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The effect of transtraumatic epidural electrostimulation (TEES) above (T5) and below (L2) spinal cord injury in the lower thoracic region (T8-T9) in combination with treadmill exercise in pigs was evaluated using electrophysiological examination methods and behavioral tests. Two weeks after spinal cord injury, motor evoked potentials of m. soleus were recorded during electrostimulation at the level of T5 and L2 segments, which indicated activation of spinal cord structures above and below the focus of injury. After 6 weeks of TEES in combination with physical training, restoration of the characteristics of M-response and H-reflex of the soleus muscle in response to stimulation of the sciatic nerve, improvement of joint mobility, and appearance of voluntary motor activity in the hindlimbs were observed. Neuromodulation with TEES had been proven to be an effective way to stimulate posttraumatic spinal cord regeneration and can be used in the development of a neurorehabilitation protocol for patients with spinal cord injury., (© 2023. Springer Science+Business Media, LLC, part of Springer Nature.)

The development of hypogravitational motor syndrome is an essential negative consequence of weightlessness for humans; an important role in the pathogenesis of this syndrome is played by changes in axons of the spinal tracts. Myelinated fibers and transcriptome of the spinal cord were studied in mice exposed to hypogravity during a 30-day flight on a biosatellite. Morphometric analysis of myelinated fibers of the spinal tracts showed a decrease in the thickness of the myelin sheath. Analysis of spinal cord transcriptome revealed a decrease in the expression of genes involved in the myelination of nerve fibers. These results suggest that the processes of nerve fiber myelination are involved in the development of the hypogravitational motor syndrome under weightless conditions; the 7-day readaptation period was found to be insufficient for reversion of the negative changes in the myelinated fibers of the spinal cord., (© 2023. Springer Science+Business Media, LLC, part of Springer Nature.)

Lysosomal storage diseases (LSDs) are a group of approximately 50 genetic disorders caused by mutations in genes coding enzymes that are involved in cell degradation and transferring lipids and other macromolecules. Accumulation of lipids and other macromolecules in lysosomes leads to the destruction of affected cells. Although the clinical manifestations of different LSDs vary greatly, more than half of LSDs have symptoms of central nervous system neurodegeneration, and within each disorder there is a considerable variation, ranging from severe, infantile-onset forms to attenuated adult-onset disease, sometimes with distinct clinical features. To date, treatment options for this group of diseases remain limited, which highlights the need for further development of innovative therapeutic approaches, that can not only improve the patients' quality of life, but also provide full recovery for them. In many LSDs stem cell-based therapy showed promising results in preclinical researches. This review discusses using mesenchymal stem cells for different LSDs therapy and other neurodegenerative diseases and their possible limitations., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Issa, Shaimardanova, Valiullin, Rizvanov and Solovyeva.)

The data obtained by transcriptome analysis of lumbar spinal cord segments, sciatic nerve, and the respiratory diaphragm of the mice performed after a space flight on board Bion-M1 biosatellite were processed by bioinformatic methods aimed at elucidation of the regularities in hypogravity-induced transcriptome changes in various compartments of motor neurons. The study revealed abnormalities of axonal transport in spinal motor neurons provoked by weightlessness. These data agree with the results of electron microscopy examination of the spinal cord in experimental animals. In space group mice sacrificed on the landing day, the content of perinuclear ribosomes in lumbar motoneurons surpassed that in control mice or in the recovery group examined 1 week after the flight. The data corroborate our hypothesis on contribution of axonal transport disturbances into pathogenesis of hypogravity motor syndrome. They can be employed as a launching pad for further study of hypogravity-triggered motor disorder mechanisms in order to elaborate the preventive therapy against the development of hypogravity motor syndrome in space flights.

