Treadmill Exercise Improves Motor Function by Suppressing Purkinje Cell Loss in Parkinson Disease Rats

Abstract

PurposeRotenone is the most widely used neurotoxin for the making Parkinson disease (PD) animal model. The neurodegenerative disorder PD shows symptoms, such as slowness of movements, tremor at resting, rigidity, disturbance of gait, and instability of posture. We investigated whether treadmill running improves motor ability using rotenone-caused PD rats. The effect of treadmill running on PD was also assessed in relation with apoptosis of cerebellar Purkinje cells. MethodsTreadmill running was applied to the rats in the exercise groups for 30 minutes once a day for 4 weeks, starting 4 weeks after birth. We used rota-rod test for the determination of motor coordination and balance. In this experiment, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining, immunohistochemistry for calbindin, glial fibrillary acidic protein (GFAP), Iba-1, and western blot analysis for Bax and Bcl-2 were performed. ResultsTreadmill running enhanced motor balance and coordination by preventing the loss of Purkinje cells in the cerebellar vermis. Treadmill running suppressed PD-induced expression of GFAP-positive reactive astrocytes and Iba-1-positive microglia, showing that treadmill running suppressed reactive astrogliosis and microglia activation. Treadmill running suppressed TUNEL-positive cell number and Bax expression and enhanced Bcl-2 expression, demonstrating that treadmill running inhibited the progress of apoptosis in the cerebellum of rotenone-induced PD rats. ConclusionsTreadmill running improved motor ability of the rotenone-induced PD rats by inhibiting apoptosis in the cerebellum. Apoptosis suppressing effect of treadmill running on rotenone-induced PD was achieved via suppression of reactive astrocyte and inhibition of microglial activation.

Forced exercise activates the NrF2 pathway in the striatum and ameliorates motor and behavioral manifestations of Parkinson's disease in rotenone-treated rats

“…They reported that rotenone injection shortened the latency time; meanwhile, treadmill running lengthened the latency to fall of the rotenone-treated. Shin et al, reported decrease in depressive-like behaviors in exercised rotenone treated rats (27,29). In accordance with our study, Chen et al (30) reported signi cant improvement of Rota rod test in treadmill exercised 6-OHDA group , and signi cant gait improvement with signi cant improvement in overlap, stride length and base width with treadmill exercise.…”

“…Recently many authors studied the effects of treadmill and other means of exercise on rat models of PD. Lee et al, and Shin et al (27,29), both studied the effects of treadmill exercise on rotenone-treated rats. They reported that rotenone injection shortened the latency time; meanwhile, treadmill running lengthened the latency to fall of the rotenone-treated.…”

Treadmill training increases the motor activity and neuron survival of the cerebellum in a mouse model of spinocerebellar ataxia type 1

“…Treadmill exercise has been approved to ameliorate motor disturbance in Parkinson's disease through inhibition of dopaminergic neuron loss and cerebellar Purkinje neuron apoptosis as well as reduce of neurodegeneration in Alzheimer's disease (AD) . However, therapeutic treadmill exercise has been regarded as heterogeneous issue due to the diversified treadmill protocols and different physical situation.…”

Basic neurourology

“…The previously mentioned somatic storage reflex, also known as the pelvic-to-pudendal or guarding reflex, can occur in situations such as laughing, sneezing, and coughing that induce a rise in vesical pressure due to increased abdominal pressure or detrusor pressure. L-glutamate, which is the primary excitatory transmitter in the reflex arc, triggers action potentials by stimulating N-methyl-D-aspartate, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid, and transmembrane ionotropic receptors, and these action potentials stimulate the secretion of acetylcholine, thereby causing contraction of rhabdosphincter muscle fibers (Lee et al, 2018). The urinary incontinence occurs because of this stress if this guarding reflex does not function properly.…”

“…The axons of LMUs pass through the efferent anterior or ventral roots, where motor nerves and autonomic nerves run when they exit the spinal cord. At that point, LMUs extend to the neuromuscular plate or neuromuscular junction, where they are responsible for innervation at muscles that are under voluntary control (Lee et al, 2018). Onuf's nucleus is a defined group of neurons that maintain continence of micturition and defecation and induce muscle contraction during orgasm.…”