta alta en grasas durante el período perinatal. Los descendientes machos (n = 52) formaron cuatro grupos experimentales: NN (hijos de madres que utilizaron alimentos de laboratorio durante la gestación y la lactancia); NH (hijos de madres que comieron dieta de laboratorio durante el embarazo y dieta con un alto contenido de grasas en la lactancia); HH (hijos de madres con una dieta alta en grasas durante el embarazo y la lactancia); HN (hijos de madres que comieron una dieta alta en grasas durante el embarazo y comida de laboratorio durante la lactancia). La ontogenia refleja, la maduración de las características físicas y los parámetros de crecimiento somático durante la lactancia fueron evaluados. Además, el índice de masa corporal (IMC), la tasa específica de aumento de peso (SRWG), el índice de Lee, el peso cerebral y los parámetros intestinales fueron analizados después del destete. La dieta alta en grasas durante el embarazo (grupos HH y HN) retrasó la maduración de reflejos y características físicas. La dieta alta en grasas afectó el crecimiento somático de manera diferente, reduciendo los parámetros de crecimiento somático en los grupos NH y HH y aumentando en el grupo HN. El SRWG más grande se encontró en el grupo HN. El SRWG y el IMC se redujeron en los grupos NH y HH. El peso relativo intestinal se redujo en los grupos NH, HH y HN. La longitud relativa del intestino delgado fue mayor en el grupo HN que en el grupo NN. La altura total de la mucosa y el tamaño de las vellosidades fueron menores en el grupo HH que en el grupo NN. En conclusión, la dieta alta en grasas tuvo consecuencias negativas para el desarrollo de los sistemas nervioso y entérico de la prole(AU)

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Sepsis is a clinical syndrome with high morbidity and mortality. It is characterized by acute inflammatory response and oxidative stress, which is implicated in cerebral dysfunction. Murici (Byrsonimacrassifolia (L.) Kunth) is a fruit rich in antioxidant compounds, which could be an alternative to prevent damage to tissues induced by sepsis . Here, we evaluated the effects of sepsis on the propagation of cortical spreading depression (CSD) and oxidative stress, and tested the action of murici antioxidant extract in prevention against the effect of sepsis. Male Wistar rats (90-210 days, n = 40) were previously supplemented, orogastrically, with murici extract (150 mg/kg/day or 300 mg/kg/day), or an equivalent volume of the vehicle solution, for fifteen days. Then the animals were subjected to experimental sepsis through cecal ligation and perforation (CLP). Subsequently, CSD recordings were obtained and brain oxidative stress was evaluated. Sepsis decelerated CSD and increased the malondialdehyde (MDA) levels in the brain cortex of the animals. In contrast, septic rats that had been previously supplemented with murici antioxidant extract in doses of 150 and 300 mg/kg/day showed an increase in CSD propagation velocity, low levels of MDA and GSH/GSSG ratio and an increase of superoxide dismutase (SOD) activity, regardless of the dose tested. Our results demonstrate that sepsis affects brain excitability and that this effect can be prevented by murici antioxidant extract. The effects of sepsis and/or murici extract on CSD may be due to the oxidative state of the brain.

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Objectives: This investigation studied whether physical exercise could modulate cortical spreading depression (CSD) propagation velocity in adult rat offspring from dams that had received a high-fat (HF) diet during lactation. Methods: Wistar male rats suckled by dams fed either control (C) or HF diet ad libitum. After weaning, pups received standard laboratory chow. From 40 to 60 days of life, half of the animals exercised on a treadmill (group E); the other half remained sedentary (group S). Two additional HF groups (E and S) received fluoxetine (F; 10 mg/kg/day, orogastrically) from 40 to 60 days of life (groups HF/EF and HF/F). Results: At 40 days of life, rats from the maternal HF diet presented higher weight, thoracic circumference, and Lee Index than C animals and remained heavier at 60 days of life. Physical exercise decreased abdominal circumference. HF diet increased CSD propagation velocity (mean ± SD; mm/min) in sedentaries (HF/S 3.47 ± 0.31 versus C/S 3.24 ± 0.26). Treadmill exercise decelerated CSD propagation in both groups C/E (2.94 ± 0.28) and HF/E (2.97 ± 0.40). Fluoxetine alone decreased CSD propagation (HF/F 2.88 ± 0.45) compared with HF/S group. The combination of fluoxetine + exercise under HF condition (2.98 ± 0.27) was similar to HF/E group. Discussion: Physical exercise is able to reduce CSD propagation velocity in rat adult brains even when they have suffered over-nourishing during lactation. The effects of exercise alone or fluoxetine alone on CSD were similar to the effects of fluoxetine + exercise, under the HF condition. Data reinforce malnutrition during lactation modifies cortical electrophysiology even when the HF condition no longer exists.

