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PubMedDate not supplied

[Synergism of picrotoxin with the endogenous convulsants kynurenine and quinolinic acid and its antagonism with their antagonists].

In experiments on mice the existence of common mechanisms of action was revealed in picrotoxin and kynurenine and quinolinic acid. Picrotoxin selectively potentiated convulsions induced by kynurenine and quinolinic acid and the antagonists of these endogenous convulsants--picolinic, kynurenic and xanthurenic acids--selectively antagonized picrotoxin convulsions. GABA-ergic preparations, effective in kynurenine convulsions and the anticonvulsants diazepam and phenobarbital, were highly effective against picrotoxin-induced convulsions also. Puphemid and trimethin indicated for treating petit mal epilepsy, proved ineffective. The obtained data suggest the possibility of action of kynurenine and quinolinic acid via picrotoxin-sensitive subunits of the benzodiazepine-GABA-receptor-ionophore complex.

Animals↗
PubMed1979

On some relationships between dopaminergic and serotoninergic mechanisms in pentylenetetrazol convulsions in albino mice.

Experiments with pentylenetetrazol convulsion model in albino mice--80 mg/kg subcutaneously--have revealed the following. The inhibitory effect of 5-HT, introduced intracerebroventricularly in a dose of 100 micrograms per mouse is eliminated by 500 mg/kg L-DOPA, 100 mg/kg amantadine, 5 mg/kg amphetamine and apomorphine, while for lower doses of the dopaminergic agent only a tendency towards antagonism is observed. The inhibitory effect of 50HTP in a dose of 200 mg/kg i. p. is eliminated by 500 mg/kg L-DOPA, 50 mg/kg amantadine and 5 mg/kg amphetamine, but it is not influenced by these drugs in doses of 250 mg/kg L-DOPA, 25 mg/kg amantadine and 5 mg/kg apomorphine, although when applied independently L-DOPA and amantadine in these lower doses potentiate convulsive reactions. The results obtained show that the dopaminergic and 5-HT-ergic systems have an antagonist effect on the convulsive reactivity in the case of pentylenetetrazol convulsion model. These results are in agreement with our views about the determining role of the balance between the various neurotransmitter systems in convulsive-seizure reactions.

5-Hydroxytryptophan↗
PubMed1988

Adaptive changes in the effects of angiotensin II on the convulsive-seizure threshold in cases of altered sensitivity of dopamine receptors.

The adaptive changes in the effects of the neuropeptide angiotensin II (AT II) on the convulsive-seizure threshold were studied. AT II was injected intracerebroventricularly (i.c.v.) at a dose of 1 micrograms/mouse and convulsive seizures were induced by timed intravenous infusion of pentylenetetrazol (PTZ) in male albino mice. The sensitivity of DA receptors was altered by: repeated (14 days) intraperitoneal (i.p.) injection of the DA receptor antagonist pimozide (1 mg.kg-1) and subsequent withdrawal of the antagonist for 7 or 21 days; and repeated (14 days) subcutaneous (s.c.) injection of the DA receptor agonist apomorphine (0.5 mg.kg-1). The convulsive-seizure-increasing effect of AT II was enhanced after multiple administration of pimozide and particularly after its withdrawal for 21 days. This effect was also enhanced though to a lesser degree by repeated treatment with apomorphine. Apomorphine applied 21 days after withdrawal of pimozide decreased the pimozide-enhanced effect of AT II. All these adaptive changes in the effects of AT II on the PTZ convulsive-seizure threshold might be associated with the altered receptor-receptor (AT II-DA-GABA) interactions in the brain structures participating in the regulation of the convulsive-seizure threshold.

Angiotensin II↗
PubMed1987

Citrate synthase and lactate dehydrogenase activities in rat cerebral cortex following the administration of the convulsants bicuculline and 3-mercaptopropionic acid.

Systemic administration of bicuculline (Bic) and 3-mercaptopropionic acid (MP) induces generalized seizure in laboratory animals. The effect of these convulsants on lactate dehydrogenase and citrate synthase activities in rat cerebral cortex was studied. Bic was administered i.p. at 1.0 mg/kg (subconvulsant dose) and 7.5 mg/kg (convulsant dose). MP was administered i.p. at 150 mg/kg (convulsant dose). Lactate dehydrogenase activity in cerebral cortex soluble and particulated fractions was not modified by the administration of Bic or MP. Citrate synthase activity in cerebral cortex homogenates increased about 40% by the administration of subconvulsant and convulsant doses of Bic. A similar increase was found after the injection of MP. No changes in the liver enzyme activity were found, suggesting tissue specificity. The finding of a higher activity of citrate synthase in cerebral cortex homogenates observed with the convulsants may be correlated with the increase in brain citrate levels reported in seizure states.

