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1.
Am J Physiol Regul Integr Comp Physiol ; 320(4): R541-R546, 2021 04 01.
Artigo em Inglês | MEDLINE | ID: mdl-33533311

RESUMO

Physical exercise attenuates the development of l-3,4-dihydroxyphenylalanine (l-DOPA)-induced dyskinesia (LID) in 6-hydroxydopamine-induced hemiparkinsonian mice through unknown mechanisms. We now tested if exercise normalizes the aberrant corticostriatal neuroplasticity associated with experimental murine models of LID. C57BL/6 mice received two unilateral intrastriatal injections of 6-hydroxydopamine (12 µg) and were treated after 3 wk with l-DOPA/benserazide (25/12.5 mg/kg) for 4 wk, with individualized moderate-intensity running (60%-70% V̇o2peak) or not (untrained). l-DOPA converted the pattern of plasticity in corticostriatal synapses from a long-term depression (LTD) into a long-term potentiation (LTP). Exercise reduced LID severity and decreased aberrant LTP. These results suggest that exercise attenuates abnormal corticostriatal plasticity to decrease LID.


Assuntos
Antiparkinsonianos/toxicidade , Córtex Cerebral/efeitos dos fármacos , Corpo Estriado/efeitos dos fármacos , Discinesia Induzida por Medicamentos/prevenção & controle , Terapia por Exercício , Levodopa/toxicidade , Plasticidade Neuronal/efeitos dos fármacos , Transtornos Parkinsonianos/tratamento farmacológico , Animais , Benserazida/toxicidade , Córtex Cerebral/fisiopatologia , Corpo Estriado/fisiopatologia , Di-Hidroxifenilalanina/análogos & derivados , Modelos Animais de Doenças , Discinesia Induzida por Medicamentos/etiologia , Discinesia Induzida por Medicamentos/fisiopatologia , Potenciação de Longa Duração/efeitos dos fármacos , Depressão Sináptica de Longo Prazo/efeitos dos fármacos , Masculino , Camundongos Endogâmicos C57BL , Atividade Motora/efeitos dos fármacos , Transtornos Parkinsonianos/induzido quimicamente , Transtornos Parkinsonianos/fisiopatologia , Corrida , Fatores de Tempo
2.
Mol Neurobiol ; 56(4): 2944-2951, 2019 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-30073506

RESUMO

Exercise can act as a disease-modifying agent in Parkinson's disease (PD), and we have previously demonstrated that voluntary exercise in running wheels during 2 weeks normalizes striatopallidal dopaminergic signaling and prevents the development of L-DOPA-induced dyskinesia (LID) in C57BL/6 mice. We now tested whether LID in Swiss albino mice could be attenuated by treadmill-controlled exercise alone or in combination with the reference antidyskinetic drug amantadine. The daily intraperitoneal (i.p.) treatment with three different doses of L-DOPA/benserazide (30/12.5, 50/25, or 70/35 mg/kg) during 3 weeks induced increasing levels of LID scores in hemiparkinsonian Swiss albino mice previously lesioned with a unilateral intrastriatal injection of 6-hydroxydopamine (6-OHDA, 10 µg). Then, we addressed the antidyskinetic effects of treadmill-controlled exercise by comparing LID, induced by L-DOPA/benserazide (50/25 mg/kg, i.p.) during 4 weeks, in sedentary and daily exercised mice. Exercise reduced LID and improved motor skills of dyskinetic mice, as indicated by decreased contralateral bias, increase in maximal load test, and latency to fall in rotarod. The antidyskinetic effect of amantadine (60 mg/kg, i.p.) was only observed in sedentary mice, indicating the absence of synergistic antidyskinetic effect of the combination of treadmill exercise plus amantadine. Finally, Western blot analysis unraveled an ability of exercise to increase the striatal immunocontent of glial cell-derived neurotrophic factor (GDNF), apart from normalizing striatal levels of tyrosine hydroxylase. These findings show that controlled treadmill exercise attenuates LID and provide the first indication that the antidyskinetic effects of treadmill exercise may involve increased striatal GDNF levels.


Assuntos
Corpo Estriado/metabolismo , Corpo Estriado/patologia , Discinesia Induzida por Medicamentos/metabolismo , Fator Neurotrófico Derivado de Linhagem de Célula Glial/metabolismo , Levodopa/efeitos adversos , Doença de Parkinson/metabolismo , Doença de Parkinson/patologia , Condicionamento Físico Animal , Animais , Corpo Estriado/efeitos dos fármacos , Modelos Animais de Doenças , Proteínas da Membrana Plasmática de Transporte de Dopamina/metabolismo , Discinesia Induzida por Medicamentos/patologia , Discinesia Induzida por Medicamentos/fisiopatologia , Levodopa/administração & dosagem , Masculino , Camundongos Endogâmicos C57BL , Atividade Motora/efeitos dos fármacos , Doença de Parkinson/fisiopatologia , Tirosina 3-Mono-Oxigenase/metabolismo
3.
Brain Res Bull ; 79(6): 452-7, 2009 Aug 14.
Artigo em Inglês | MEDLINE | ID: mdl-19463920

