A study of molecular mechanisms of the neurobiological effects of the combined exposure to 10‑day antiorthostatic suspension (AnOS), daily γ-irradiation, and irradiation with carbon ions in rats was carried out. Analysis of molecular changes in dopamine receptors of the hippocampus revealed changes in irradiated rats; in particular, increased expression of monoamine oxidase A, the substrates of which are serotonin, adrenaline, norepinephrine and histamine, was found. The spectral and amplitude–frequency EEG characteristics of rats after the specified influences were studied. Comparison of primary EEG results revealed a tendency towards a decrease in the frequencies of the first peak in irradiated rats regardless of rhythms. In irradiated animals, a tendency towards a decrease in the center frequencies and amplitudes of the most pronounced peak of the EEG spectrum and a decrease in the center frequency and amplitude within the delta rhythm of the maximum peak of the spectrum was observed. Increased anxiety and somewhat accelerated learning in the Morris tests and conditioned reflexes of active avoidance in the shuttle chamber were observed in the behavior of rats, which was consistent with changes in some metabolites of dopamine and serotonin in the hippocampus.

The study of the role of typological characteristics of higher nervous activity of rats in the neurobiological effects (rat behavior and its neurochemical mechanisms) of combined exposure to a 10-day antiorthostatic suspension, γ-, and high-energy proton and carbon ion ( 12 C) irradiation demonstrated that the 12 C ion irradiation caused more marked distortion of the ratio of orientation and exploratory behavior and passive defensive behavior/anxiety in rats of the excitable anxious emotional type. In the experiment with proton irradiation, the differences between typological groups were more smoothed out, though some parameters of passive defensive behavior in the rats of the experimental groups were also increased. These changes were accompanied by decreased monoamine metabolism in the prefrontal cortex.

Skeletal muscle myosin phenotype (i.e., the predominance in the muscle of a particular isoform or isoforms of myosin heavy chains (MyHC)) determines the properties of muscle, such as contraction speed and fatigue. The aim of this study was to identify the functional relationship between the decrease of the nitric oxide (NO) content, the GSK-3β phosphorylation (leading to the GSK-3β activation), the NFATc1 amount in the muscle nuclei, and the MyHC I(β) isoform expression in the rat soleus muscle under gravitational unloading. Male Wistar rats were divided into five groups: the vivarium control group; the group of animals with a 7-day hind limb suspension receiving placebo; the group of animals with a hind limb suspension receiving a NO donor (L-arginine); the group of animals with a hind limb suspension receiving a NO donor and a NO-synthase inhibitor (L-NAME); and the group of animals with a hind limb suspension receiving a GSK-3β inhibitor. We have shown that a 7-day unloading leads to a NO content decrease in the soleus muscle, and this effect is prevented by L-arginine administration. In addition, administration of L-arginine blocks the GSK-3β phosphorylation decrease, NFATc1 export from the muscle nuclei, and MyHC I(β) expression decrease caused by unloading. The L-arginine effect in each case can be blocked by the NO-synthase inhibitor. Administration of the GSK-3β inhibitor prevents the unloading-induced NFATc1 export from the muscle nuclei and a decrease of the MyHC I(β) expression. The prevention of the MyHC I(β) expression decrease and the NFATc1 export from the nucleus by the selective GSK-3β inhibition confirms the hypothesis on the NO influence on the MyHC I(β) expression and the NFATc1 export from the nucleus via the GSK-3β phosphorylation decrease. Thus, the NO level decrease in the rat soleus muscle in unloading leads to the GSK-3β activation, which in turn, promotes the NFATc1 export from the nucleus and stabilization of the fast myosin phenotype.