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Biomedical subjects

B I Kotlyar

Publications and source records attributed to B I Kotlyar.

At least 19 recordsLinked to original sources
PubMedDate not supplied

Transformation of the afferent tactile signal into a motor command in the cat motor cortex.

Activity of 112 neurons of the precruciate motor cortex in cats was studied during a forelimb placing reaction to tactile stimulation of its distal parts. The latent period of response of the limb to tactile stimulation was: for flexors of the elbow (biceps brachii) 30-40 msec, for the earliest responses of cortical motor neurons about 20 msec. The biceps response was observed for 5-10 msec after the end of stimulation of the cortex with a series of pulses lasting 25 msec. Two types of excitatory responses of the neurons were identified: responses of sensory type observed to each tactile stimulation of the limb and independent of the presence or absence of motion, and responses of motor type, which developed parallel with the motor response of the limb and were not observed in the absence of motion. The minimal latent period of the responses of motor type was equal to the latent period of the sensory responses to tactile stimulation (20 +/- 10 msec). Stimulation of the cortex through the recording microelectrode at the site of derivation of unit activity, which increased during active flexion of the forelimb at the elbow (11 stimuli at intervals of 2.5 msec, current not exceeding 25 microA), in 70% of cases evoked an electrical response in the flexor muscle of the elbow.

Action Potentials↗
PubMedDate not supplied

Regulation by calcium of short-term plasticity of the cholinoreceptors of RPa3 and LPa3 neurons of the edible snail.

The pharmacological influences which change the intracellular content of free Ca2+ reversibly change the rate and depth of the extinction of the inward current of RPa3 and LPa3 neurons of the edible snail, elicited by repeated iontophoretic applications of acetylcholine to the soma. Suppression by a calcium-free extracellular medium and by verapamil (100-150 mumoles/liter) of the influx of Ca2+ into the cell, induced by the activation of cholinoreceptors, reversibly attenuates the extinction. An increase in the level of intracellular Ca2+ by ruthenium red blockade (5-10 mumoles/liter) of the specific transport of Ca2+ by the mitochondria and by caffeine mobilization (1-4 mmoles/liter) of Ca2+ deposited by the endoplasmic reticulum increases and intensifies extinction. The results obtained indicate that the short-term plasticity of the cholinoreceptors of these neurons is positively regulated by Ca2+ which has entered the cell along chemoregulated ion channels, and has been mobilized from the intracellular Ca depots.

Acetylcholine↗
PubMedDate not supplied

Arachidonic acid and its acyclic derivatives regulate short-term plasticity of the cholinoreceptors of neurons of the edible snail.

The influence of eicosanoids on the dynamics of the extinction of the inward current, induced by repeated iontophoretic applications of acetylcholine to the soma has been demonstrated in identified RPa3 and LPa3 neurons of the edible snail by means of bielectrode recording of the membrane potential. The extracellular action of arachidonic acid (50-100 mumole/l) intensifies the extinction. Quinacrine (100-600 mumole/l), an inhibitor of phospholipase A2, which decreases the content of arachidonic acid in the cells, acts ambiguously. Nordihydroguaiaretic acid (3-10 mumole/l), which is an inhibitor of the lipoxygenase oxidation of arachidonic acid, attenuates the extinction. Indomethacin (10-50 mumole/l), a blocker of cyclooxygenase oxidation of arachidonic acid, does not influence extinction. All of the compounds investigated decrease the amplitude of the inward current induced by acetylcholine. The results obtained make it possible to hypothesize that arachidonic acid and its acyclic metabolites, which are formed as a result of lipoxygenase oxidation, regulate short-term plasticity of the cholinoreceptors of neurons of the edible snail. The cyclic eicosanoids which are formed during the cyclooxygenase oxidation of arachidonic acid do not exert a regulatory effect on the plasticity of the cholinoreceptors.

Animals↗
PubMedDate not supplied

Calmodulin blockers decrease short-term plasticity of the cholinoreceptors of neurons of the edible snail.

A reversible decrease in the rate and depth of the extinction of the reactions of the cholinoreceptive membrane to repeated iontophoretic applications of acetylcholine to the soma by a number of calmodulin blockers was demonstrated in identified RPa3 and LPa3 neurons in the edible snail using the method of recording transmembrane ionic currents: R 24571 (20-50 mumols/liter), trifluoperazine (50-200 mumols/liter), chlorpromazine (20-60 mumols/liter), and prenylamine lactate (30-400 mumols/liter). The results obtained attest to the positive regulation of short-term plasticity of the cholinoreceptors of the neurons in question by calmodulin.

Acetylcholine↗
PubMedDate not supplied

Temporal specificity in the action of stimuli during the formation of associative ultrastructural reorganizations in neurons of the cerebral cortex.

A morphometric investigation of various components of the synapses of neurons of the sensorimotor region of the cerebral cortex of rats with different variants of combined and uncombined repeated microiontophoretic application of glutamate and acetylcholine has been carried out. A substantial dependence of the character and expressivity of the reorganizations of the thickness of the postsynaptic density (PSD), of the width of the synaptic cleft, and the length of the active zone of the synapses, on the temporal relationships in the action of mediators has been identified: significant changes in the thickness of the PSD appeared only with the combined applications of the stimuli (neuromediators); the maximum thickening of the PSD was induced by the combined action of glutamate and acetylcholine with a 3-second delay in the latter. A hypothesis is presented according to which the temporal specificity in the integration of associable signals arriving at neurons is determined by the kinetics of the various interacting biochemical regulator mechanisms.

Acetylcholine↗