3-Mercaptopropionic Acid↗
PubMed1986

Inherited convulsive disorders in mice.

In this chapter, we review the major inherited convulsive disorders found in mice and discuss their possible relationship to specific clinical seizure disorders in humans. These disorders in mice include audiogenic seizures, the epilepsy (El) mouse, various spontaneous seizures, the tottering/leaner syndrome, seizures associated with cerebellar abnormalities, seizures associated with myelin disorders, and alcohol withdrawal seizures. We find that for most major types of epilepsy in humans, there exists a similar counterpart in the mouse. Because human and rodent nervous systems respond similarly to seizure-provoking stimuli, it is possible that biochemical and physiological mechanisms of naturally occurring convulsive disorders are also similar in these species. The use of recombinant inbred (RI) and congenic mouse strains for genetic and biochemical studies of audiogenic seizures is presented. Using these strains, we have identified a major gene, Ias, that inhibits the spread of seizure activity. This gene was found through its close linkage with the Ah locus on chromosome 17. We also found that juvenile-onset and adult-onset audiogenic seizures are controlled by different genetic systems. The problem of juvenile-onset audiogenic seizure susceptibility is especially interesting because these seizures are genetically associated with an ecto-Ca2+-ATPase deficiency among the RI strains. This deficiency is the first neurochemical trait found to be inherited together with an idiopathic convulsive disorder, and may represent a potentially important basic mechanism of epilepsy. Because the brains of human epileptics are generally inaccessible for neurochemical research, the epileptic mouse mutants offer a convenient means of pursuing this type of research. The well-known genetic constitution of the mouse, together with the availability of numerous physiologically distinct convulsive disorders, makes the mouse ideally suited for molecular, genetic, and biochemical studies of convulsive behavior.

Acoustic Stimulation↗
PubMed1985

Effects of glycine and other inhibitory amino acid neurotransmitters on strychnine convulsive threshold in mice.

The effects of glycine and other inhibitory amino acid neurotransmitters on strychnine convulsive threshold were studied in mice. The mean intravenous threshold dose for strychnine to produce its convulsive effects in briefly restrained mice was determined to be 1.386 +/- 0.035 mg/kg. The dose of strychnine produced 100% postconvulsive mortality in all the mice tested. Intraperitoneal administration of various doses (100-500 mg/kg) of glycine, beta-alanine and L-threonine, 15-20 minutes prior to strychnine infusion produced an increase of 13.92%, 25.73% and 17.15% respectively in strychnine convulsive threshold in mice. Diazepam, known to produce its anticonvulsant, sedative and muscle relaxant effects through its interaction either with central GABA or glycine receptors was found to be the most potent (48.39%) in increasing strychnine convulsive threshold. Taurine and Baclofen were found to be ineffective in raising strychnine convulsive threshold in mice. These observations favor the possible use of either glycine or beta-alanine in addition to diazepam in treating clinical cases of strychnine neurotoxicoses.

Alanine↗
PubMed1977

On some relationships between gamma-aminobutyric acid (GABA) and the cholinergic mechanisms in pentylenetetrazol convulsions.

In experiments on albino mice with pentylenetetrazol convulsions it has been found that GABA, introduced intracerebroventricularly in a dose of 100 microgram/mouse, has a marked anticonvulsive effect. Scopolamine in doses of 1, 10 and 50 mg/kg i. p. does not influence significantly the convulsive-seizure reactions, while spasmolytin inhibits them only in large doses (80 mg/kg weight). The inhibitory effect of GABA does not change significantly on the background of scopolamine, while spasmolytin in a dose of 50 mg/kg (and to a lesser extent 80 mg/kg) antagonizes the inhibitory effect of GABA. Arecoline in doses of 1 and 10 mg/kg inhibits to a certain extent the convulsive-seizure reactions, and in doses of 10 mg/kg it potentiates the effect of GABA. Physostigmine in doses of 0.1 and 0.5 mg/kg has no significant effect, while in a dose of 0.3 mg/kg its effect is inhibitory. On the background of the two higher physostigmine doses, however, the anticonvulsive effect of GABA is markedly decreased. The results show that changes in the functional activity level of the brain cholinergic systems lead to changes in the inhibitory effect of GABA on the convulsive reactivity. The mechanisms of these correlations are complex. However, the results are in support of the view that the balance between the different neurotransmitter systems in the brain and not a separate specifically responsible neurotransmitter system, are of decisive significance for the convulsive excitability and reactivity.

