Objective: We investigated the effect of early-in-life administration of L-arginine, combined wit... more Objective: We investigated the effect of early-in-life administration of L-arginine, combined with physical exercise, on cortical spreading depression (CSD) in young and adult rats. Methods: L-arginine (300 mg/kg/day, n = 40) or distilled water (vehicle, n = 40) was given to the rats during postnatal days 7-35 by gavage. Physical exercise (treadmill) was carried out during postnatal days 15-35 in half of the animals in each gavage condition described above. The other half (non-exercised) was used for comparison. When the animals reached 35-45 days (young groups) or 90-120 days of age (adult) CSD was recorded on two cortical points during 4 hours and CSD propagation velocity was calculated. Results: L-arginine-treated + exercised rats had increased body weight, but not brain weight, in adult age compared to L-arginine + non-exercised ones (P < 0.05). In both young and adult animals, L-arginine increased, whereas exercise decreased the CSD propagation velocity. Analysis of variance revealed a significant interaction between gavage treatment and age (P < 0.001), and also between gavage treatment and exercise (P = 0.004), but not between age and exercise. An additional control group of young rats, treated with 300 mg/kg of L-histidine, presented CSD velocities comparable to the corresponding water-treated controls, suggesting that the CSD acceleration seen in the L-arginine group was an L-arginine-specific effect, rather than an effect due to a non-specific amino acid imbalance. Discussion: L-arginine and exercise affect CSD differentially (L-arginine accelerated, while exercise decelerated CSD), and both effects did interact. Probably, they depend on developmental plasticity changes associated with the treatments.
Biochimica et Biophysica Acta (BBA) - General Subjects, 2014
Background: Our previous study demonstrated that essential fatty acid (EFA) dietary restriction o... more Background: Our previous study demonstrated that essential fatty acid (EFA) dietary restriction over two generations induced midbrain dopaminergic cell loss and oxidative stress in the substantia nigra (SN) but not in the striatum of young rats. In the present study we hypothesized that omega-3 deficiency until adulthood would reduce striatum's resilience, increase nitric oxide (NO) levels and the number of BDNF-expressing neurons, both potential mechanisms involved in SN neurodegeneration. Methods: Second generation rats were raised from gestation on control or EFA-restricted diets until young or adulthood. Lipoperoxidation, NO content, total superoxide dismutase (t-SOD) and catalase enzymatic activities were assessed in the SN and striatum. The number of tyrosine hydroxylase (TH)-and BDNF-expressing neurons was analyzed in the SN. Results: Increased NO levels were observed in the striatum of both young and adult EFA-deficient animals but not in the SN, despite a similar omega-3 depletion (~65%) in these regions. Increased lipoperoxidation and decreased catalase activity were found in both regions, while lower tSOD activity was observed only in the striatum. Fewer TH-(~40%) and BDNF-positive cells (~20%) were detected at the SN compared to the control. Conclusion: The present findings demonstrate a differential effect of omega-3 deficiency on NO production in the rat's nigrostriatal system. Prolonging omega-3 depletion until adulthood impaired striatum's anti-oxidant resources and BDNF distribution in the SN, worsening dopaminergic cell degeneration. General significance: Omega-3 deficiency can reduce the nigrostriatal system's ability to maintain homeostasis under oxidative conditions, which may enhance the risk of Parkinson's disease.
Objective: We investigated the effect of early-in-life administration of L-arginine, combined wit... more Objective: We investigated the effect of early-in-life administration of L-arginine, combined with physical exercise, on cortical spreading depression (CSD) in young and adult rats. Methods: L-arginine (300 mg/kg/day, n = 40) or distilled water (vehicle, n = 40) was given to the rats during postnatal days 7-35 by gavage. Physical exercise (treadmill) was carried out during postnatal days 15-35 in half of the animals in each gavage condition described above. The other half (non-exercised) was used for comparison. When the animals reached 35-45 days (young groups) or 90-120 days of age (adult) CSD was recorded on two cortical points during 4 hours and CSD propagation velocity was calculated. Results: L-arginine-treated + exercised rats had increased body weight, but not brain weight, in adult age compared to L-arginine + non-exercised ones (P < 0.05). In both young and adult animals, L-arginine increased, whereas exercise decreased the CSD propagation velocity. Analysis of variance revealed a significant interaction between gavage treatment and age (P < 0.001), and also between gavage treatment and exercise (P = 0.004), but not between age and exercise. An additional control group of young rats, treated with 300 mg/kg of L-histidine, presented CSD velocities comparable to the corresponding water-treated controls, suggesting that the CSD acceleration seen in the L-arginine group was an L-arginine-specific effect, rather than an effect due to a non-specific amino acid imbalance. Discussion: L-arginine and exercise affect CSD differentially (L-arginine accelerated, while exercise decelerated CSD), and both effects did interact. Probably, they depend on developmental plasticity changes associated with the treatments.
Biochimica et Biophysica Acta (BBA) - General Subjects, 2014
Background: Our previous study demonstrated that essential fatty acid (EFA) dietary restriction o... more Background: Our previous study demonstrated that essential fatty acid (EFA) dietary restriction over two generations induced midbrain dopaminergic cell loss and oxidative stress in the substantia nigra (SN) but not in the striatum of young rats. In the present study we hypothesized that omega-3 deficiency until adulthood would reduce striatum's resilience, increase nitric oxide (NO) levels and the number of BDNF-expressing neurons, both potential mechanisms involved in SN neurodegeneration. Methods: Second generation rats were raised from gestation on control or EFA-restricted diets until young or adulthood. Lipoperoxidation, NO content, total superoxide dismutase (t-SOD) and catalase enzymatic activities were assessed in the SN and striatum. The number of tyrosine hydroxylase (TH)-and BDNF-expressing neurons was analyzed in the SN. Results: Increased NO levels were observed in the striatum of both young and adult EFA-deficient animals but not in the SN, despite a similar omega-3 depletion (~65%) in these regions. Increased lipoperoxidation and decreased catalase activity were found in both regions, while lower tSOD activity was observed only in the striatum. Fewer TH-(~40%) and BDNF-positive cells (~20%) were detected at the SN compared to the control. Conclusion: The present findings demonstrate a differential effect of omega-3 deficiency on NO production in the rat's nigrostriatal system. Prolonging omega-3 depletion until adulthood impaired striatum's anti-oxidant resources and BDNF distribution in the SN, worsening dopaminergic cell degeneration. General significance: Omega-3 deficiency can reduce the nigrostriatal system's ability to maintain homeostasis under oxidative conditions, which may enhance the risk of Parkinson's disease.
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Papers by Monara Angelim