Taurine/Pilocarpine Interaction in the Malnourished Rat Brain: A Behavioral, Electrophysiological, and Immunohistochemical Analysis.

This study aimed to evaluate the possible protective role of taurine on anxiety-like behavior, brain electrical activity and glial cell immunoreactivity in well-nourished and malnourished rats that were treated with a subconvulsing dose of pilocarpine. Newborn Wistar rats were subjected to normal or unfavorable lactation conditions, represented by the suckling of litters with 9 or 15 pups, resulting in well-nourished and malnourished animals, respectively. Each nutritional group was split into five subgroups that were treated from postnatal day (PND) 35 to 55 with 300 mg/kg/day of taurine + 45 mg/kg/day of pilocarpine (group T + P), taurine only (group T), pilocarpine only (group P), vehicle control (group V), or not treated control (group naïve; Nv). At PND56-58, the groups were subjected to the elevated plus-maze behavioral tests. Glycemia was measured on PND59. Between PND60 and PND65, the cortical spreading depression (CSD) was recorded in the cerebral cortex, and the levels of malondialdehyde and microglial and astrocyte immunoreactivity were evaluated in the cortex and hippocampus. Our data indicate that treatment with taurine and pilocarpine resulted in anxiolytic-like and anxiogenic behavior, respectively, and that nutritional deficiency modulated these effects. Both treatments decelerated CSD propagation and modulated GFAP- and Iba1-containing glial cells. Pilocarpine reduced body weight and glycemia, and administration of taurine was not able to attenuate the effects of pilocarpine. The molecular mechanisms underlying taurine action on behavioral and electrophysiological parameters in the normal and altered brain remain to be further explored.

Brain effects of the lectin from Canavalia ensiformis in adult rats previously suckled in favorable and unfavorable conditions: A spreading depression and microglia immunolabeling study.

OBJECTIVE: To evaluate in adult rats, previously suckled under favorable and unfavorable conditions, the brain electrophysiological and microglial effects of the treatment early in life with the lectin (ConA) from Canavalia ensiformis. METHODS: Male Wistar newborn rats (n = 89) were suckled under favorable or unfavorable conditions, represented by litters with 6-7 pups or 12-14 pups (groups N6 and N12, respectively). From postnatal days 5-24, they were treated intraperitoneally with 1 or 10 mg/kg ConA (groups L1 and L10, respectively), or with saline solution (group Sal), or no treatment (group Naïve). At 90-120 days of age, cortical spreading depression (CSD) was recorded at two parietal points for 4 hours, and CSD parameters (velocity of propagation and amplitude and duration of the DC slow potential change) were measured. Fixative-perfused brain sections were reacted with anti-Iba1 antibodies to quantify immunolabeled microglia. RESULTS: Compared with the control groups, ConA-treated animals dose-dependently presented with reduced CSD propagation velocities and increased amplitude and duration of the CSD slow potential change. Microglia Iba-1 immunoreactivity was lower in both nutritional groups treated with ConA, in comparison with the control groups. The CSD hemisphere presented with higher immunoreactivity compared with the CSD-free hemisphere. DISCUSSION: Attenuation in CSD propagation and microglia reaction was associated in adulthood with ConA treatment during brain development, indicating that the lectin can affect the electrophysiological and microglial development, and suggesting long-lasting protective action of the lectin on the rat brain, which is not impeded by the unfavorable suckling condition.

Spreading depression features and Iba1 immunoreactivity in the cerebral cortex of developing rats submitted to treadmill exercise after treatment with monosodium glutamate.

Physical exercise and excessive consumption of monosodium glutamate (MSG) can affect the morphological and electrophysiological organization of the brain during development. However, the interaction of both factors remains unclear. We analyzed the effect of this interaction on the excitability-related phenomenon known as cortical spreading depression (CSD) and the microglial reaction expressed as Iba1-immunolabeled cells in the rat motor cortex. MSG (2g/kg or 4g/kg) was administered every other day during the first 14 postnatal days. Treadmill exercise started at 21-23 days of life and lasted 3 weeks, 5 days/week, for 30min/day. At 45-60 days, CSD was recorded for 4h at two cortical points and the CSD parameters (velocity, amplitude, and duration of the negative potential change) calculated. Confirming previous observations, exercised rats presented with lower CSD velocities (3.29±0.18mm/min) than the sedentary group (3.80±0.18mm/min; P<0.05). MSG increased CSD velocities in the exercised rats compared to saline-treated and exercised animals in a dose-dependent manner (3.49±0.19, 4.05±0.18, and 3.27±0.26 for 2g/kg MSG, 4g/kg MSG, and saline, respectively; P<0.05). The amplitude (ranging from 14.3±5.9 to 18.7±6.2mV) and duration (46.7±11.1 to 60.5±11.6s) of the negative slow potential shift of the CSD were similar in all groups. Both exercise and MSG treatment increased Iba1 immunolabeling. The results confirm that physical exercise decelerates CSD propagation. However, it does not impede the CSD-accelerating action of MSG. These effects were accompanied by a cortical microglia reaction. Therefore, the data suggest that treadmill exercise early in life can influence the development of cortical electrical activity.

Neonatal treatment with monosodium glutamate lastingly facilitates spreading depression in the rat cortex.

