Abstract
Parkinson’s disease is associated with hyperactivity of the subthalamic nucleus (STN), contributing to motor and gait disturbances. Although deep brain stimulation of the STN alleviates certain motor dysfunction, its specific effect on gait abnormalities remains controversial. This study investigated the long-term changes in locomotion following direct infusions of botulinum toxin-A into the globus pallidus internal segment (GPi) to suppress the flow of information from the STN to the GPi in a hemiparkinsonian rat model. Static and dynamic gait parameters were quantified using a CatWalk apparatus. Interestingly, botulinum toxin-A at 0.5 ng significantly reduced only the dynamic gait parameters of hemiparkinsonian rats at 1 week and 1 month post-infusion, while static gait parameters did not change. This study offers new insights into the complexity of basal ganglia in locomotor control and shows the potential of central infusion of botulinum toxin-A as a novel intervention in the study of experimental hemiparkinson’s disease.
Highlights
Parkinson’s disease (PD) is the second most common neurodegenerative disorder after Alzheimer’s disease
This progressive neurodegenerative disorder is characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc), leading to a functional re-organization of the basal ganglia (BG) circuitry including hyperactivity of the subthalamic nucleus (STN) [2,3]
We have demonstrated that intrapallidal injection of Botulinum toxin type-A (BoNT-A) has the potential to selectively impair overactive glutamate transmission from the STN in the unilateral 6-hydroxydopamine (6-OHDA) rodent model of PD [40]
Summary
Parkinson’s disease (PD) is the second most common neurodegenerative disorder after Alzheimer’s disease. It is estimated that PD affects over 7 million individuals globally and about 1% of the population over 60 years of age [1]. This progressive neurodegenerative disorder is characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc), leading to a functional re-organization of the basal ganglia (BG) circuitry including hyperactivity of the subthalamic nucleus (STN) [2,3]. Gait is defined as the pattern of leg movements used to complete a stride. In PD, the automatic and rhythmic pattern of movement required for gait is abnormal leading to short, shuffling
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