Spinal Cord Stimulation Prevents Progressive Motor Deterioration in an
α-Synuclein-Based Rat Parkinson’s Disease Model
Abstract
Spinal cord stimulation is a functional neurosurgery proposed for
treating motor symptoms in patients with Parkinson’s disease, yet the
mechanisms underlying motor symptom relief have not been elucidated.
While preclinical studies suggest that long-term motor improvements may
be due to neuroprotection of the nigrostriatal pathway, this evidence is
limited to neurotoxic models. To evaluate the effect of spinal cord
stimulation on nigrostriatal pathway neuroprotection in a genetic model
of Parkinson’s disease, male Sprague-Dawley rats were unilaterally
injected into the substantia nigra with empty or α-synuclein-coding
adeno-associated viruses. Thirty-two days later, the rats were treated
with 300 Hz spinal cord stimulation for ten weeks (two sessions/week).
Ninety-one days post-injection treated α-synuclein rats had better motor
performance than the untreated group, and no differences compared to the
control group. However, spinal cord stimulation could not counteract the
loss of dopaminergic neurons in the nigrostriatal pathway and did not
cause changes in the total dopamine levels in the striatum, dopamine
transporter, or tyrosine hydroxylase expression in the substantia nigra.
The current study suggests that spinal cord stimulation prevents motor
impairment in a genetic model of PD through a mechanism independent of
the nigrostriatal pathway degeneration induced by α-synuclein
overexpression.