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A I Roitbak

Publications and source records attributed to A I Roitbak.

15 recordsLinked to original sources
PubMed1992

Stimulus-evoked slow potential shifts and changes in [K+]0 of the frog optic tectum.

In 17 frogs (Rana esculenta var ridibunda) immobilised with succinyl choline the optic tectal surface was stimulated by trains of electrical pulses or by a flash to the contralateral eye. Sustained potential shifts (SPSs) and changes in extracellular potassium concentration (delta[K+]0) were simultaneously recorded. In response to electrical stimulation SPSs of maximal amplitudes (1.19 +/- 0.1 mV) were recorded between 50 and 200 microns in depth and maximal delta[K+]0 (0.69 +/- 0.08 mM) between 100 and 350 microns. The changes of SPS and delta[K+]0 showed a close similarity in experiments with changes in voltage, pulse duration and frequency of stimuli within a train. The induced SPS had a duration of 28 +/- 1.54 s, the delta[K+]0 of 32 +/- 1.23 s. The flash stimulus induced an SPS and delta[K+]0 of maximal amplitudes between 50 and 200 microns in depth with values of 0.57 +/- 0.1 mV and 0.29 +/- 0.03 mM respectively. An additional wave with a latency of ca 1 s and a duration of ca 3 s arose on the background of the SPS to a flash stimulus, associated with an additional increase in [K+]0. It is considered that the accumulation of K+ in extracellular space, with neuronal activity, results in depolarization of radial processes of ependymal glia. This is reflected in the neuropil of the upper layers of the optic tectum as an SPS.

Animals↗
PubMed1987

Contribution of glia and neurons to the surface-negative potentials of the cerebral cortex during its electrical stimulation.

In 20 cats anaesthetized with pentobarbital the suprasylvian gyrus was stimulated by single stimuli or by trains of 50 s stimuli and the potentials from the cortical surface and the intracellular potentials from glial and nerve cells were recorded. Glial cells were identified according to conventional electrophysiological criteria: the absence of action potentials and postsynaptic potentials; slow depolarization in response to electrical stimulation. The slow negativity of direct response to a single stimulus is similar in shape and time course to the depolarization of the cortical glial cells and is unlike the hyperpolarization of the cortical neurons. Quantitative analysis showed that the basic part of the slow negativity is the glial component, whereas the neuronal component--inhibitory postsynaptic potential--plays a much lesser role. The negative shift of the potential on the cortical surface evoked by its high-frequency stimulation is similar in shape and time course to the depolarization shift of the membrane potential of the cortical glial cells (the mean value and standard error of time to peak for glial depolarization were 567.6 +/- 26.8 ms and 427 +/- 24 ms for negative shift of potential). (The results are based on recordings from 37 cells.) The negative shift decays much quicker; it is not similar in shape and time course to the hyperpolarization shift of the neuronal membrane potentials (the mean value and standard error of time to peak for inhibitory postsynaptic potential was 44.9 +/- 4.5 ms). According to the quantitative analysis, the negative shift of the potential reflects mainly the depolarization of the cortical glial cells. The contribution of the hyperpolarization of neurons to the surface-negative shift can be distinctly observed during the first 0.2-0.3 s of stimulation. It is supposed that accumulation of K+ ions in intercellular clefts results in depolarization of glial syncytium, which is reflected on the cortical surface as a slow negativity and a negative shift of the potential.

Animals↗
PubMed1984

On the possible nature of the processes induced by unconditioned stimulation in the cerebral cortex.

Tetanic stimulation of the cortex elicits in some cortical neurons a hyperpolarizing change of the membrane potential and inhibition of impulse activity; after cessation of stimulation often an enhanced discharge occurs. Other neurons respond to stimulation with high-frequency discharges. At the site of stimulation [K+]o is increased more than by 2 mM. If tetanic stimulations are applied at less than 2 min intervals they result in an attenuated K+ release. During tetanic stimulation of the cortex a depolarizing shift of the glial cell membrane potential develops at all strata of the cortex. It is known that conditioned reflex may be elaborated when the electrical stimulation of the motor cortex is used as unconditioned stimulus if the intertrial intervals are not too short. It is hypothesized that the effectiveness of the stimulation of the cortex in eliciting the K+ release and in promoting a conditioned reflex acquisition are interrelated. According to this hypothesis an increase in [K+]o is a signal for myelin formation, and myelination of the naked axonic terminals which convey conditioned signal is the basis for the conversion of the potential connections into the actual ones.

Action Potentials↗
PubMed1980

The importance of I. M. Sechenov's electrophysiological research.

In his electrophysiological studies I. M. Sechenov described for the first time the spontaneous electrical activity of the isolated brain, the physical electrotonus in the CNS, the amplifying action of anodic polarization on spontaneous and induced electrical activity, phenomena of inhibition of spontaneous and induced electrical oscillations of the brain upon tetanization of sensory nerves and negative shifts in the potential of the brain. Thus Sechenov discovered some basic electrical manifestations of the activity of the CNS and initiated fundamental electrophysiological studies of the brain.

Action Potentials↗
PubMed1975

Spreading depression resulting from cortical punctures.

In acute experiments on cats under deep Nembutal anesthesia punctures of the cortex caused a prolonged negative shift of its surface potential (up to 15 mv, 5.5 min), which was followed by a prolonged positive shift. During these shifts of the potential, both components of the direct response were depressed. The changes in potential and the depression of electric activity spread over the cortex at a mean rate of 65 micrometers/s. The phenomenon arised when the punctures are made with a pipet 20 micrometers and above in diameter. A puncture of the surface structures was critical; passage of the pipet through the middle and deep layers was ineffective. It is assumed that when cortical punctures are made the SD is caused by K(+) ions which leak out of the destroyed glial structures.

Animals↗