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OBJECTIVE: This study aimed to analyze whether exposure to environmental enrichment (EE) during the juvenile phase of life interferes with the electrical activity of the adult rat brain. In addition, the present research also investigated whether this putative effect on brain electrical activity could be affected by prior overnutrition during lactation. Electrophysiology was measured through cortical spreading depression (CSD), a phenomenon related to brain excitability. METHODS: Wistar rats were suckled in litters of either nine or three pups, forming the nourished (N) or overnourished (ON) groups, respectively. At 36 days old, half of the animals from each nutritional condition were exposed to EE. The other half was kept in the standard environment (SE). At 90-120 days of life, each animal was anesthetized for CSD recordings. RESULTS: Overnutrition during lactation caused increases (p < 0.05) in body and brain weights. The EE decelerated CSD propagation velocity regardless of nutritional state during lactation (p < 0.001). The CSD deceleration in the N-EE group was 23.8% and in the ON-EE group was 15% in comparison with the N-SE and ON-SE groups, respectively. CONCLUSION: Our data demonstrated that EE exposure in the juvenile phase of the rat's life reduced brain excitability, and this effect was observed even if animals were overnourished during lactation. An EE could be considered an adjuvant therapeutic resource to modulate brain excitability.

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ABSTRACT Objective: This study aimed to analyze whether exposure to environmental enrichment (EE) during the juvenile phase of life interferes with the electrical activity of the adult rat brain. In addition, the present research also investigated whether this putative effect on brain electrical activity could be affected by prior overnutrition during lactation. Electrophysiology was measured through cortical spreading depression (CSD), a phenomenon related to brain excitability. Methods: Wistar rats were suckled in litters of either nine or three pups, forming the nourished (N) or overnourished (ON) groups, respectively. At 36 days old, half of the animals from each nutritional condition were exposed to EE. The other half was kept in the standard environment (SE). At 90-120 days of life, each animal was anesthetized for CSD recordings. Results: Overnutrition during lactation caused increases (p < 0.05) in body and brain weights. The EE decelerated CSD propagation velocity regardless of nutritional state during lactation (p < 0.001). The CSD deceleration in the N-EE group was 23.8% and in the ON-EE group was 15% in comparison with the N-SE and ON-SE groups, respectively. Conclusion: Our data demonstrated that EE exposure in the juvenile phase of the rat's life reduced brain excitability, and this effect was observed even if animals were overnourished during lactation. An EE could be considered an adjuvant therapeutic resource to modulate brain excitability.

RESUMO Objetivo: Este estudo analisou se a exposição ao ambiente enriquecido durante a fase juvenil da vida interferiria na atividade elétrica do cérebro de ratos adultos. Além disso, a presente pesquisa também investigou se esse provável efeito na atividade elétrica cerebral poderia ser afetado pela hipernutrição durante a lactação. A eletrofisiologia foi medida através da depressão alastrante cortical, um fenômeno relacionado à excitabilidade cerebral. Métodos: Ratos Wistar foram amamentados em ninhadas de nove ou três filhotes, formando os grupos nutridos ou hipernutridos, respectivamente. Aos 36 dias, metade dos animais de cada condição nutricional foram expostos ao ambiente enriquecido. A outra metade foi mantida na condição de ambiente padrão. Aos 90-120 dias de vida, foram obtidos os registros da depressão alastrante cortical. Resultados: A hipernutrição durante a lactação causou incrementos (p < 0,05) nos pesos corporal e cerebral.O Ambiente Enriquecido desacelerou a velocidade de propagação da depressão alastrante cortical independentemente do estado nutricional durante a lactação (p < 0,001). A desaceleração da depressão alastrante cortical no grupo nutrido/ambiente enriquecido foi de 23,8% e no grupo hipernutrido/ambiente enriquecido foi de 15% em comparação com os grupos nutrido/ambiente padrão e hipernutrido/ambiente padrão, respectivamente. Conclusão: Nossos dados demonstram que a exposição ao ambiente enriquecido na fase juvenil da vida do rato reduz a excitabilidade cerebral, e esse efeito pode ser observado mesmo se os animais estiverem hipernutridos durante a lactação. O ambiente enriquecido pode ser considerado um recurso terapêutico adjuvante para modular a excitabilidade cerebral.

