Exercise improves motor deficits and alters striatal GFAP expression in a 6-OHDA-induced rat model of Parkinson’s disease

Abstract

Astrocytic changes have been demonstrated in several neurodegenerative diseases, showing that these cells play an important role in functional recovery/maintenance against brain damage. Physical exercise is known to contribute to this process; however, the cellular mechanisms involved are not fully understood. This study investigated the effects of physical exercise on motor deficits and the expression of glial fibrillary acidic protein (GFAP) in a model of Parkinson's disease (PD). Rats were divided into four groups: sham sedentary (SS) and sham trained (ST); lesioned sedentary (LS) and lesioned trained (LT). 6-OHDA was infused unilaterally into the medial forebrain bundle. Behavioral tasks were applied to evaluate motor abilities. Tyrosine hydroxylase (TH-in substantia nigra) and GFAP (in striatum) immunoreactivities (ir) were semi-quantified using optical density. The animals submitted to treadmill training completed fewer pharmacological-induced rotations when compared with sedentary animals and they also showed ameliorated motor impairments. Interestingly, although no change in TH-ir, the exercise led to restored striatal GFAP expression in the LT group while there was no effect in the ST group. This study is the first study to show data indicating the recovery of GFAP expression post-exercise in this model and further research is necessary to determine the precise action mechanisms of exercise on astrocytes in the PD.

Role of movement in long-term basal ganglia changes: implications for abnormal motor responses

“…These results may appear to contrast with recent studies in experimental animals and PD patients that demonstrate how performance of movement in the form of physical training and exercise may improve motor deficits and even ameliorate dyskinesias (Goodwin et al, 2008; Döbrössy et al, 2010; Frazzitta et al, 2010; Dutra et al, 2012; Frazzitta et al, 2012; Aguiar et al, 2013). In this regard, it is worth considering that extensive neuroplasticity takes place in the striatum, which regulates movement performance, that physical activity may interfere with these neuroplastic phenomena, eventually influencing the execution of movement at a later time, and that neuroplasticity can be profoundly modified in conditions of dopamine denervation (Tillerson et al, 2001; Packard and Knowlton, 2002; Smith and Zigmond, 2003; Schouenborg, 2004; Graybiel, 2005).…”

Dyskinesia in Parkinson's disease: mechanisms and current non‐pharmacological interventions

“…; Dutra et al . ). Amelioration of parkinsonian‐like symptoms may also be elicited by the performance of voluntary exercise, as indicated by studies showing that 6‐OHDA‐lesioned rats allowed access to a running wheel exhibited scarce contralateral rotational behavior in response to apomorphine, compared with sedentary hemiparkinsonian rats (Mabandla et al .…”

Effect of Exercise on Oxidative Stress in Neurological Disorders

“…Studies on the effect of exercise in animal models of PD have indicated that exercise not only protects dopaminergic neurons from the toxic effects of neurotoxins (1-methyl-4-phenyl-1,2,3,6-tetrahydro-pyridine, MPTP), but also improves cognitive function in the neurotoxin treated animals. Although, exercise has no effect on tyrosine hydroxylase immunoreactivity in striatum, but it restores striatal GFAP expression (Dutra et al 2012). Recent studies have also indicated that exercise in the form of intensive treadmill running facilitates neuroplasticity through increased expression of striatal dopamine D2 receptors (DA-D2Rs), a process most evident in the MPTP-mediated injured brain (Vuckovic et al 2010).…”