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Biomedical subjects

A I Roĭtbak

Publications and source records attributed to A I Roĭtbak.

At least 19 recordsLinked to original sources
PubMed1990

[I. S. Beritashvili and his school in the critical period of 1948-1953].

Cynically violating the principles of science, the organizers of the scientific session of the USSR Acad. Sci. and Acad. Med. Sci. in 1950 made an attempt to make null and void of the contributions of Academician I. S. Beritashvili and his associates to the physiological science. At the special sessions of the "Pavlovian Council" in April 1951, Beritashvili's concept on the psychonervous activity was qualified as anti-Pavlovian, idealistic. The hypothesis developed by him and his associated on the process of inhibition was rejected as dualistic; the use of the notion "spontaneous electrical activity" was qualified as the deviation from the principles of determinism. In the resolution adopted, "vicious aims" of I. S. Beritashvili were censured, and soon he was exempted from the post of Director of the Institute of Physiology. The campaign against I. S. Beritashvili and his School ceased in 1953; it proved to be a vivid example of the form of leadership pernicious for science.

Academies and Institutes↗
PubMed1987

[Changes in the concentration of extracellular potassium in the cerebral cortex with different parameters of electrical stimulation].

In anesthetized cats, a recording macroelectrode, a K+-sensitive microelectrode and a stimulating electrode were placed on the surface of the suprasylvian gyrus. As the duration or intensity of stimulus increased, the amplitude of K+-potential reflecting the changes in the extracellular concentration of K+ ions (delta [K+]o) was augmented, while the half time of decay decreased. delta [K+]o also increased when the number of stimuli increased. Repetitive tetanic stimulation resulted in impairment of the effect also in the case when [K+]o following the preceding stimulus, reached the initial level. K-potential started to decay in the course of prolonged tetanic stimulation; impairment of the neuronal activity is supposed to underlie this event.

Animals↗
PubMed1984

[Post-tetanic potentiation of the dendritic potentials of the cerebral cortex].

In acute experiments on anesthetized cats, the post-tetanic potentiation (PTP) of cortical dendritic potentials lasted for over 30 min. The PTP did not occur after cooling of the cortex below 31 degrees C or after ouabain application to the cortex. In presentation of paired stimuli during the PTP, mathematical analysis revealed an enhancement of relative depression of the dendritic potential at the second stimulus. The PTP of dendritic potentials seems to be associated with metabolic processes in presynaptic fibers of the 1 layer which have synaptic contacts with apical dendrites.

Animals↗
PubMed1983

[Glial origin of negative shifts in the surface potential of the brain upon tetanic stimulation: microelectrode study and mathematical analysis].

It is shown in experiments on anesthetized cats that negative shift of the cortical surface potential evoked by its tetanic stimulation is similar in form and time course to the depolarization of glial cells. On the contrary, hyperpolarizing shifts of neuronal membrane potential are dissimilar in form and time course to the negative shift of the cortical surface potential. A conclusion is made that the contribution of neuronal hyperpolarization to the surface-negative shift of the potential can distinctly be seen only at the beginning of tetanization--in the first 200-300 ms; negative shift of the cortical surface potential is mainly produced by depolarization of glial cells.

Animals↗
PubMed1983

[Changes in the concentration of extracellular potassium and the slow negative potential in the somatosensory area of the cortex in response to stimulation of the ventroposterolateral nucleus of the thalamus in the cat].

A single electrical stimulus applied to the VPL nucleus with intensity, strong enough to elicit in gyrus sigmoideus posterior slow negativity following the primary response, caused a local increase in [K+]0 reaching 0.2 mM. On the basis of this finding it is supposed that the slow negativity reflects mainly depolarization.

Animals↗
PubMed1983

[Changes in the concentration of intracellular potassium and the phenomenon of dendritic potential depression against a slow negative potential background in the cat cerebral cortex].

Two stimulating electrodes (S1 and S2), a recording macroelectrode and a K+-selective microelectrode were placed on g. suprasylvius of cat. A stimulus applied through S1 elicited slow negativity and an increase in [K+]0. At this time the dendritic potential evoked by stimulation through S was depressed. The depression of the dendritic potential was found to correlate with [K+]0.

Animals↗
PubMed1982

[Glial origin of the slow negative potential of the direct cortical response: microelectrode study and mathematical analysis].

Slow negative potential of a direct cortical response is similar in configuration, time-course and reaction to repeated stimuli to depolarization of the cortical glial cells and differs from IPSP of the cortical neurons. According to data of digital spectral (frequency) analysis, slow negative potential is based on the glial component formed by summing up the constituents, which coincide with glial depolarization within a constant factor. The neuronal component, whose contribution is comparatively much smaller, is an indirect result of IPSP.

Animals↗
PubMed1980

[Changes in the extracellular potassium concentration and the slow negative potential in the cerebral cortex].

Changes of potassium concentration in the extracellular space ([K+]0) of the g. suprasylvius of cat cerebral cortex were recorded by means of K+ selective microelectrodes; the electrical field potential was recorded simultaneously. Under deep anesthesia a single electrical stimulus, applied to the cortical surface, at intensity enough to elicit the slow negativity, caused a local increase of [K+]0 reaching 0.1-1.5 mM. The time course of the K+ signal coincide with the course of the slow negativity. It is supposed that the slow negativity reflects glial depolarizaion arising under the action of K+ ions.

Animals↗