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PURPOSE: To investigate the effects of Murici extract on the brain excitability-dependent phenomenon known as cortical spreading depression (CSD) and on brain oxidative stress. METHODS: Adult and aged Wistar rats were supplemented with murici extract (150 mg/kg/day or 300 mg/kg/day) by gavage for fifteen days. Afterwards, the animals were submitted to a CSD electrophysiological recording and to brain oxidative stress evaluation. RESULTS: Our results showed that aging decreased CSD propagation velocity, catalase activity and glutathione/oxidized glutathione ratio (GSH/GSSG) in the brain cortex of the rats, and increased malondialdehyde (MDA) concentrations and superoxide dismutase (SOD) activity. The highest dose (300 mg/kg/day) of murici extract accelerated CSD, whereas the lowest (150mg/kg/day) decelerated, in both adult and aged animals. In contrast, aged animals supplemented with murici extract in both doses presented low MDA levels and high GSG/GSSG ratio in comparison to the control-aged animals. CONCLUSION: Murici extract supplementation seems to revert detrimental effects in aged brains and could be considered as a strategy in the treatment of pathologies related to aging and cortical spreading depression.

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Purpose: To investigate the effects of Murici extract on the brain excitability-dependent phenomenon known as cortical spreading depression (CSD) and on brain oxidative stress. Methods: Adult and aged Wistar rats were supplemented with murici extract (150 mg/kg/day or 300 mg/kg/day) by gavage for fifteen days. Afterwards, the animals were submitted to a CSD electrophysiological recording and to brain oxidative stress evaluation. Results: Our results showed that aging decreased CSD propagation velocity, catalase activity and glutathione/oxidized glutathione ratio (GSH/GSSG) in the brain cortex of the rats, and increased malondialdehyde (MDA) concentrations and superoxide dismutase (SOD) activity. The highest dose (300 mg/kg/day) of murici extract accelerated CSD, whereas the lowest (150mg/kg/day) decelerated, in both adult and aged animals. In contrast, aged animals supplemented with murici extract in both doses presented low MDA levels and high GSG/GSSG ratio in comparison to the control-aged animals. Conclusion: Murici extract supplementation seems to revert detrimental effects in aged brains and could be considered as a strategy in the treatment of pathologies related to aging and cortical spreading depression.(AU)

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Abstract Purpose: To investigate the effects of Murici extract on the brain excitability-dependent phenomenon known as cortical spreading depression (CSD) and on brain oxidative stress. Methods: Adult and aged Wistar rats were supplemented with murici extract (150 mg/kg/day or 300 mg/kg/day) by gavage for fifteen days. Afterwards, the animals were submitted to a CSD electrophysiological recording and to brain oxidative stress evaluation. Results: Our results showed that aging decreased CSD propagation velocity, catalase activity and glutathione/oxidized glutathione ratio (GSH/GSSG) in the brain cortex of the rats, and increased malondialdehyde (MDA) concentrations and superoxide dismutase (SOD) activity. The highest dose (300 mg/kg/day) of murici extract accelerated CSD, whereas the lowest (150mg/kg/day) decelerated, in both adult and aged animals. In contrast, aged animals supplemented with murici extract in both doses presented low MDA levels and high GSG/GSSG ratio in comparison to the control-aged animals. Conclusion: Murici extract supplementation seems to revert detrimental effects in aged brains and could be considered as a strategy in the treatment of pathologies related to aging and cortical spreading depression.

