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The role of the posterior parahippocampal area of the brain in spatial types of memory in conditions of one-trial visual perception of the positions of objects was studied by training eight cats to remember the spatial positions of either two different objects covering two of three feeders placed on a test tray (tests for the "object-place" association) or the positions of two of three feeders (tests for place). Each trial used new objects and new positions for the two of three feeders. After training, four cats were subjected to electrolytic lesioning of the posterior parahippocampal area, primarily the parahippocampal cortex, parasubiculum, and presubiculum; the remaining four cats underwent all the surgical procedures except electrocoagulation of nervous tissue; this was the sham-operated control group. Cats of this group showed no impairment to the performance of tests of both types, while the experimental group showed similar levels of impairment to the performance of both tests. Thus, memory for one-trial perception of "object-place" associations and, more simply, two different object places in cats were critically dependent on the posterior parahippocampal area.

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To determine the contribution of the posterior parahippocampal region to spatial form of one-trial memory in cats, we trained 8 cats to remember the spatial positions of either two different trial-unique objects overlying two of three feeders in a feeder test tray (object-place trials) or simply two of the three feeders (place trials). Four cats then received electrolytic lesions restricted to the posterior parahippocampal region (experimental group) including mainly parahippocampal cortex, parasubiculum and presubiculum. Four other cats comprised sham-operated control group. This group was found to be completely unaffected postoperatively in both types of trials, whereas experimental group showed impaired performance in both types of trials equally. Thus, one-trial memory for object-place association and one-trial memory for two different places in cats appear to be critically dependent on the posterior parahippocampal region.

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Memory for visual recognition in primates is at least partially mediated by the peripheral and entorhinal (i.e., rhinal) areas of the cerebral cortex. The roles of these structures in visual recognition in cats was studied by producing electrolytic combined lesions of the rhinal (perirhinal + entorhinal) areas in a group of cats trained in a modified Wisconsin test apparatus to delayed selection of an object on the basis of its image on presentation of a new object in every trial in the test. Control groups consisted of intact and sham-operated cats. Animals with rhinal lesions were no different from sham-operated and intact animals in the initial training to the rules for correct responding to the objects presented; they also showed no difference at the minimum delay period of 5 sec used in these experiments. However, a statistically significant difference was seen on testing with a delay of 10 sec, demonstrating impairment of intrinsic visual recognition memory.

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Visual recognition memory in primates is mediated at least in part by the perirhinal and entorhinal (i.e., rhinal) cortices. To examine the role of these structures in cats' visual recognition memory, we performed combined electrolytic rhinal (perirhinal and entorhinal) lesions in a group of cats trained in visual delayed matching-to-sample with trial-unique objects in the modified Wisconsin General Testing Apparatus. Sham-operated and intact cats were used as control groups. Cats with rhinal lesions did not differ from the control sham-operated and unoperated groups in initial learning of the rules of the task; difference between experimental and control groups under conditions of minimum 5-sec delay was nonsignificant as well. However, significant difference between experimental and control groups was revealed under conditions of testing with 10-sec delay. This finding suggests a disorder in the visual recognition memory.

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A metabolite of an anticonvulsant drug Benzonal was isolated from the guinea pig blood serum and identified by high performance liquid chromatography (HPLC). By using HPLC as well as ultraviolet-, infrared- and mass-spectrometry it was established that in the guinea pig intestine Benzonal undergoes alkaline hydrolysis with the formation of phenobarbital. The native Benzonal in the guinea pig blood serum was not found.

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A study was made of metabolism of the new antiepileptic drug halonal in guinea-pigs. It was established that on oral administration halonal was not absorbed from the intestinal tract and only its metabolite, phenobarbital, was detectable in blood serum. It is assumed that halonal produces a therapeutic action only thanks to phenobarbital, its pharmacologically active metabolite.

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In cats the hypothalamus proved capable of the primary epileptogenesis. It suggests the principal feasibility of diencephalic (hypothalamic) epilepsy.

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Inversion of the early component of IPSPs in neurons of the sensorimotor cortex by artificial hyperpolarization of the membrane was demonstrated in cats immobilized by myorelaxants in acute experiments. The late component of IPSP was not inverted. Amplitudes of the early component of IPSPs were decreased by the membrane depolarization while the late component was completely reduced. The input resistance of the membrane which decreased during the early component of IPSPs was restored to the initial level during the late component.

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Major pharmacokinetic parameters of the Soviet anticonvulsive drug benzobarbital used with different regimens of administration (single and prolonged) are described. The authors have studied the interrelationship between benzobarbital and carbamazepine when these drugs are used in combination and drawn a conclusion as to their weak pharmacokinetic synergism. On the basis of the established pharmacokinetic parameters a number of practical inferences pertaining to the mode of benzobarbital administration have been made.