We studied immunohistochemical and morphometric characteristics of the spermatogenic epithelium in rats against the background of peroral administration of nanoparticles containing titanium dioxide. Substantial degenerative changes in the spermatogenic epithelium were revealed: thinning, disorganization of layers, and detachment of sperm cells from the basement membrane. Immunohistochemical analysis revealed reduced proliferative activity and differentiation potential of epithelial cells, which was confirmed by changes in the expression of Ki-67 and c-kit markers. Our data attest to unfavorable effects of titanium dioxide nanoparticles on the structural and functional characteristics of the reproductive system in male rats leading to spermatogenesis disturbances.

The results of axonal regeneration in peripheral nerves and of the modulating effect of estrogens on the posttraumatic plasticity of motor neurons through the classical and alternative genomic mechanisms involving the activation of estrogen receptors ERalpha and ERbeta and increased transcription of specific neuroprotective control genes. New mechanisms of the neuroprotective effect of estrogens related to the cross interaction of estrogens with intracellular signaling cascades of many other biologically active compounds, in particular, vascular endothelial growth factor and endothelin, are proposed.

We studied parameters of the frog sartorius muscle contraction initiated by ryanodine receptor agonists in the presence of ROS donors. We hypothesized that sodium nitroprusside and hydrogen peroxide inhibit initiation of contractions by N-ethylmaleimide and that this effect of ROS donors on parameters of N-ethylmaleimide-induced contractions is due to a direct effects of sodium nitroprusside and hydrogen peroxide on N-ethylmaleimide, but not to inactivation of ryanodine receptors in the sarcoplasmatic reticulum of frog skeletal muscle.

Expression of slow myosin in fast lumbrical muscle during unilateral damage to the sciatic nerve was studied in rats. Four weeks after unilateral excision of sciatic nerve segment or its crushing, the content of slow fiber in the lumbrical muscle of the contralateral leg tended to increase (detected using monoclonal antibodies against slow myosin). The extrapyramidal system seems to modulate the phenotype of muscle fibers via motoneurons of the spinal cord, while the compensatory activation of this system manifests in pronounced "deceleration" of both the fast and slow muscles in the hind legs.

Immunohistochemical study with monoclonal antibodies against fast myosin heavy chains showed that excision of a fragment of sciatic nerve does not change, while compression of the nerve decreased the relative content of fast muscle fibers in rat soleus muscle. The content of fast fibers in the muscles of contralateral limbs decreased in both models of denervation. Hence, contralateral limbs cannot be used as the control in experiments with disturbed neurotrophic function. Possible mechanisms underlying changes in the immunohistochemical profiles of experimental and contralateral limbs are discussed.

The authors studied the ability for anaphylactic contraction in vitro of musculus plantaris, diaphragmatic muscle and musculus soleus of guinea pig. The muscles of double sensitized pigs were denervated and 4 weeks after the nerve cut the muscles' specimens were studied for anaphylactic contraction. The addition of the resolving dose of the specific antigen to incubation medium resulted in anaphylactic contraction of the diaphragmatic muscle and musculus soleus. Musculus plantaris did not respond. Mechanisms of anaphylactic contraction of the skeletal muscle are discussed.

Membrane potential (MP) of the diaphragm muscle fibers of the rats was registered in the different periods of ischemia in vitro. The ability to normalization of MP up to 6 h of ischemia and an irreversible decrease of MP after 6.5 h of ischemia was revealed. It is concluded that the ability of diaphragm muscle fibers to restore their MP lost beginning from 6 h of artificial ischemia.

After transferrin injection to the slow m. soleus of guinea pig no immunohistochemical changes in myosin composition with monoclonal antibodies (AB) against fast myosin heavy chain (HCf) have been found. All muscles fibers in intact and experimental animals were identified as slow ones (type I of muscle fibers). After colchicine treatment of nerve trunk innervating slow muscle, some muscle fibers reacting with monoclonal AB against myosin HCf have been found. However, after colchicine treatment of nerve trunk and transferrin injection also some muscle fibers in slow muscle reacting with monoclonal AB against myosin HCf have been found. In appears that transferrin probably can not be the factor of neurotrophic control for myosin composition in skeletal muscle.