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Nutritional status during development can modify the brain's electrophysiological properties and its response to drugs that reduce the serotonin availability in the synaptic cleft. Here we used cortical spreading depression (CSD) in the rat as a neurophysiological parameter to investigate the interaction between nutritional status and treatment with tianeptine, a serotonin uptake enhancer. From postnatal day 2 to 24, well-nourished and early-malnourished rat pups were s.c. injected with tianeptine (5 or 10mg/kg; 10 ml/kg) or equivalent volume of saline solution (control group). When the animals were 25-30 days old, CSD was recorded on the brain cortical surface. In the well-nourished rats, but not in the malnourished group, systemic tianeptine dose-dependently increased the CSD propagation velocity, with 10mg/kg producing a significant (P<0.05) effect. An experiment in adult rats showed that cortical topical application of tianeptine solutions (5mg/ml, 10mg/ml, and 20mg/ml) increased the CSD propagation in both the well-nourished and early-malnourished conditions. In well-nourished animals, 0.5mg/ml topical tianeptine did not affect CSD propagation, and 2mg/ml produced a small, but significant CSD acceleration. Our results indicate a facilitating action of tianeptine on CSD propagation, probably via tianeptine's pharmacological action on the serotonin system. These findings support previous data suggesting an antagonistic role of the serotoninergic system on CSD.

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Chronic ethanol ingestion, mostly in young adults, constitutes a frequent drug-abuse situation, which is associated to a wide variety of pathological disturbance affecting a number of organs, including liver, kidney, heart, pancreas and brain. The ethanol effects are more prominent when occurring at the perinatal period of life, generating, among other disabilities, brain developmental and functional impairments, as well as the so-called "fetal alcoholic syndrome". However, low doses of ethanol, although not producing conspicuous signs of physiological impairment, may affect the developing organism, impairing the renal and cardiovascular system, among others. As a consequence of increased oxidative stress produced by ethanol intake and its subsequent oxidation, lipid peroxidation increases, enhancing reactive oxygen species formation, which is potentially injurious to the brain tissue. When occurring during gestation, lipid peroxidation may occur in the placenta, an event that would partially be responsible for fetal nutrition disturbance and consequently late physiological impairment. In this short review, data on ethanol effects on the nervous and cardiorenal structure and function are analyzed at the light of the most relevant hypotheses concerning ethanol mechanisms of action. Additionally, experimental data from the authors' laboratories are presented and discussed, focusing particular attention to the possibility of differential neural and cardiorenal ethanol effects as a function of the dose used in distinct experimental models.

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Ketogenic diets influence brain function and have been therapeutically used for anti-epileptic purposes. We investigated the effects of maternal ketogenic diets on the development of somatic and reflex responses in rat pups. These were born from mothers receiving: (i) normal fat (7%) + normal protein (17%); (ii) high-fat (55.4%) + normal protein; (iii) normal fat + low protein (8%); and (iv) high-fat + low protein (respectively, called N-17, K-17, N-8 and K-8). Ketogenic diets, but not the normal-fat diets, delayed the development of reflex and somatic responses. The effects were more evident when the ketogenic diet was associated with low protein content. The results suggest that fat excess can alter brain maturation, and this action is intensified by early protein-deficiency. Data raise concerns about the therapeutic use of ketogenic diets in newborn children.

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SUMMARY: Brain excitability diseases like epilepsy constitute one factor that influences brain electrophysiological features. Cortical spreading depression (CSD) is a phenomenon that can be altered by changes in brain excitability. CSD propagation was presently characterized in adult male and female rats from a normal Wistar strain and from a genetically audiogenic seizure-prone strain, the Wistar audiogenic rat (WAR), both previously submitted (RAS(+)), or not (RAS(-)), to repetitive acoustic stimulation, to provoke audiogenic kindling in the WAR-strain. A gender-specific change in CSD-propagation was found. Compared to seizure-resistant animals, in the RAS(-) condition, male and female WARs, respectively, presented CSD-propagation impairment and facilitation, characterized, respectively, by lower and higher propagation velocities (P<0.05). In contraposition, in the RAS(+) condition, male and female WARs displayed, respectively, higher and lower CSD-propagation rates, as compared to the corresponding controls. In some Wistar and WAR females, we determined estrous cycle status on the day of the CSD-recording as being either estrous or diestrous; no cycle-phase-related differences in CSD-propagation velocities were detected. In contrast to other epilepsy models, such as Status Epilepticus induced by pilocarpine, despite the CSD-velocity reduction, in no case was CSD propagation blocked in WARs. The results suggest a gender-related, estrous cycle-phase-independent modification in the CSD-susceptibility of WAR rats, both in the RAS(+) and RAS(-) situation.

