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The central nervous system (CNS) plays a critical role in the regulation of muscle relaxation, which is not merely a passive process but involves active neural mechanisms. Muscle relaxation requires specific cortical activation and suppression of excitatory pathways that control muscle contraction. Key molecules involved include GABAergic interneurons, acetylcholine (ACh), and related receptors. The process involves termination of neural signals, repolarization of the muscle fiber membrane, calcium reuptake into the sarcoplasmic reticulum, and detachment of cross-bridges between actin and myosin filaments. Neuroimaging studies show decreased corticospinal tract excitability and increased intracortical inhibition during voluntary or imagined muscle relaxation. Clinical muscle relaxants often target these CNS pathways to promote overall skeletal muscle relaxation.
Enhancement of inhibitory neurotransmission (e.g., GABAergic pathways) or reduction of excitatory drive in the CNS.
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