ABSTRACT
Myelinated fibers and myelin-forming cells in the spinal cord at the L3-L5 level were studied in C57BL/6N mice that had spent 30 days in space. Signs of destruction of myelin in different areas of white matter, reduction of the thickness of myelin sheath and axon diameter, decreased number of myelin-forming cells were detected in "flight" mice. The stay of mice in space during 30 days had a negative impact on the structure of myelinated fibers and caused reduced expression of the markers myelin-forming cells. These findings can complement the pathogenetic picture of the development of hypogravity motor syndrome.
Subject(s)
Nerve Fibers, Myelinated/metabolism , Space Flight , Spinal Cord/metabolism , Weightlessness/adverse effects , Animals , Male , Mice , Nerve Fibers, Myelinated/pathology , Spinal Cord/pathologySubject(s)
Hindlimb/innervation , Nerve Fibers, Myelinated/metabolism , Spinal Cord/metabolism , Animals , Hindlimb Suspension , Lumbosacral Region/physiology , Male , Mice , Mice, Inbred C57BL , Myelin P2 Protein/genetics , Myelin P2 Protein/metabolism , Myelin Proteins/genetics , Myelin Proteins/metabolism , Nerve Fibers, Myelinated/physiology , Nerve Fibers, Myelinated/ultrastructure , Spinal Cord/physiology , Spinal Cord/ultrastructureABSTRACT
The spontaneous quantum secretion of neurotransmitter and its regulation through the system of presynaptic acetylcholine receptors have been studied on a neuromuscular preparation of rat m. soleus of intact animals and animals in which the axonal transport was blocked via the application of colchicine to the sciatic nerve. It was shown that, after six days of colchicine application, the spontaneous quantum secretion, the reaction of presynaptic membrane, and the reaction of neurosecretory apparatus to the depolarization of nerve endings via increase of the content of potassium ions in the environment and to the activation of presynaptic receptors by carbachol are not disturbed. Keeping in mind a rather short half-life of proteins that take part in the exocytosis and its regulation, it may be concluded that their functioning does not depend on the state of the axonal transport. These data correspond to the hypothesis put forward earlier that the synthesis of some proteins performing their function in nerve terminals occurs directly at the site of their utilization but not in the perikaryon, as it has been traditionally assumed.
Subject(s)
Axons/metabolism , Motor Neurons/metabolism , Protein Biosynthesis , Acetylcholine/metabolism , Animals , Axonal Transport/physiology , Colchicine/pharmacology , Electromyography , Exocytosis , In Vitro Techniques , Male , Membrane Potentials , Neuromuscular Junction/metabolism , Protein Biosynthesis/drug effects , Protein Synthesis Inhibitors/pharmacology , Rats , Rats, Wistar , Receptors, Cholinergic/physiology , Receptors, Presynaptic/physiology , Sciatic Nerve/physiology , Sciatic Nerve/ultrastructureABSTRACT
Experiments on rat diaphragm muscle showed that the nitric oxide (NO) donors sodium nitroprusside SNP) and S-nitroso-N-acetylpenicillamine (SNAP). as well as L-arginine. a substrate for NO synthesis. decreased the level of muscle fiber hyperpolarization (the H effect) after blockade of cholinoceptors on the postsynaptic membrane by d-tubocurarine in conditions of irreversible inhibition of acetylcholinesterase with armine. Conversely, disruptions to NO synthesis in muscle fibers by the NO synthase blocker NG-nitro-L-arginine methyl ester (L-NAME) led to increases in the H effect both in vitro and in vivo. Inactivated solutions of sodium nitroprusside and inactive forms of arginine and NAME (D-arginine. D-NAME) had no effect on the magnitude of the H effect, while hemoglobin, which efficiently binds NO molecules, blocked the inhibitory effects of sodium nitroprusside. SNAP, and L-arginine on the magnitude of the H effect. All these points provide evidence that NO can function as a modulator of non-quantum mediator release in the neuromuscular junctions of warm-blooded animals.