Aminobutyrates↗
PubMed1984

[Clinical, biochemical and electroencephalographic findings in children with a post-traumatic convulsive syndrome].

Clinical, biochemical and electroencephalographic examinations were carried out in 96 children with the post-traumatic convulsive syndrome. The time of the development of convulsive syndrome and its clinical manifestations are reviewed. In 75 children, convulsive attacks took the course of traumatic arachnoiditis; in 21 children, the clinical picture of the disease with consideration for the characteristics and frequency of convulsive seizures and changes in the character of the children was suggestive of epilepsy development. Possible pathogenetic mechanisms of the development of convulsive attacks in children who have had a closed craniocerebral injury are analyzed.

Adolescent↗
PubMed1982

Catecholamines and pinealectomy-induced convulsions in the gerbil (Meriones unguiculatus).

Within three hours after surgery nine out of ten pineal-ectomized gerbils will convulse; dopamine (DA) levels in the telencephalon of the gerbils do not change after pinealectomy (PX), however, norepinephrine (NE) concentrations decrease in the telencephalon from 1-12 hours after PX (Philo and Reiter, 1980). Administration of L-dihydroxyphenylalanine (L-DOPA, 50 mg/kg) will prevent the convulsions and maintain normal levels of norepinephrine. Administration of alpha-methyl-p-tyrosine (alpha MPT, 250 mg/kg), a tyrosine hydroxylase inhibitor, increases the number of convulsions. Injections of L-DOPA counter the facilitatory actions of alpha MPT on PX-induced convulsions. Studies with the monoamine oxidase inhibitor pargyline indicate a decrease in production of norepinephrine after PX in the gerbil. The diminished levels of neurotransmitter apparently facilitate the onset of convulsions caused by the epileptogenic stimulus of PX.

Animals↗
PubMed1980

[Convulsive syndrome activation in mice after administration of ADPT vaccine].

The experimental model of chemical convulsions allowed to establish the fact that the death of mice immunized with adsorbed DPT vaccine was accelerated, in comparison with the control group, as a result of convulsive fits caused by the injection of thiosemicarbazide. Immunization with adsorbed DPT vaccine was also found to induce a qualitative change in convulsive fits. The fact that an increase in convulsive activity occurs in the animals immunized with absorbed DPT vaccine may be related to the appearance of some forms of convulsive states in children during the postvaccination period.

Animals↗
PubMedDate not supplied

On some electrolytic and water metabolism modifications in rats susceptible to audiogenic convulsions.

Following our research in the relationship between mechanisms of blood transportation of sodium and cerebral excitability, we studied adult rats (males-180-230 gm), divided into two groups according to their level of excitability to noise: 1. Rats susceptible to audiogenic convulsions and, 2. Rats with normal response to acoustic stimulation. In the two groups we determined the following parameters: 1. mechanisms of blood transportation of sodium; 2. general free motor behaviour; oriented behaviour (to satisfy motivation for sodium or water); nature and intensity of motivation expressed as milliliters of liquid and grams of sodium consumed; 3. influence of the variable sodium intake on the renal elimination of sodium, potassium and water. Also the influence of the variable water intake on the renal elimination of water. Results obtained show that: cerebral hyperexcitability manifested as susceptibility to audiogenic convulsions is associated with several modifications expressed as follows: 1) Sodium transportation in blood serum occurs in a free state in rats susceptible to audiogenic convulsions, while in normal rats it occurs in a state of interaction with serum proteins; 2) In animals susceptible to audiogenic convulsions one can notice significant hypermotricity in the behaviour cage; 3) Hyperexcitable animals consume significantly more sodium chloride solution which they freely choose, in a motivational manner, than animals with a normal excitability; 4) Increased, motivational consumption of sodium chloride is associated with increased renal elimination of sodium in animals susceptible to audiogenic convulsions. Increased renal elimination of sodium is accompanied by increased elimination of water, therefore with the protection of renal concentration mechanisms; 5) If we take the Na/K ratio as an indicator for the function of the corticosuprarenal and represent it as a function of the sodium intake, the data presented show that ratio is greater in animals with cerebral hyperexcitability, which is in concordance with the data presented, also involving the mineralcorticoid hormones in this response, a similar picture to that of loading the body with sodium; 6) The data presented seem to advocate once more for the idea that normal cerebral excitability is compatible with the existence of mechanisms that transport sodium in a state of oligoenergetic interaction with blood proteins.

