Ultrastructural changes in the autonomic interneuronal synapse during activation in the presence of acetylcholinesterase suppression

Structural-functional reconstructions of the frog autonomic interneuronal synapsis have been studied at its activation with endogenic acetylcholine under conditions of acetylcholinesterase suppression. The investigation has been performed with preparations of isolated sympathetic trunk of Rana temporaria treated with armine (5 X 10(-6) M) and subjected to electrostimulation (5 imp/sec) up to a complete block of the synaptic transmission. Certain structural changes are revealed in the axo-somatic synapses, demonstrating an increased adhesive properties of the membranes, ("hatch-like" membranes, numerous submembranous aggregates, aggregates of the intercellular cleft and neuronal-glial contacts). In the terminals changed according to the "light type", with poorly manifested changes, light synaptic vesicles loose their spheric form, their diameter decreases. In the boutons with more intensive changes, the vesicles gradually change into the mass of cluster-floccular material. In the boutons with intensively manifested disorders in the ultrastructure, a complete destruction of the light vesicles is observed. The great part of the ganglionic neuron bodies changes according the "dark type". In their neuroplasm a great amount of subsuperficial cisterns of the endoplasmic reticulum and formation of powerful fasciculi of microfilaments are noted to appear.     

Dynamics of ultrastructural transformations of paired biological membranes in the nervous system

The paper describes ultrastructural mechanisms of formation of nanoscopic pores and large syncytial perforations of paired membranes located between neurons, between neuron and glia, in multiglial envelopes, as well as in the endoplasmic reticulum and Golgi apparatus. The mechanisms of pores and perforation formation are similar in all cases. Adjacent membranes fuse or form either continuous or punctate tight junctions. The pores and their extensions—perforations—are formed only on the basis of the tight junctions; the intermembrane cleft acquires a varicose, bead-like shape. The pore between the “beads” is formed as a result of transformation of the ellipsoid shape of the bead into the spherical one. Upon autoamputation of the varicose structures, they are transformed into residual bodies in the lumen of perforations.     

ST-segment elevation associated with allergic reaction to echocardiographic contrast agent administration

We report a case of an allergic reaction after the administration of an echocardiographic contrast agent which resulted in ST-segment elevation. Hypersensitivity and allergic reactions are known causes of acute cardiovascular events. However, only limited reports are available which suggest the exact mechanism of the occurrence of angina or myocardial infarction during severe allergic reactions. In our case, through invasive imaging (coronary angiography and IVUS) we have shown for the first time a transient coronary spasm in the absence of intra-coronary thrombus and only minimal neointimal hyperplasia.     

Glio-neuronal and glio-glial syncytial cytoplasmic connections in peripheral nerve trunks of the crayfish Astacus leptodactylus

The paper considers various aspects of glial sheaths of neuritis in the crayfish peripheral nerve trunks and roots. There are revealed dotted glio-neurite tight junctions and a varicose deformation of the intercellular glio-neurite cleft. Rupture of membranes in the area of contact leads to formation of the glio-neurite pore (less than 10 nm) that is enlarged and forms wide (up to 240 nm) syncytial perforations. At the edge of perforation, either remnants of tight junctions are present or damaged membranes that fuse and are rounding. The lumen of perforations always contains residual membranous bodies in the form of vesicles. Their deviation from the median line can indicate a mutual translocation of substances of the glio- and neuroplasm. In the adjacent layers of the multilayer glial sheath there is noted a similar phenomenon of formation of the glio-glial syncytial connection terminating by fusion of neighbor glial layers, which is terminated by fusion of neighbor glial layers into the single lamina. The process begins from the varicose deformation of interglial clefts, which appears as a result of massive formation of dotted and expanded tight membranous contacts. As a result of transformation of ellipsoid varicose deformations into the spherical ones, syncytial pores (less than 10 nm) between them are formed, which are enlarged and break the paired gliolemmas into fragments. As a result, the adjacent glial layers are united. Since this process in intact animals occurs on the background of undamaged nerve structures, a suggestion is put forward about its reversibility and the functional nature.     

Effect of the ponderomotive force on the development of beam-plasma instability

The amplitude of the wave generated in a plasma during the development of beam-plasma instability is nonuniform in the longitudinal direction. The ponderomotive force associated with this nonuniformity leads to a redistribution of the plasma density; as a result, the wave amplitude and its spatial distribution change. As the beam current grows, the ponderomotive force plays an increasingly important role and radically changes the mechanism by which the beam-plasma instability saturates. Ion acoustic waves generated by the ponderomotive force propagate in the direction opposite to the propagation direction of the beam, thereby ensuring distributed feedback and giving rise to a strong low-frequency self-modulation of the wave amplitude and phase. Results are presented from experimental investigations of the self-modulation regime of the beam-plasma instability in a magnetized plasma waveguide. Theoretical estimates of the parameters of the low-frequency self-modulation agree well with the experimental data.     

Platelets Recognize Brain-Specific Glycolipid Structures,Respond to Neurovascular Damage and Promote Neuroinflammation

Platelets respond to vascular damage and contribute to inflammation, but their role in the neurodegenerative diseases is unknown. We found that the systemic administration of brain lipid rafts induced a massive platelet activation and degranulation resulting in a life-threatening anaphylactic-like response in mice. Platelets were engaged by the sialated glycosphingolipids (gangliosides) integrated in the rigid structures of astroglial and neuronal lipid rafts. The brain-abundant gangliosides GT1b and GQ1b were specifically recognized by the platelets and this recognition involved multiple receptors with P-selectin (CD62P) playing the central role. During the neuroinflammation, platelets accumulated in the central nervous system parenchyma, acquired an activated phenotype and secreted proinflammatory factors, thereby triggering immune response cascades. This study determines a new role of platelets which directly recognize a neuronal damage and communicate with the cells of the immune system in the pathogenesis of neurodegenerative diseases.