Effect of pantogam, nicotinamide, and phenazepam on seizure activity

Gn, Kryzhanovskiĭ; Aa, Shandra; Ls, Godlevskiĭ; Ev, Nikushkin

doi:10.1007/bf00835630

Cited by 5 publications

(12 citation statements)

References 2 publications

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“…If the pathological exposure to the epileptogen were not prolonged, epileptogenesis would not have developed, which is proven by experimental data: no epileptization of the brain develops after discontinuation of pentylenetetrazole treatment at the initial stage of kindling. On the whole, the data indicate that epileptogenesis is a dysregulation condition [4].…”

Section: Resultsmentioning

confidence: 98%

“…However, the stages and characteristics of the development of elevated convulsive readiness of the brain in kindling remains poorly studied. One of the mechanisms of the convulsive threshold reduction in kindling is attenuation of the inhibitory antiepileptic GABAergic processes in the CNS [3,4,7,8]. We studied the status of Cl -conduction of the GABA receptor/Cl -ionophore complex (GABA A -RC) at the early stages of the development of elevated convulsive readiness of the brain induced by pentylenetetrazole (pharmacological kindling).…”

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confidence: 99%

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Cl− conduction of GABAA receptor complex on synaptic membranes in rat cortex at the early stage of chronic cerebral epileptization

et al. 2006

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Experiments on Wistar rats showed that muscimol-stimulated Cl(-) conduction of synaptoneurosomes, isolated from the cerebral cortex increased after 5-day systemic treatment with subconvulsive doses of pentylene tetrasole during the initial stage of pharmacological pentylene tetrasole kindling, characterized by gradually augmenting convulsive readiness of the brain. This indicates an increase in functional activity of the GABA(A) receptor/Cl(-) ionophore complex.

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Section: Resultsmentioning

confidence: 98%

mentioning

confidence: 99%

Cl− conduction of GABAA receptor complex on synaptic membranes in rat cortex at the early stage of chronic cerebral epileptization

et al. 2006

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“…Electrical stimulation (ES) of caudate portions of the vermis during regular use of the benzodiazepines diazepam or phenazepam potentiates the anticonvulsive effect of the drugs both during and after ES and eliminates the factors promoting epileptogenesis [1,4].…”

Section: Abstract: Diazepam; Cerebellum; Electrostimulation; Epileptmentioning

confidence: 99%

Increasing the efficacy of antiepileptic effect of diazepam by cerebellar cortex electrostimulation

Brusentsov¹

1998

Bull Exp Biol Med

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Diazepam effects on epileptic foci induced by benzylpeniciUin application to the posterior sigmoid gyrus were studied in acute experiments on cats. Diazepam more effectively decreased the activity of the foci after preliminary electrostimulation of the IX and X lobules of the vermis than without such a pretreatment. Our purpose was to assess the opposite effect: stimulation of antiepileptic action of diazepam by preliminary ES of the cerebellar cortex. MATERIALS AND METHODSThe study was performed on 27 cats of both sexes weighing 2.5-3.5 kg. Tracheostomy, trephination, implantation of constantan bipolar electrodes (0.12-0.15 ~t, distance between the electrodes 0.25 mm) in the cerebellar cortex (IX-X lobules of the vermis according to [5]), and catheterization of the femoral vein were carried out under ether rausch narcosis. Electrodes were f'Lxed to the skull bones by rapidly hardened Noracryl. The animals were transferred to forced respiration after intraperitoneal injection of 0.25 mg/kg d-tubocurarine (Orion). Follow-up started from 22.5 h after the end of ether narcosis. Twenty sessions of ES of cerebellar cortex (rectangular pulses, 100-300 Hz, 300-400 ~tA, pulse duration 0.25 msec, ES duration 5-7 see) were performed every 3 min with an ESU-2 electrostimulator. To Odessa State Medical University control animals, electrodes were similarly implanted, but no ES was performed.After opening the dura mater, a focus of epileptic activity (EpA) was created by applying a filter paper (2x2 mm) moistened with fresh-prepared benzylpenicillin sodium solution (10,000 U/ml) onto the posterior sigmoid gyrus. Activity of EpA was recorded through monopolar electrodes by an electroencephalograph (Medicor) with indifferent electrodes f'Lxed in the nasal bones.EpA of the foci was expressed in arbitrary units: a mean amplitude of 1 mV at 1 charge/min generation was taken for one unit. A 1-min Bpoque of charge generation was taken for estimating the level of EpA, and the life span of foci was determined as the period from the first to the last spike [3]. Diazepam (Gedeon Richter) was injected intravenously in doses 0.5 and 1.5 mg/kg during generation of stable activity in the foci. Controls were injected with 0.5 ml normal saline.Results were statistically processed using ANOVA tests with subsequent processing by the NeumannKeuls test. Differences were considered significant at p<0.05. RESULTSAfter application of benzylpenicillin (in 3-7 min), the first spike charges were generated in the focus. The amplitude and frequency of these charges in-

