Exercise exerts neuroprotective effects on Parkinson's disease model of rats

Abstract

Recent studies demonstrate that rehabilitation ameliorates physical and cognitive impairments of patients with stroke, spinal cord injury, and other neurological diseases and that rehabilitation also has potencies to modulate brain plasticity. Here we examined the effects of compulsive exercise on Parkinson's disease model of rats. Before 6-hydroxydopamine (6-OHDA, 20 microg) lesion into the right striatum of female SD rats, bromodeoxyuridine (BrdU) was injected to label the proliferating cells. Subsequently, at 24 h after the lesion, the rats were forced to run on the treadmill (5 days/week, 30 min/day, 11 m/min). As behavioral evaluations, cylinder test was performed at 1, 2, 3, and 4 weeks and amphetamine-induced rotational test was performed at 2 and 4 weeks with consequent euthanasia for immunohistochemical investigations. The exercise group showed better behavioral recovery in cylinder test and significant decrease in the number of amphetamine-induced rotations, compared to the non-exercise group. Correspondingly, significant preservation of tyrosine hydroxylase (TH)-positive fibers in the striatum and TH-positive neurons in the substantia nigra pars compacta (SNc) was demonstrated, compared to the non-exercise group. Additionally, the number of migrated BrdU- and Doublecortin-positive cells toward the lesioned striatum was increased in the exercise group. Furthermore, brain-derived neurotrophic factor and glial cell line-derived neurotrophic factor increased in the striatum by exercise. The results suggest that exercise exerts neuroprotective effects or enhances the neuronal differentiation in Parkinson's disease model of rats with subsequent improvement in deteriorated motor function.

Exercise Therapy for Parkinson's Disease: Pedaling Rate Is Related to Changes in Motor Connectivity

“…Experiments in animal models of PD have shown that exercise can improve motor function and have a neuroprotective effect (Fisher et al, 2004;Petzinger et al, 2007Petzinger et al, , 2013Tajiri et al, 2010;Tillerson et al, 2003;Zigmond et al, 2009). These animal models generally utilize either 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) or 6-hydroxydopamine (6-OHDA) lesioning to induce degeneration of dopaminergic neurons .…”

Hypoxic Preconditioning Increases the Neuroprotective Effects of Mesenchymal Stem Cells in a Rat Model of Spinal Cord Injury

“…Bdnf and Becn1 mRNA expression levels at the spinal cord lesion site of rats in the H-MSC group were significantly higher than those in the Ctrl group. BDNF plays an important role in survival and differentiation of various neural cells types during neural development and after brain injury, which affect functional recovery [34][35][36]. Although BDNF was reported to play a role in regulating VEGF expression [37,38], it has been recently confirmed that BDNF expression and action are dependent on the vascular endothelial growth factor receptor-2 identifying BDNF as a downstream signaling partner of VEGF [39,40].…”

GDNF and PD: Less Common Points of View

“…On the other hand, exercise for 2 weeks after intrastriatal injection of 6-OHDA results in partial recovery of TH labeling and axonal fiber projection to the striatum (Yoon et al, 2007). Treadmill exercise starting the day after intrastriatal 6-OHDA infusion induces significant preservation of TH-positive fibers in the striatum and TH-positive neurons in the substantia nigra pars compacta as compared to the non-exercised group (Tajiri et al, 2010). An increase in TH labeling in the substantia nigra pars compacta of MPTP-treated mice receiving treadmill exercise was also recently reported (B.A.…”

“…These discrepancies might be related to differences in the lesion regimen/extension and exercise paradigm. Physical exercise increases the expression of GDNF in the nigrostriatal system, and this correlates with the protection of dopaminergic neurons against MPTP toxicity (Faherty et al, 2005), and amelioration of motor impairment due to a 6-OHDA lesion (Cohen et al, 2003;Tajiri et al, 2010). Exercise in the running-wheel markedly accelerates spontaneous recovery after a 6-OHDA lesion as animals exercised on the running-wheel prior or after a unilateral striatal 6-OHDA injection show a faster motor recovery compared to nonexercised animals (O'Dell et al, 2007).…”