Studies in long-term isolated areas of the rat neocortex were performed to investigate the dynamics of the numbers and areas of nerve cell bodies in layer V and to compare these data with the degree of synchronization of epileptic discharges evoked by application of penicillin. Decreases in the number of pyramidal neurons with body areas of 200-350 microm2 in isolated strips after maintenance for 30 and 90 days led to decreases in the degree of synchronization of epileptiform potentials. Large pyramidal neurons are known to have long horizontal axon collaterals, spreading into layers V and VI of the neocortex. It is suggested that the neural networks formed by large pyramidal neurons by means of their long horizontal collaterals mediate the process of intracortical synchronization.

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Spatial organization of intracellular organelles of stretch receptor neurons as an indicator of their different functional states.

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Sprouting and electric activity parameters of the rat sensorimotor cortex after damaging a symmetric part of the contralateral hemisphere.

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[An improved method for isolating a section of the rat neocortex].

Neocortical island chronically isolated from surrounding cortical and subcortical structures with preserved pial blood supply has long been a model for research into the mechanisms of cortex functioning. To fully cut the cortex we improved the type of knife by using a retractable tungsten wire. The tip of a syringe needle was bent and cut away all but the beginning of the bend. In anesthetized rats the somatosensory cortex was exposed, the guide needle was lowered down to the desired depth into the cortex avoiding blood vessels. The wire then was pulled out through the curved needle tip until the tip of the wire touched the pia mater. The device was then raised, lowered, rotated to achieve complete separation of the cortical island from the surrounding tissues. The wire was retracted into the needle before withdrawal of the device. Analysis of neocortical slices 8 weeks later showed lesions of the white matter and transcortical cuts.

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[Neurobiological problems of brain ischemia and post stroke epilepsy].

A review. Current literature data concerning pathophysiological mechanisms of cerebral ischemia and poststroke epilepsy are presented. Results of investigations of structural-functional changes in activity of inhibitory inter neurons, mechanisms of brain plasticity, and main components of neuroprotection in ischemia are also discussed. The presented data confirm the current concept of apoptosis and necrosis as a consequence of injuring action of ischemia, the role of excitotoxicity in pathogenesis of ischemia and poststroke epilepsy, and different kinds of plasticity in recovery of brain functions.

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[Simulation of local cerebral hemorrhage in different brain structures of experimental animals].

A standardized experimental model of intracerebral hemorrhagic stroke in small laboratory animals is developed and advanced for chronic neurobiological studies of normal and pathological higher nervous activity as well as disorders developed after acute hemorrhages. A device is advanced which allows a researcher to destroy appropriate brain structures (tissues and local blood vessels) with necessary precision by four-six rotations of curved stereotaxically inserted mandrel-wire knife and, subsequently, to inject autoblood into the area of the lesion. The advanced model is convenient for the reproduction of lesions in different brain regions (for the purpose of experimental knockouts) in neurophysiological, neuropharmacological, and clinical investigations.

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[Aldosterone binding by compensatory hypertrophic kidney with disturbed neurotrophic supply in rats].

We studied certain aspects of interaction between (3H)aldosterone and the cytoplasmic as well as nuclear receptors of renal cells in the rats during compensatory renal hypertrophy at the background of reflex renal dystrophy. The dystrophy developing in the kidney after cutting the sciatic nerve blocks the compensatory increase in specific accumulation of (3H)aldosterone in the cytoplasm of the renal tubular cells. (3H)Aldosterone transport from the cytoplasmic receptors to the nuclear receptors during rat reflex dystrophy of compensatory hypertrophied kidney is lower as compared to the control. The reflex dystrophy induced by a sciatic nerve injury proved to have no effect on the degree of hypertrophy of the only kidney.

Aldosterone↗

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[Intracortical synchronization of the epileptiform field potentials at different stages of ultrastructural reorganizations in neuronally isolates island in rats].

A temporal delay (parameter of synchronization) between the incidence of epileptiform discharges in cortical sited located at a distance of 4 mm from each other was studied in rat intact cortex and neuronally isolated cortical slab using the cross-correlation function. Experiments were carried out at different stages of axonal sprouting. By 30 days of isolation, a significant increase in the number of boutons in the V cortical layer coincided with a significant decrease in the delay, whereas a reduction of the number of boutons by 90 days corresponded to its increase. These findings convincingly testify that the newly formed boutons form a basis for increase in synchronization and thus affect the epileptogenesis. The results obtained in this work and literature data suggest that under pathological conditions large pyramids of the V layer form a neuronal network which provides exclusively cortical synchronization of epileptiform field potentials.

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[Effect of beta-adrenergic blocker propranolol during reflex renal degeneration induced by sciatic nerve transection].

We present the data on functional status of the mineralocorticoid receptor system in rat kidney in the course of renal reflex degeneration induced by sciatic nerve transection at the background of both renal denervation and injections of beta blocker propranolol. According to the status of renal mineralocorticoid receptors, simultaneous blocking of both neural and humoral pathological stimuli incoming to the kidney after the nerve injury to a higher extent inhibited cytochemical changes in the organ as compared to blocking the neural transmission alone. We propose that both the central neural transmission and humoral mechanisms control the activity of the molecular structures responsible for aldosterone reception in renal tubular cells.

Adrenergic beta-Antagonists↗