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“…Presumably, the emergence of substances of a particular type reflects activation either of the pathological system underlying the disease process or of an antisystem that limits its development. Thus, when cerebellar nuclei pertaining to an Laboratory for General Pathology of the Nervous System and Laboratory for Pathophysiology or Pain, Research Institute of General Pathology and Pathophysiology, Russian Academy of Medical Sciences, Moscow antiepileptic system were activated, epileptic activity was suppressed or weakened, and substances capable of depressing epileptic activity in recipient animals were then detected in the brain and cerebrospinal fluid of donor animals [7]. Similar substances have been found to appear in animal and human cerebrospinal fluid after an epileptic seizure [3,7].…”

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confidence: 99%

“…Thus, when cerebellar nuclei pertaining to an Laboratory for General Pathology of the Nervous System and Laboratory for Pathophysiology or Pain, Research Institute of General Pathology and Pathophysiology, Russian Academy of Medical Sciences, Moscow antiepileptic system were activated, epileptic activity was suppressed or weakened, and substances capable of depressing epileptic activity in recipient animals were then detected in the brain and cerebrospinal fluid of donor animals [7]. Similar substances have been found to appear in animal and human cerebrospinal fluid after an epileptic seizure [3,7]. The present study was designed to determine which substances -pro-or antiepileptic -occur in the spinal cord when a pain syndrome (PS) of spinal origin is developing in rats under the influence of the GPEE formed in the dorsal horns of lumbosacral segments.…”

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confidence: 99%

Analgesic effects of spinal cord peptide factors produced during the establishment and development of generators of pathologically enhanced excitation in the rat spinal cord

et al. 1994

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In rats with a pain syndrome caused by the production of a generator of pathologically enhanced excitation, substances of peptide nature with analgesic properties were found to be produced in the nociceptive system of the spinal cord. Spinal cord extracts derived from rats with such syndromes (pain syndrome of spinal origin or adjuvant arthritis) exerted analgesic effects when injected intraventricularly into recipient rats with a pain syndrome of spinal origin. The highest analgesic activity was displayed by extracts obtained from the region where the generator of pathologically enhanced excitation had been set up. The analgesic activity of the extracts was directly related to the severity and duration of the pain syndrome in the donor rats.

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Effect of pantogam, nicotinamide, and phenazepam on seizure activity

Cited by 5 publications

References 2 publications

Cl− conduction of GABAA receptor complex on synaptic membranes in rat cortex at the early stage of chronic cerebral epileptization

Cl− conduction of GABAA receptor complex on synaptic membranes in rat cortex at the early stage of chronic cerebral epileptization

Increasing the efficacy of antiepileptic effect of diazepam by cerebellar cortex electrostimulation

Analgesic effects of spinal cord peptide factors produced during the establishment and development of generators of pathologically enhanced excitation in the rat spinal cord

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