AIMS: Monosodium glutamate (MSG) is a neuroexcitatory amino acid used in human food to enhance flavor. MSG can affect the morphological and electrophysiological organization of the brain. This effect is more severe during brain development. Here, we investigated the electrophysiological and morphological effects of MSG in the developing rat brain by characterizing changes in the excitability-related phenomenon of cortical spreading depression (CSD) and microglial reaction. MAIN METHODS: From postnatal days 1-14, Wistar rat pups received 2 or 4 g/kg MSG (groups MSG-2 and MSG-4, respectively; n=9 in each group), saline (n=10) or no treatment (naïve group; n=5) every other day. At 45-60 days, CSD was recorded on two cortical points for 4h. The CSD parameters velocity, and amplitude and duration of the negative potential change were calculated. Fixative-perfused brain sections were immunolabeled with anti-IBA-1 antibodies to identify and quantify cortical microglia. KEY FINDINGS: MSG-4 rats presented significantly higher velocities (4.59 ± 0.34 mm/min) than the controls (saline, 3.84 ± 0.20mm/min; naïve, 3.71 ± 0.8mm/min) and MSG-2 group (3.75 ± 0.10mm/min). The amplitude (8.8 ± 2.2 to 11.2 ± 1.9 mV) and duration (58.2 ± 7.1 to 73.6 ± 6.0s) of the negative slow potential shift was similar in all groups. MSG-treatment dose-dependently increased the microglial immunolabeling. SIGNIFICANCE: The results demonstrate a novel, dose-dependent action of MSG in the developing brain, characterized by acceleration of CSD and significant microglial reaction in the cerebral cortex. The CSD effect indicates that MSG can influence cortical excitability, during brain development, as evaluated by CSD acceleration. Data suggest caution when consuming MSG, especially in developing organisms.

Hypercaloric high-lipid diet and brain development: effects on cortical spreading depression in adult rats.

UNLABELLED: Nutritional conditions early in life constitute one of the environmental factors that can influence brain electrophysiology, as evaluated through the phenomenon denominated as cortical spreading depression (CSD). OBJECTIVE: To evaluate the effects of hypercaloric diet intake in different phases of life on CSD features in adult rats. METHODS: Newborn Wistar rats were suckled by dams fed a high-lipid (cafeteria) hypercaloric diet during the lactation period. After suckling, part of the pups remained in the high-lipid diet until the end of the experiment in adulthood (group 'full-life' FL), and the other part received the control (lab chow) diet (group L). A third group received the hypercaloric diet only at adulthood (group Ad). When the animals reached 90-93 days of life, CSD was recorded. RESULTS: CSD propagation velocities (in mm/minute) and CSD amplitudes (in mV) were reduced (P < 0.05) in the groups L (2.77 ± 0.07 and 7.1 ± 2.0 for velocity and amplitude, respectively) and FL (3.05 ± 0.17 and 8.5 ± 1.9), but not in the group Ad (3.36 ± 0.11 and 10.7 ± 2.0), in comparison with a control group (C), fed the lab chow diet during the entire life (3.52 ± 0.18 and 10.8 ± 2.2). DISCUSSION: CSD velocity changes observed in adulthood were associated with the hypercaloric dietary treatment during brain development, constituting evidence in favor of permanent or at least long-lasting electrophysiological effects related to the prevailing nutritional status during the period of brain growth spurt.

Impacto da multimistura no estado nutricional de pré-escolares matriculados em creches / Impact of a dietary supplement on the nutritional status of preschool children enrolled in day care centers

OBJETIVO: Avaliar o impacto da suplementação da dieta com multimistura sobre o estado nutricional de crianças em fase pré-escolar em risco nutricional. MÉTODOS: Trata-se de estudo tipo duplo cego com duração de dois meses e acompanhamento longitudinal de 135 crianças na faixa etária de um a seis anos. As crianças foram divididas em três grupos: intervenção 1 (GI1 n=48), intervenção 2 (GI2 n=45) e controle (GC n=42), recebendo 5g e 10g de multimistura e placebo, respectivamente. O estado nutricional das crianças em estudo foi avaliado antes e após a suplementação. RESULTADOS: Não houve diferença significativa nos indicadores peso/idade, altura/idade e peso/altura entre os grupos estudados na linha base (p=0,251 p=0,248 e p=0,399, respectivamente). Após a intervenção a diferença na prevalência de déficit antropométrico entre os grupos também não foi significante (p=0,100 p=0,435 e p=0,210, respectivamente). A comparação das médias antes e depois da intervenção, igualmente, não demonstrou diferenças (p>0,05 utilizando os métodos estatísticos de Kruskall - Wallis e Análise de Variância). CONCLUSÃO: Frente ao impacto das pequenas quantidades consumidas de suplemento, no caso a mistura de farelo de cereais, não se justifica esperar alterações significativas sobre a recuperação de crianças em risco nutricional, já que esses suplementos contêm somente pequenas quantidades de calorias e de macro e micronutrientes.

Métodos inovadores do tratamento da obesidade / Innovative Methods to Treat Obesity

A obesidade tornou-se uma patologia epidêmica e prioritária para estudo, e seu controle foi aconselhado em caráter emergencial pela OMS. Os resultados obtidos no controle da obesidade subsidiado por tratamento médico e dietoterapia não têm se mostrado tão eficazes. O emprego da psicologia social no tratamento da obesidade deveria ser mais explorado, considerando-se que através de abordagem cognitivo-comportamentais, tem-se obtido êxito na modificação de comportamento ligados à saúde, especialmente a Teoria da Ação Racional, que busca medir a intenção pessoal de aderir a uma modificação de hábitos para, através de comunicações persuasivas específicas, promover a adesão a comportamentos mais saudáveis. Verifica-se ainda um número pequeno de estudos contemplando Nutrição e Psicologia. Estas disciplinas estão separadas pela tradição acadêmica, mas interligam-se inevitavelmente no contexto da Saúde Pública, especialmente no tratamento da obesidade. Espera-se que futuramente a utilização desta teoria conjuntamente com o tratamento nutricional inovador leve os pacientes obesos a assumir comportamentos mais favoráveis à perda de peso, aumentando sua persistência terapêutica