Motoneuron excitability in Parkinson's disease: effects of dopaminergic medication

Dopamine is a critical neuromodulator of motor function. In Parkinson's disease (PD), the degeneration of dopaminergic neurons not only disrupts motor function but may also alter motoneuron excitability, contributing to motor deficits. The aim of this study was to investigate motoneuron excitability in people with PD during ON and OFF medication states and to compare these responses with those of controls of similar age. Fourteen people with PD (4 females) were tested in two sessions (ON and OFF medication), and 13 controls (5 females) completed the same protocol in one session. Participants performed slow triangular elbow flexion isometric contractions to 30% of their maximum voluntary contraction (MVC). Motor unit discharge rates, recruitment threshold, discharge rate hysteresis (ΔF), brace height, acceleration and attenuation slopes, ascending and descending rate modulations, and self-sustained discharge duration were calculated. People with PD showed higher initial discharge rates (P < 0.05) and lower recruitment thresholds (P < 0.001) in both medication states compared with controls, with no significant differences between the OFF and ON conditions (P > 0.05). ΔF and acceleration slope were both elevated in the OFF state compared with controls (P = 0.04 and P = 0.05, respectively), with no significant medication effects on either measure (P > 0.05). Motoneuron excitability was higher in people with PD compared with controls, and dopaminergic medication does not fully normalize motoneuron excitability or suppress persistent inward current (PIC)-related amplification. These findings raise the possibility that changes associated with long-term monoaminergic loss may not be fully restored by medication.NEW & NOTEWORTHY This study provides new evidence that motoneuron excitability is consistently elevated in people with Parkinson's disease (PD) independent of dopaminergic medication. People with PD showed higher initial discharge rates, lower recruitment thresholds, and greater indicators of persistent inward currents than controls, pointing to lasting spinal adaptations driven by chronic monoaminergic deficits. The persistence of these abnormalities despite dopamine replacement therapy indicates that chronic monoaminergic depletion produces enduring plasticity within the spinal circuits that persists despite dopamine replacement.