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Spreading depression was characterized in adult rats rendered epileptic by pilocarpine (350 mg/kg, i.p.) and thereafter made hyperglycemic with (i.p.) 60 mg/kg streptozotocin. Groups treated with only one of the above drugs, as well as control groups treated with their vehicles (saline and citrate buffer, respectively) were also studied. The animals treated with pilocarpine or streptozotocin presented, as a common feature, a reduction in the spreading depression propagation rate. However, they differed by the fact that pilocarpine, in some cases, blocked spreading depression propagation, whereas streptozotocin did not block it at all. In early-malnourished animals, streptozotocin-effects, but not pilocarpine-effects on spreading depression were attenuated. The treatment with both drugs did not potentiate their individual reducing effects on spreading depression propagation, irrespective of the animals' early nutritional status. These results extend previous observations on rats treated with both drugs separately, confirming their impairing action on spreading depression propagation. They also indicate that early malnutrition is more effective in changing the streptozotocin effects on spreading depression, as compared to the pilocarpine-effects. Since such effects were observed at adulthood, they indicate that the early malnutrition-induced cortical changes responsible for the here-described effects are long-lasting.

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This study investigated the effects of repeated l-arginine administration during lactation, combined with different suckling conditions, on morphometric parameters of primary visual cortex NADPH-diaphorase-positive neurons. Wistar rat pups reared in "normal-size litters" or "large litters" (N- and L-conditions; litters formed by 6 and 12 pups, respectively) received, from postnatal day 7 to 28, either arginine (300 mg/kg/day, per gavage) or distilled water (control). At 90-120 days of life, they were perfused with saline + formaldehyde, and their brains were processed for histochemical reaction to reveal NADPH-diaphorase-positive neurons (malic enzyme indirect method). Compared to the normal-size litters, L-rats had lower body weights (P < 0.05), confirming the effectiveness of the L-condition in affecting pup development. Concerning NADPH-d histochemistry, arginine treatment was associated with increased (P < 0.05) density of dendrite varicosities and of dendrite branching frequency, suggesting a plastic response of the developing brain to that treatment, even in previously malnourished rats. No difference was seen, however, in dendrite orientation, total number of neurons, soma area and perimeter, as well as dendrite bifurcation points, fractal dimension, and area and volume of dendrite field, suggesting that NADPH-d cells are resistant to arginine and nutritional changes, regarding these features. Data are considered of interest for studies of synaptic plasticity during neural development and its relationships to aggressive agents like malnutrition.

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Cortical spreading depression is a neural phenomenon present in several animal species. Spreading depression features, like velocity of propagation, depends on several chemical and metabolic factors, as for example, anti-oxidants. Here we studied spreading depression-velocity changes in weaned rat-pups born from dams treated on a daily basis, either during gestation or lactation, with a carotenoid ethanolic extract (30 microg/kg/day) prepared from shrimp waste (heads). These pups were compared with age-mated ones, whose mothers were treated either with the vehicle (ethanol) or with distilled water. Compared to the distilled water-group (mean values, in mm/min, per hour of recording ranging from 3.02+/-0.26 to 3.15+/-0.27 [treatment during gestation; n=7], and from 3.03+/-0.25 to 3.22+/-0.30 [lactation; n=11]), ethanol-treated rats displayed higher spreading depression-velocities (from 3.74+/-0.06 to 3.82+/-0.08 [gestation; n=7], and from 4.26+/-0.32 to 4.33+/-0.34 [lactation; n=11]; p<0.05). Compared to the ethanol-group, carotenoid-treatment lead to lower spreading depression-velocities (p<0.05), ranging from 3.38+/-0.09 to 3.42+/-0.12, n=7 (gestation) and 3.58+/-0.13 to 3.62+/-0.17, n=12 (lactation). Carotenoid-treatment during lactation was shown to be significantly more effective than that during gestation (p<0.05), in lowering spreading depression-velocity. The results suggest a protective action of shrimp carotenoids against the ethanol effects on spreading depression. This protective effect could be related to the carotenoid antioxidant properties, as previously indicated by evidence showing spreading depression-effects of other antioxidants.

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