[Structural changes in dendritic spines of the pyramidal neurons of layer III of the rat sensory-motor cortex during remote postischemic period]. / Strukturnye izmeneniia dendritnykh shipikov piramidnykh neironov sloia III sensomotornoi kory bol'shogo mozga krys v otdalennom postishemicheskom periode.

The combination of Golgi method with the lipid phosphorilate mark Dil (1,1'-dioctadecyl-3,3,3 cents, 3 cents-tetramethyl-indocarbocyanine perchlorate) and confocal laser scanning microscope for demonstration of the structure of dendritic tree and dendritic spines enables exact determination of spatial organization of small dendrites and their spines at significant distances in norm and especially in postischemic period. The regularities of dendritic spine reorganization in layer III pyramidal neurons of the cerebral sensory-motor cortex during 9 months after short-term (10 min) total brain ischemia were established.

Effect of transplantation of embryonic nervous tissue on reorganization of interneuronal relationships after mechanical damage to sensorimotor cortex.

The effect of implanted embryonic nervous tissue on restoration of axonal connections in the cerebral cortex after mechanical injury was studied on albino rats using fluorescent lipophilic probe DiI (1,1'-dioctadecyl-3,3,3',3'-tetramethyl-indocarbocyanine perchlorate) and confocal laser scanning microscope. Implantation of embryonic tissue to damaged area promotes the growth of axons through the transplant to adjacent tissue. The damaged area is impenetrable for axons growing without implantation.

[Postischemic reorganization of dendritic architectonics of the hippocampal CA3 region in albino rats predisposed to seizures]. / Postishemicheskaia reorganizatsiia dendritoarkhitektoniki sektora CA3 gippokampa belykh krys s vysokoi sudorozhnoi gotovnost'iu mozga.

Total short term ischemia of brain was induced experimentally in albino rats (10 min long clamp of heart vascular bundle). Using Golgi Silver nitrate impregnation geometry of pyramidal neurons dendritic tree was studied in sector of hippocampus in norm, postischemic period (d 1.30 and 90) healthy animals and those predisposed to cramps. Significant reduction of dendrite volume, total length, dendrite territory, parameters of dendrite arborization were shown on the background of stable numerical density of neurons in all animals who survived brain ischemia. The extent of reduction, volume and duration of changes of parameters of dendritic tree geometry was higher in animals predisposed to cramps than in high threshold animals without cramps. Possible mechanisms of postischemic neuron "epileptization" were discussed.

The cellular distribution of GAP-43 immunoreactivity in human neocortical areas using immunofluorescence and confocal microscopy: post-ischemic influence.

The distribution of growth associated protein-43 (GAP-43) immunoreactive (IR) neurons were studied in human neocortical areas, using immunofluorescence and confocal microscopy. The GAP-43-IR cells were generally localised close to blood vessels, and contained fewer lipofuscin granules than GAP-43 negative cells. Quantification of the relative number of GAP-43-IR cells in control cases showed that the highest number of GAP-43-IR cells were present in layers III and V in the motor and visual cortices, fewer in the temporal cortex, and the lowest number in the frontal cortex. After general ischemia, GAP-43-IR cells were significantly reduced at various survival times, with the counts being lowest in the 1 week surviving case, and higher, but still subcontrol, in the 1 year post-ischemic case.

Quantitative analysis of synaptophysin immunoreactivity in human neocortex after cardiac arrest: confocal laser scanning microscopy study.

Transient global ischaemia caused by cardiac arrest results in lesions that involve all brain structures. The aim of this study was to investigate the condition of synapses in patients surviving, but remaining in a persistent vegetative state, following resuscitation after cardiac arrest. We performed a quantitative analysis of the distribution and density of elements containing a synaptic vesicle protein--synaptophysin (p38)--in human neocortex in cases which survived for 1 week, 2 months, and 1 year after the cardiac arrest. Neurologically healthy cases that died following an accident served as control. Dual-channel confocal laser scanning microscopy (CLSM) was used to image p38-immunoreactivity (IR) and lipofuscin autofluorescence. In control cases no statistically significant differences were found for p38-IR between layers II-III and V-VII. However, the temporal cortex had a higher density of p38-immunoreactive structures than the motor cortex. In postischaemic cases a reduction in the density of p38-IR elements was apparent, mainly in the frontal and motor cortices and less pronounced in the temporal cortex. The least decrease compared with controls was observed in the visual cortex. In the 1 week survival case, a maximal decrease in p38-IR (35% below control) was found. In this case, the number of p38-IR elements per visual field was decreased, and big aggregates of p38-IR structures were observed. In general, the amounts of p38-IR structures were higher in all of the control cases compared with the postischaemic cases.

An ultrastructural study into the effect of global transient cerebral ischaemia on the synaptic population of the cerebellar cortex in rats.