RESUMO

Previous studies have shown that cognitive deficits precede the classical motor symptoms seen in Parkinson's disease (PD) and that physical exercise may exert beneficial effects on PD. We have recently verified that the monoamine-depleting drug reserpine - at doses that do not modify motor function - impairs memory processes in rats. Here, we evaluated the potential of physical exercise to improve cognitive and motor deficits induced by reserpine. Adult Wistar rats were assigned to six groups: (1) untrained-vehicle; (2) untrained-reserpine; (3) running wheel (RW)-vehicle; (4) RW-reserpine; (5) treadmill-vehicle; and (6) treadmill-reserpine. Exercise groups were given free nocturnal access to RW or continuous treadmill exercise (20-25 min/day) for 5 days/week over 4 weeks. The animals were injected subcutaneously with reserpine (1.0 or 5.0mg/kg) or vehicle 48 h after the end of physical program, and 24h later they were tested in a battery of behavioral paradigms. RW and treadmill improved the motor deficits induced by a high reserpine dose (5.0mg/kg), as evaluated in the rotarod and open-field tests. Moreover, untrained rats treated with a low reserpine dose (1.0mg/kg) presented short-term social memory deficits (without motor or olfactory disturbance) that were selectively improved by the exercise training. Our results reinforce the potential of low to moderate physical exercise as a useful tool in the prevention of motor and cognitive impairments associated to CNS monoaminergic depletion.


Assuntos
Transtornos da Memória/terapia , Transtornos dos Movimentos/terapia , Condicionamento Físico Animal , Percepção Social , Análise de Variância , Animais , Discriminação Psicológica/efeitos dos fármacos , Discriminação Psicológica/fisiologia , Relação Dose-Resposta a Droga , Masculino , Transtornos da Memória/induzido quimicamente , Atividade Motora/efeitos dos fármacos , Atividade Motora/fisiologia , Percepção Olfatória/efeitos dos fármacos , Percepção Olfatória/fisiologia , Distribuição Aleatória , Ratos , Ratos Wistar , Reconhecimento Psicológico/efeitos dos fármacos , Reconhecimento Psicológico/fisiologia , Reserpina , Fatores de Tempo
4.
J Neural Transm (Vienna) ; 115(9): 1251-5, 2008 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-18629433

RESUMO

This study examined the effects of downhill treadmill exercise on brain-derived neurotrophic factor (BDNF) protein on the hippocampus and striatum of mice. Twenty-four adult mice were assigned to three groups: non-runners control, level or downhill (16 degrees decline) running exercise. The exercise schedule consisted of progressive treadmill running for 5 days week(-1) over 8 weeks. Blood lactate levels classified exercise intensity as moderate to high. Both training types increased citrate synthase activity of the soleus muscle when compared to untrained controls. While level running increased BDNF levels selectively in the hippocampus (68.5%), the eccentric running resulted in a pronounced BDNF increase in both the hippocampus (137.0%) and the striatum (49.9%). Further studies will specify whether the observed alterations in BDNF are due to downhill-induced upregulation or complex learning-induced mechanisms that influence BDNF levels in these brain regions.


Assuntos
Fator Neurotrófico Derivado do Encéfalo/metabolismo , Corpo Estriado/metabolismo , Hipocampo/metabolismo , Condicionamento Físico Animal/fisiologia , Esforço Físico/fisiologia , Regulação para Cima/fisiologia , Animais , Citrato (si)-Sintase/metabolismo , Metabolismo Energético/fisiologia , Teste de Esforço , Ácido Láctico/sangue , Aprendizagem/fisiologia , Masculino , Camundongos , Músculo Esquelético/enzimologia , Corrida/fisiologia
5.
J Neural Transm (Vienna) ; 115(12): 1643-50, 2008 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-18795225

RESUMO

Considerable evidence has indicated a pro-oxidant status in the brain of people with Down's syndrome (DS), which may contribute to motor and cognitive impairments verified in this condition. On the other hand, previous studies addressing the role of physical exercise on oxidative stress and antioxidant status in DS have indicated conflicting results. Here, we investigated the effects of a supervised judo training of controlled intensity and monitored on the basis of lactate threshold on the blood oxidative stress status and motor coordination in 21 young adults with DS. The training extended over a period of 16 weeks and consisted of three sessions per week. The exercise improved the motor function and significantly decreased lactate production in the DS subjects. However, blood markers of oxidative damage to lipids (TBARS and lipid peroxides) and proteins (carbonyls) were increased by the judo training. Moreover, superoxide dismutase and catalase activity also increased, while glutathione peroxidase activity remained unaltered after exercise. These results reinforce the notion that physical exercise can improve motor disabilities in people with DS. More importantly, our findings demonstrate that the beneficial effects are accompanied by some degree of oxidative stress, suggesting that young adults with DS may be more susceptible to physical training-induced oxidative stress than adolescents with DS, which should be taken into account in physical training programs for this population.


Assuntos
Encefalopatias Metabólicas Congênitas/terapia , Síndrome de Down/complicações , Tolerância ao Exercício/fisiologia , Transtornos dos Movimentos/terapia , Estresse Oxidativo/fisiologia , Aptidão Física/fisiologia , Adulto , Antioxidantes/metabolismo , Biomarcadores/sangue , Encéfalo/metabolismo , Encéfalo/fisiopatologia , Encefalopatias Metabólicas Congênitas/metabolismo , Encefalopatias Metabólicas Congênitas/fisiopatologia , Catalase/sangue , Síndrome de Down/metabolismo , Síndrome de Down/fisiopatologia , Terapia por Exercício/efeitos adversos , Humanos , Ácido Láctico/sangue , Peroxidação de Lipídeos/fisiologia , Masculino , Transtornos dos Movimentos/metabolismo , Transtornos dos Movimentos/fisiopatologia , Oxirredução , Superóxido Dismutase/sangue , Substâncias Reativas com Ácido Tiobarbitúrico/metabolismo , Resultado do Tratamento , Adulto Jovem
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