Final answer:
Rapid dystonia parkinsonism affects membrane potential via changes in ion channel function and excitotoxicity, and targeting NMDA receptor subunits has shown promise in treating symptoms in animal models and humans.
Step-by-step explanation:
Rapid dystonia parkinsonism, a neurological condition, affects membrane potential through mechanisms that may involve glutamate-mediated excitotoxicity and alterations in ion channel function. In understanding this, the study of calcium-permeable AMPA receptors becomes significant, where their excess activity can lead to neuronal damage. The membrane potential is the distribution of charge across the cell membrane and plays a crucial role in cellular function, including neurotransmission and muscle contraction. Membrane depolarization occurs when there is an influx of ions, such as sodium, that reverses the usually negative membrane potential, which can be part of normal physiological processes or contribute to pathological states like excitotoxicity in neurological disorders.
In animal models of Parkinson's disease, experiments have shown that drugs targeting the NR2B subunit of the NMDA receptor may alleviate some symptoms by potentially mitigating excitotoxic mechanisms. Specific compounds like Traxoprodil have shown promise in treating dyskinetic symptoms in humans, suggesting a link between these receptors and changes in membrane potential relevant to rapid dystonia parkinsonism pathophysiology.