The immunohistochemical profile of intact and denervated soleus muscle of guinea pigs after sensibilization was studied. It is shown, that intact soleus muscle consists of slow fibers, which have low ATP-ase activity and don't react with monoclonal antibodies against fast myosin heavy chain. No changes of immunohistochemical profile were found after denervation or sensibilization. At the same time, the fibers, reacting with monoclonal antibodies against fast myosin heavy chain and having low ATP-ase activity, were found in denervated muscles after sensibilization. It is concluded, that the synthesis of fast myosin is induced after sensibilization of denervated muscles. Validity of myosin ATP-ase histochemistry for muscle fibers typing is discussed.

The influence of hypothermia on the development of the ischemic disorders was studied using allotransplantation of the rat skeletal muscle (m. lumbricalis) to the anterior chamber of the eye after different period of ischemia. The morphological and immunohistochemical (monoclonal antibodies to heavy chain of the fast myosin, PAP-method) data were found confirming that hypothermia (2-4 degrees C) prolongs the period of the ischemic disorders first appearance by 5 h (from 6 to 11 h) if compared with development of ischemia in the muscle at 21-23 degrees C.

The ability of muscle fibers to survive the ischemic condition was examined. After 0 to 11 h of ischemia of the rat m. lumbricalis was transplanted to the anterior chamber of the rats eye. Using a morphological and immunohistochemical (monoclonal antibodies to heavy chain of the fast myosin, PAP-method) methods it was revealed that population of surviving muscle fibers reduced significantly beginning from 6 h of ischemia. After 9 h of ischemia there were no muscle fibers in the transplant but one could observe the new formed muscle tubules. It is concluded that up to 6 h the muscle fibers of m. lumbricalis ischemia still preserve the ability to recover.

After experimental cease of neurotrophic control of skeletal muscle by denervation no changes in myosin ATP-ase histochemistry and immunohistochemical profile in slow (m. soleus) muscle of guinea pig were found. All muscle fibers in intact muscle fibers). However after colchicine blockade of axoplasmic transport in this slow muscle some muscle fibers reacting with monoclonal antibodies against fast myosin heavy chain were found. At the same time no changes in histochemical ATP-ase profile were observed. Validity of myosin ATP-ase histochemistry for muscle fibers typing as well as possible influence of nerve activity and neurotrophic control itself were discussed.

Denervation of the guinea-pig fast (m. plantaris) and slow (m. soleus) muscles, administration of alpha-thyroxine (T4) to animals followed by denervation and T4 injection entail changes in the relative content of different types of muscle fibers. The slow muscle shows fast muscle fibers after T4 injection, denervation and T4 injection. Moreover, myosin isolated from the m. soleus shows the precipitation band with antibodies to fast muscle myosin. These data attest to partial reprogramming of myosin synthesis by the m. soleus, pointing to the role played by thyroxine in myosin synthesis regulation.

L-thyroxin prevents neither the postdenervation decrease of resting MP, nor the increase of input resistance, nor the extrajunctional sensitivity to acetylcholine, but after the injection the cross-sectional areas of muscle fibers decrease more rapidly than after a mere denervation and muscle fibers of new type by myosin-ATPase activity do not appear. The same doses of hormone do not affect properties of muscle fiber membrane but increase the input resistance of membrane and decrease cross-sectional areas of muscle fibers. l-thyroxin seems unable to prevent the appearance of the postdenervation changes in skeletal muscle fibers in adult frog and does not take part in regulation of its differentiation.

Myosin ATPase and succinic dehydrogenase activity and fast myosin (indirect immunochemical test) were assayed in m. soleus of guinea-pigs after the administration of T4 (200 micrograms/kg) to animals every day for 3 weeks. This was followed by the application of 10 mM colchicine solution to sciatic nerve for 6 min. Fast muscle fibers and the line of precipitation with antiserum to fast myosin were revealed in soleus muscle of experimental animals after the application of colchicine and T4 injection.