Acoustic Stimulation↗
PubMedDate not supplied

Convulsions in childhood shigellosis and antimicrobial resistance patterns of shigella isolates.

Drug resistance patterns of 68 shigella strains were investigated prospectively in Kayseri during a period of approximately two years. The resistance was highest with ampicillin (58.8%) followed by co-trimoxazole (50%) and ampicillin-sulbactam (13%). Only 2.8 percent of cases were resistant to gentamicin, and all serogroups were sensitive to ceftriaxone. We conclude that in children with severe shigellosis, treatment with ceftriaxone is effective and better than ampicillin and co-trimoxazole for obtaining a clinical cure. We followed 18 children who experienced convulsions associated with shigellosis. Only one child had a history of febrile convulsions, and two children had histories of convulsive disorders. The majority of the children had generalized, self-limited convulsions which lasted less than ten minutes. Due to the benign and self-limited nature of most of the convulsions, neither diagnostic procedures nor drug therapy are usually necessary. These measures should, however, be considered in complicated cases characterized by focal or prolonged seizures.

Adolescent↗
PubMed1998

[A case of convulsion induced by propofol].

A 71-year-old man was scheduled for laryngomicrosurgery under total intravenous anesthesia. Anesthesia was induced and maintained with propofol. Seven to eight minutes after induction of anesthesia, convulsion was observed first on his lower limbs and then on his all limbs and the head. This clonicotonic convulsion of a few minute duration lasted for 25 minutes. Later neurological examination revealed normal functions. Although the etiology of convulsion by propofol is controversial, the convulsion observed in our patient seems to be related to glycinergic as well as glutamate receptors. When we administer propofol to patients, we should be careful about the occurrence of convulsion.

Aged↗
PubMed1997

Convulsions in hemodialysis (HD) patients with elevated polymorphonuclear leukocyte elastase (PMNE) levels.

Eight hemodialysis (HD) patients with convulsions of unknown cause were monitored for serum levels of uremic toxins such as methylguanidine(MG), and polymorphonuclear leukocyte elastase (PMNE). Twenty HD patients without convulsions served as controls. In the convulsion group, MG and PMNE were high. In 2 patients, convulsions subsided after daily hemodiafiltration (HDF). Although PMNE was thought to be a mediator of injury in the present series, no significant correlation was found between PMNE and either neutrophil numbers or endotoxin levels. PMNE may indicate the over production of cytokines not associated with serious infection or septicemia. In patients with renal failure and complications of unknown cause, intensified dialysis therapy such as frequent HDF may be useful when combined with treatment of the underlying disease producing the toxins. PMNE measurement is useful in assessing the uremia caused by high cytokine levels and, together with methylguanidin (MG) serum levels, can indicate the severity of the convulsion.

Aged↗
PubMed1976

[Influence of diazepam and phenytoin on penicillin-induced cerebral convulsions (author's transl)].

The effects of diazepam and phenytoin on penicillin-induced EEG changes and convulsions were studied in 32 rabbits. EEG changes and convulsions were elicited by 2.4 g/kg benzylpenicillin i.v. over 50 min. The dosages of the anticonvulsants were 1, 5 and 10 mg of diazepam and 10, 20 and 30 mg/kg of phenytoin. The qualitative and semiquantitative evaluation of the electroencephalograms revealed no reduction of spike frequency or spike amplitude for either of the two drugs. However, in contrast to phenytoin, diazepam was highly effective in preventing the development of generalized convulsions. None of the 12 diazepam-treated animals developed a convulsion, whereas in most of the phenytoin treated animals and in most of the controls generalized convulsions appeared. The results suggest that diazepam should be used in the treatment of penicillin-encephalopathy.

Animals↗
PubMed1996

Thermodynamics and kinetics of t-butylbicyclophosphorothionate binding differentiate convulsant and depressant barbiturate stereoisomers acting via GABAA ionophores.