The density of synapses, the shape and size of presynaptic dense projections (PDP), and the curvature of synaptic appositions in the molecular layer of the cerebellum cortex of rat at 10 min ischaemia and after 90 min, 1, 3, 7, 30 days of re-circulation were examined using quantitative ultra-structural techniques. The numerical density of mature junctions decreased significantly (44.0%) after 1 and 3 days of re-circulation, and was increased to 149.8% of the value in the control animals after 7 days of re-circulation. The restoration of the population of mature synaptic junctions was accompanied by a considerable increase of the number of immature junctions. We found a close association between the synaptic curvature and the size of PDP. The curvature of the larger junctions was consistently associated with a reduced height of PDP and a rounder shape. Synaptic curvature increased from 0.0885 (control) to 0.2041 (3 days of re-circulation) and to 0.2128 (7 days re-circulation). The maximum reduction in synaptic numerical density and larger junction curvature was found in zones of irreversibly damaged Purkinje cells. Our results revealed that the synaptic curvature and the height of the pre-synaptic dense projections undergo reciprocal changes after global transient cerebral ischemia. It is tempting to hypothesize that the positive synaptic curvature occurs as a result of changes in morphological conditions for the PDP filaments and in the shape and size of PDP and depends on the level of Ca2+ in synaptic appositions.

Dendritic changes of the pyramidal neurons in layer V of sensory-motor cortex of the rat brain during the postresuscitation period.

Experiments were performed on 40 Wistar rats. Total brain ischemia was induced by 10 min clamping of the cardiac blood vessels. The brains were examined in control rats, after 90 min and after 1, 3, 7, 30 and 90 days during the postresuscitation period. Histological sections were stained with the Golgi method. Morphometrical parameters, 12, of dendritic changes of the pyramidal neurons in layer V of sensory motor cortex (SMC) in rat brain were studied at different intervals of the postresuscitation period. Reduction of the dendrites of the pyramidal neurons due to the loss of the terminal branches of the oblique apical dendrites in layer III-IV was detected from the first day after ischemia. The maximal dendritic change was detected 3 and 7 days after ischemia. Decrease the volume of dendritic territory (54, 4%), the total dendritic length of the whole dendritic territory (56, 0%) and branching of dendrites, and decrease in the number of dendritic spines on apical dendrites in layers I-II (46, 1%) were the main changes during this period. Reduction of the total length of dendrites occurred mostly due to disappearance of the 2nd and 3rd order branches of the apical and basal dendrites. The change of dendrites neurons had returned to control levels after 30 days. By that time the diameter of the dendrites had increased, the varicosities on oblique apical and basal dendrites had disappeared, and the number of 2nd and 3rd order dendrites and of dendritic spines had increased.

Structural basis of information capacity changes of sensory-motor cerebral cortex of rat brain during post-resuscitation period.

In a rat model of asphyxial cardiac arrest the volume of the sensory-motor cortex and the number of neurons and synapses were determined 90 min, 6 h, and 1, 3, 7, 14, and 30 days post-resuscitation. The number of synapses was determined from serial fragmental sections, using selective contrast in ethanol solution of phosphorotungsten acid (PTA), and by cytoarchitectonic analysis on medium-thick sections. The sensory-motor cortex (SMC) volume did not change significantly during the subsequent 30 days after resuscitation. The number of neurons decreased from 2.462 +/- 0.082) x 10(6) pre-insult to (1.441 +/- 0.098) x 10(6) 30 days after resuscitation. Damage was most severe in the small neuronal cell complexes of layers III-IV, which serve as an afferent cortical 'entrance'. Damage was least in the large neuronal cell complexes of layer V, which serves as an efferent cortical 'outlet'. The number of SMC synapses decreased from (5.920 +/- 0.51) x 10(9) pre-insult to (3.441 +/- 0.305) x 10(9) 30 days after resuscitation. Damage was most severe in the synaptic pool of the cortical SMC 'entrance'. An increase in the number of high-efficiency hypertrophic synaptic contacts was observed during the post-resuscitation period, which may significantly change interneuronal relationships.

[The dendritic plasticity of the pyramidal neurons in layer V of the rat sensorimotor cortex in the postischemic period]. / Plastichnost' dendritov piramidnykh neironov sloia V sensomotornoi kory krys v postishemicheskom periode.

Dendrites plasticity of pyramidal neurons in layer V of rat sensomotor cortex was analyzed during postischemic period. Oblique dendrites and their spines of pyramidal neurons were more reactive for ischemia after 1 day aa manifested by decrease in their length, branching, the volume of dendritic territory and number of dendritic spines. This testifies to high sensitivity to the ischemic influence of stimulating aditus of pyramidal neurons of layer V in the sensomotor cortex of rat. At 7 days of postischemic damage, dendrites of pyramidal neurone were mostly reduced. The quantitative parameters of dendritic geometry recovered after 30 and 90 days of ischemia.