A 1983 neuropharmacologic perspective of space sickness.
Space sickness is generally considered a variant of motion sickness although not fully proved as such. Understanding space sickness requires objective and quantitative characterization of the disorder. Vomiting is a quantifiable physiological event performed by the respiratory muscles which generate the pressures that evacuate the gut. Vomiting from all causes is coordinated by the vomiting center in the medulla oblongata. The emetic chemoreceptor trigger zone (CTZ) in the area postrema is thought to be an indispensable element in the afferent pathway of motion sickness. About 30 potential neurotransmitters exist in the vomiting control mechanism which includes at least eight chemical transmission steps through the reflex pathway of motion sickness. Individual synaptic transmitters do not likely mediate specific functions, but particular combinations of those transmitters might well serve distinct functions. Adaptation to the cause of space sickness probably results from readjustment of a cerebellar circuit or of a humoral factor acting on the CTZ, rather than from stimulus-receptor desensitization. Space sickness must, for purposes of investigation, be treated as a unique disorder engendered by weightlessness until proved equivalent to any emetic syndrome that occurs on earth.
D000222:Adaptation, Physiological; D000337:Aerospace Medicine; D002531:Cerebellum / Q000503:physiopathology; D006801:Humans; D008526:Medulla Oblongata / Q000503:physiopathology*; D009041:Motion Sickness / Q000503:physiopathology*; D018377:Neurotransmitter Agents / Q000502:physiology*; D012018:Reflex / Q000502:physiology; D012154:Reticular Formation / Q000503:physiopathology; D013577:Syndrome; D014839:Vomiting / Q000503:physiopathology
D018377:Neurotransmitter Agents