The temperature dependence of [35S]-t-butylbicyclophosphorothionate (TBPS) binding to the convulsant sites of the GABAA receptor complex was studied in membrane preparations of rat forebrain. Although specific [35S]TBPS binding was maximal around 20 degrees C, the rate constants of dissociation decreased monotonously between 37 degrees C and 2 degrees C. The displacing potencies of the convulsant S(+) enantiomer of 1-methyl-5-phenyl-5-propyl-barbituric acid (MPPB) (IC50 = 1250 +/- 30 microM) and the depressant R(-) MPPB (IC50 = 310 +/- 5 microM) did not show significant changes between 19 degrees C and 37 degrees C. Therefore barbiturate binding seems to be driven by entropic, rather than enthalpic changes. An excess of MPPB enantiomers elicited accelerated and polyphasic dissociations of [35S]TBPS as compared to the monophasic dissociation by TBPS. Arrhenius analysis was applied to the measurable initial rate constants of dissociation. Arrhenius plots were linear between 2 degrees C and 37 degrees C. Activation parameters were similar when [35S] TBPS dissociation was triggered by the convulsants TBPS and S(+) MPPB. It can be attributed to similar conformations of the closed ionophore complex. In contrast, the depressant R(-) MPPB strongly decreased the activation energy of TBPS dissociation from the open ionophore ternary complex. In whole-cell patch-clamp experiments R(-) MPPB, but not S(+) MPPB, elicited chloride currents in rat primary cortical cultures with an EC50 value of 560 +/- 30 microM and a Hill coefficient of 2.9 +/- 0.2. These currents were similar to those elicited by GABA and blocked by TBPS. A kinetic scheme is proposed for the dissociation of TBPS and to explain the different effects of MPPB enantiomers. Submillimolar R(-) MPPB is supposed to bind to (about three) barbiturate sites on GABAA-ionophores and to open them in a cooperative manner to result in a decreased activation energy for accelerated displacement of convulsant binding.

Animals↗
PubMedDate not supplied

The influence of the delta-sleep-inducing peptide on convulsive activity.

Data are presented in this paper on the influence of the delta-sleep-inducing peptide (DSIP) on various forms of convulsive activity. The capacity of this peptide to suppress convulsive activity in foci created in the cerebral cortex by the application of strychnine has been demonstrated in experiments on cats. It has been established in experiments on rats that DSIP determines the later development of the convulsive kindling syndrome, and prevents the development of convulsions in mice induced by bicuculline, picrotoxin, and corazol, but is devoid of such action in relation to thiosemicarbazide and strychnine. It was demonstrated that the anticonvulsant action of DSIP is associated with its influence on the reticular portion of the substantia nigra. The lowest level of this peptide itself has been discovered, in the reticular portion of the substantia nigra at the late stages of pharmacological kindling. It is inferred that DSIP may represent one of the factors of the endogenous control of the excitability of the brain.

Animals↗
PubMed1991

Exploring the pharmacology of the pro-convulsant effects of alpha 2-adrenoceptor antagonists in mice.

The effects of selective and specific alpha 2-adrenoceptor antagonists on electroshock seizure threshold in mice were investigated. Idazoxan, at low doses, efaroxan, RX811059 and RX821002 significantly lowered seizure threshold. The alpha 1-agonist St 587 and the beta-agonist isoprenaline were also pro-convulsant. On the other hand the alpha 2-agonists clonidine and UK 14,304 produced small increases in seizure threshold. Anticonvulsant effects were also produced by low doses of the noradrenaline uptake inhibitor desipramine. This compound increases levels of noradrenaline in the synaptic cleft which could subsequently act at post-synaptic alpha 2-adrenoceptors. The pro-convulsant action of alpha 2-adrenoceptor antagonists could be explained in terms of two mechanisms: a) blockade of endogenous noradrenaline which may normally exert a tonic anti-convulsant influence on seizure threshold, through post-synaptic alpha 2-receptors and/or b) increased activation of alpha 1- and beta-adrenoceptors by elevated synaptic noradrenaline levels following blockade of pre-synaptic alpha 2-adrenoceptors. Of the alpha 2-antagonists tested, idazoxan was unusual in that high doses were not pro-convulsant; this difference may be explained by alpha 1-adrenoceptor mediated actions or be related to its recently described affinity at a non-adrenoceptor site--a function for which is currently unknown.

Adrenergic alpha-Agonists↗