摘要：SummaryProgressive neuromuscular decline in microgravity is a prominent health concern preventing interplanetary human habitation. We establish functional dopamine-mediated impairments as a consistent feature across multiple spaceflight exposures and during simulated microgravity inC. elegans. Animals grown continuously in these conditions display reduced movement and body length. Loss of mechanical contact stimuli in microgravity elicits decreased endogenous dopamine andcomt-4(catechol-O-methyl transferase) expression levels. The application of exogenous dopamine reverses the movement and body length defects caused by simulated microgravity. In addition, increased physical contact madecomt-4and dopamine levels rise. It also increased muscular cytoplasmic Ca2+firing. Indop-3(D2-like receptor) mutants, neither decrease in movement nor in body length were observed during simulated microgravity growth. These results strongly suggest that targeting the dopamine system through manipulation of the external environment (contact stimuli) prevents muscular changes and is a realistic and viable treatment strategy to promote safe human deep-space travel.Graphical abstractDisplay OmittedHighlights•Dopamine levels, movement and body are reduced inC. elegansgrown under microgravity•Loss of mechanical contact in microgravity activates a D2-like dopamine receptor•Reinstating physical contact stimulation improves these reductionsSpace medicine; Aerospace Engineering