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One of the metabolites of the anticonvulsant drug Benzonal (BZL) has been isolated and its chemical structure studied. High-performance liquid chromatography (HPLC) was utilized for isolation of the metabolite from the blood plasma in patients after a single oral BZL dose of 100 mg. Using this technique and ultraviolet, infrared and mass spectrometries BZL was found to be partially metabolized into phenobarbital by human organism.

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In acute experiments on immobilized cats intracellular injection of Ca+ decreased of IPSP and postburst hyperpolarization amplitudes in pyramidal neurons of the sensorimotor cortex. Intracellular injection of ethylene glycol tetraacetic acid had almost the same effect. This substance also reduced the late part of spike afterhyperpolarization, while the early part remained practically unchanged. It is concluded that Ca2+-dependent K+-conductance might play an important role in the genesis of IPSP, postburst and spike afterhyperpolarization in the membrane of pyramidal neurons of the cat sensorimotor cortex.

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Chromatographic methods of a quantitative determination of phenobarbital, carbamazepine, sodium valproate and ethosuximide in the blood plasma are proposed. The methods are characterized by a good reproducibility and a high sensitivity with a small volume of the sample under study.

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In 14 epileptic patients the authors determined concentrations of carbamazepine, its total and relative clearance, the period of half-elimination and the elimination constant. Blood levels of carbamazepine were assayed by gas liquid chromatography. The pharmacokinetic parameters have been found to be important for specifying the causes of dissociation between the level of blood anticonvulsant and the therapeutic effect when the attacks cannot be controlled or there were signs of intoxication. The mean diagrams of fluctuations of blood concentrations of the drug in the interval between single doses indicate the dependence of the clinical effect on the amplitude of fluctuations and create the prerequisites for the optimization of anticonvulsive therapy.

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Evoked potentials to stimulation of the ventrolateral and intralaminar thalamic nuclei, the surface of the sensomotor cortex, and the pyramidal pathways, derived from the same point, and also corresponding postsynaptic responses of pyramidal neurons were studied in acute experiments on cats anesthetized with ether or superficially with pentobarbital (25-30 mg/kg, intraperitoneally), and immobilized with muscle relaxants. Surface application of strychnine inhibits the slow negative potential arising in response to direct and primary responses, and the corresponding slow potentials of the IPSP. The action of iontophoretic application of strychnine on IPSP of pyramidal neurons and responses of cortical glial cells also were studied. Both methods of application of strychnine block mainly the early component of the IPSP, during which the input resistance is significantly lower than that during the late component, evidence of their different genesis. The results of the investigation show that slow negative potentials are a reflection of hyperpolarization of pyramidal neurons, and that the separate components of the responses have a common genesis.

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Intracellular correlates of evoked rhythmic cortical "spike-and-wave" potentials produced in sensorimotor cortex during 3/s stimulation of the thalamic relay nucleus (VPL) and of self-sustained "spike-and-wave" afterdischarges following 8-14/s stimulation of the same nucleus were studied in acute experiments on cats immobilized by myorelaxants. Intracellular recordings of pyramidal tract neurons revealed that different components of evoked "spike-and-wave" potentials, i. e. the spike-like negative wave and the long lasting negative wave, are postsynaptic in origin: the first is due to EPSPs with spike discharges, and the latter--to IPSPs of cortical neurons. Components of "spike-and-wave" afterdischarge mostly reflect the paroxysmal depolarizing shifts of the membrane potential of cortical neurons. After cessation of sustained "spike-and-wave" activity the long-lasting hyperpolarization accompanied by inhibition of spike discharges and subsequent recovery was observed in cortical neurons. It is presumed that the negative wave of the evoked "spike-and-wave" potential as well as slow negative potentials of direct cortical and primary responses reflect IPSPs of deeper parts of pyramidal tract neurons, while the waves of the sustained "spike-and-wave" afterdischarges are due to paroxysmal depolarizing shifts in cortical neurons.

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The intracellular activity of pyramidal tract neurons during electrical stimulation of ventro-lateral and ventro-postero-lateral nuclei of thalamus was studied in acute experiments on cats immobilized by myorelaxants. Both somatic and presumably dendritic spikes (d-spikes) were observed. The latter were characterized by relatively low and variable (5-60 mV) amplitude; d-spikes occurred both spontaneously and in response to single shock and tetanic (8-14/s) stimulation of the thalamus. They were also induced by intracellular depolarizing current pulses and thalamic stimulation following iontophoretic application of strychnine. Simultaneously generated somatic and d-spikes revealed no collision between each other. Intracellular hyperpolarizing current pulses abolished only somatic spikes, while d-spikes were not affected. Dendritic origin with multiple generation zones of these variable spikes is suggested. Possible functional role of d-spike is discussed.

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