ArticleMetabolic brain disease2012
Effect of maternal separation on mitochondrial function and role of exercise in a rat model of Parkinson's disease.
Article in Metabolic brain disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- A history of maternal separation drives systemic aging-associated signatures in middle-aged male rats.Frontiers in cellular neuroscience · 2026Article
- Neonatal stress disrupts the glymphatic system development and increases the susceptibility to Parkinson's disease in later life.CNS neuroscience & therapeutics · 2024Article
- Early Life Stress AffectsInternational journal of molecular sciences · 2022Review
- Transcriptional Profiling Reveals Brain Region-Specific Gene Networks Regulated in Exercise in a Mouse Model of Parkinson's Disease.Frontiers in aging neuroscience · 2022Article
- Impact of Maternal Separation on Dopamine System and its Association with Parkinson's Disease.Neuromolecular medicine · 2020Review
- Aerobic Exercise Training Alleviates Renal Injury by Interfering with Mitochondrial Function in Type-1 Diabetic Mice.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Exercise During Adolescence Attenuated Depressive-Like Behaviors and Hippocampal Mitochondrial Dysfunction Following Early Life Stress in Adult Male Rats.Iranian journal of pharmaceutical research : IJPR · 2018Article
- Neurotrophic factors in women with crack cocaine dependence during early abstinence: the role of early life stress.Journal of psychiatry & neuroscience : JPN · 2014Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Early life stress, such as maternal separation, causes adaptive changes in neural mechanisms that have adverse effects on the neuroplasticity of the brain in adulthood. As a consequence, children who are exposed to stress during development may be predisposed to neurodegenerative disorders in adulthood. A possible mechanism for increased vulnerability to neurodegeneration may be dysfunctional mitochondria. Protection from neurotoxins, such as 6-hydroxydopamine (6-OHDA), has been observed following voluntary exercise. The mechanism of this neuroprotection is not understood and mitochondria may play a role. The purpose of this study was to determine the effects of maternal separation and exercise on mitochondrial function in a rat model of Parkinson's disease. Maternally separated (pups separated from the dam for 3 h per day from postnatal day (P) 2-14) and non-separated rats were placed in individual cages with or without attached running wheels for 1 week prior to unilateral infusion of 6-OHDA (5 μg/4 μl, 0.5 μl/min) into the left medial forebrain bundle at P60. After 2 h recovery, rats were returned to their cages and wheel revolutions recorded for a further 2 weeks. On P72, the rats' motor function was assessed using the forelimb akinesia test. On P74, rats were sacrificed for measurement of mitochondrial function. Exercise increased the respiratory control index (RCI) in the non-lesioned hemisphere of 6-OHDA-lesioned rats. This effect was evident in the striatum of non-separated rats and the prefrontal cortex of maternally separated rats. These results suggest that early life stress may reduce the adaptive response to exercise in the striatum, a major target of dopamine neurons, but not the prefrontal cortex in this model of Parkinson's disease.
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Registered trials
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