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Paramembranous specialized formations of the synaptic cytoskeleton -dense projections and postsynaptic condensation of axospinous synapses of the molecular layer of white rat sensorimotor and cerebellar cortex -in health and acute total ischemia are studied by selective contrast staining with phosphotungstic acid. A direct relationship is revealed between the pattern and degree of deformation of the contact plane, on the one hand, and the postsynaptic condensation and ratio of the volumes of pre-and postsynaptic accumulations of paramembranous fdaments, on the other. Key Words: neocortex; cerebellum; interneuronal synapse; ischemiaSynaptic deformation is regarded as the basis of morphological characterization of synapse shape [3]. Experimental findings attest to a relationship between the pattern of deformation of the plane of a synaptic contact and its functional state [2,3,7]. The factors determining the type (positive or negative) and degree of deformation include various external and internal factors (state of the synaptic cytoskeleton, type of transmitter metabolism, size of the synapse, complexity of arrangement of the contact, its localization on the neuron, and its appurtenance to a particular brain compartment) [2,3,5,6]. Discrepancies in the data, however, leave unsolved the problem of the basic structural mechanisms of synapse formation in health and disease.In this study we assessed the effect of the spatial organization of the system of paramembranous fdamentous formations (dense projections, postsynaptic condensation) on the degree of changes in the deformation of the synaptic contact plane in health and ischemia. MATERIALS AND METHODSThe objects of this study were the axospinous synapses of the molecular layer of the sensorimotor cortex (SMC) and the cerebellar cortex, which differ appreciably in biochemical composition and in the spatial arrangement of postsynaptic condensation [4]. Experiments were carried out with 6 male white rats weighing 190 to 210 g under ether narcosis. Acute total ischemia of the brain was induced by 10-rain clamping of the cardiac vascular bundle [1]. The brain was fixed by perfusion of a mixture of 1% glutaraldehyde, 4% paraformaldehyde, and 5% sucrose in phosphate buffer (pH 7.4) through the left ventricle of the heart for 15 min, and then postfixed for 2 h in the same solution at 4"C. Oriented pyramidal fragments of SMC and cerebellar cortex were contrast-stained in ethyl solution of phosphotungstic acid as described elsewhere [7]. The fragments were embedded in an epon-araldite mixture. Ultrathin slices were prepared in a tangential plane at the level of the molecular layer of the SMC and cerebeUar cortex. The slices were examined under an EVM 100AK electron microscope; 30 random visual fields of the neuropil were photographed at the standard 15,000

Studies on white mongrel rats addressed the reorganization of the synaptoarchitectonics of layer I of the cerebral cortex in diffuse-focal injuries. The experiments used models of acute arrest of the systemic circulation (clinical death) resulting from exposure to mechanical asphyxia for 6 min, clamping of the common carotid arteries for 20 min (ischemia), and imposition of sublethal rotatory trauma by the Noble-Collip method (craniocerebral trauma). Electron microscopy and morphometric analysis showed that reductions in the total number density of synapses were accompanied by changes in the relative and absolute contents of the major types of synaptic apparatuses. There were increases in the numbers of large simple and perforated contacts and synapses with invaginated synaptic membranes, mitochondria, and spine apparatuses. These changes were interpreted as the structural basis for the mechanisms of synaptic plasticity in diffuse-focal brain injuries.

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Цель исследования-сравнительное изучение структурно-функционального состояния нейро-глио-сосудистых микроструктурных комплексов соматосенсорной коры (ССК), СА1 гиппокампа и миндалевидного тела (МТ) головного мозга белых крыс в норме и после острой ишемии, вызванной 20-минутной окклюзией общих сонных артерий. Материалы и методы. В эксперименте с помощью электронной и флуоресцентной микроскопии (окраска DAPI) были изучены нейроны, астроциты, эндотелиоциты, перициты, базальная мембрана микрососудов головного мозга в норме (n=5) и реперфузионном периоде (1-, 3-, 7-, 14-, 21-и 30-е сут.; n=30). Морфометрический анализ провели с помощью программы ImageJ 1.46. Результаты. В восстановительном периоде после ишемии отметили реактивные (отек-набухание, тинкториальные свойства клеток) и компенсаторно-восстановительные (гиперплазия, гипертрофия, пролиферация, усиление трансцитоза) изменения нейро-глио-сосудистых комплексов. После ишемии количество нейронов уменьшалось (на 8,7%-55,3%), а содержание глиальных клеток возрастало в 2-3 раза. Увеличение нейроглиального индекса (НГИ) сопровождалось: 1) появлением микрососудов с многочисленными разветвленными отростками перицитов, 2) усложнением пространственной организации базальных мембран, 3) структурными признаками активации процессов трансцитоза (большое количество кавеол, гладких и клатриновых везикул, крупных везикул) в перицитах и эндотелиальных клетках. Заключение. Полученные данные свидетельствуют об компенсаторно-восстановительных изменениях компонентов нейро-глио-сосудистых комплексов ССК, СА1 гиппокампа и МТ головного мозга белых крыс после 20-минутной окклюзии общих сонных артерий. Наиболее полно реализация механизмов защиты и восстановления поврежденных нейронов происходит в ССК и МТ, обладающих высоким НГИ.