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The hypogravity motor syndrome (HMS) is one of the deleterious impacts of weightlessness on the human body in orbital space missions. There is a hypothesis that disorders of musculoskeletal system as part of HMS arise in consequence of changes in spinal motor neurons. The study was aimed at bioinformatic analysis of transcriptome changes in lumbar spinal cords of mice after a 30-day spaceflight aboard biosatellite Bion-M1 (space group, S) and subsequent 7-day readaptation to the Earth’s gravity (recovery group, R) when compared with control mice (C group) housed in simulated biosatellite conditions on the Earth. Gene ontology and human phenotype ontology databases were used to detect biological processes, molecular functions, cellular components, and human phenotypes associated with HMS. Our results suggest resemblance of molecular changes developing in space orbit and during the postflight recovery to terrestrial neuromuscular disorders. Remarkably, more prominent transcriptome changes were revealed in R vs. S and R vs. C comparisons that are possibly related to the 7-day recovery period in the Earth’s gravity condition. These data may assist with establishment of HMS pathogenesis and proposing effective preventive and therapeutic options.

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Antiorthostatic hindlimb suspension (unloading) decreased the resting membrane potential (RMP) of skeletal muscle fibers in fast extensor digitorum longus (EDL) and slow soleus (SOL) muscle of the rat by about 10 % within 7 days and more. Inactivation of the membrane Na+, K+-pump by ouabain brought about similar depolarization as unloading. The increased sodium permeability of the membrane was excluded as the major cause of this depolarization by experiments in which TRIS was substituted for Na+ in the medium. On the other hand, the decrease in the electrogenic participation of the Na+,K+-pump is apparently one of the causes of RMP decrease during hypogravity, in EDL muscle in particular.

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