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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.

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.

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.

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.

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.

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.