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PubMed1985

Changes in responsiveness to mu and kappa opiates following a series of convulsions.

After a series of seven electroconvulsive shocks, mice (C57BL/6J) showed a marked change in their response to opiates. Although very large doses of mu agonists induce convulsions in normal control mice, our evidence indicated that this was accomplished through nonopiate mechanisms: they could not be blocked by naltrexone and the pattern of drug potencies (codeine greater than morphine greater than levorphanol) was not consistent with an opiate response. In contrast, after electroconvulsive shock small doses of mu agonists induced convulsions that could be blocked by naltrexone and the pattern of drug potency (levorphanol greater than morphine greater than codeine) was consistent with an opiate mechanism. Kappa drugs, on the other hand, produced convulsions in both control and ECS animals, although there was an enhanced responsiveness in the latter. Furthermore, the convulsions produced by kappa drugs were blocked by naltrexone and showed stereoselectivity in both control and ECS animals. The changes in responsiveness to mu and kappa opiates cannot be explained on the basis of a general increase in seizure susceptibility, as sensitivity to the nonopiate convulsant, strychnine, was not enhanced after electroconvulsive shock. The results point to a qualitative change in response to mu agonists after electroconvulsive shock, but only a change in sensitivity to kappa agonists.

Animals↗
PubMed1986

Convulsions may alter the specificity of kappa-opiate receptors.

Morphine, a mu-opiate agonist, and ethylketazocine, a kappa-opiate agonist, produce distinct behavioral, pharmacologic, and biochemical effects. In the mouse, large doses of morphine produce convulsions that are usually lethal and that cannot be blocked by naltrexone, whereas ethylketazocine produces nonlethal clonic convulsions that can be blocked by naltrexone. Moreover, mice made tolerant to morphine failed to show cross-tolerance to ethylketazocine, suggesting that the convulsions induced by these drugs are not mediated via a common opioid mechanism. Following a series of electroconvulsive shocks, both morphine and ethylketazocine produced clonic convulsions that were not lethal and that could be blocked by naltrexone. Furthermore, electroconvulsive shock-treated animals made tolerant to morphine-induced convulsions showed cross-tolerance to ethylketazocine. These data suggest that electroconvulsive shock may alter kappa-opioid systems in such a way as to allow mu-agonists to be functional at these sites.

Animals↗
PubMed1995

Value of brain CT scan in children with febrile convulsions.

Studies specifically dealing with the value of brain CT scans in different types of febrile convulsion are lacking when compared to the large amount of studies on other favorable convulsive disorders. This study is correlation study between children who presented with febrile convulsions (n = 38) and the results of their brain CT scans. Twenty four patients had risk factors for subsequent epilepsy (group A), 3 of them had abnormal CT scans in the form of mild diffuse brain atrophy, and all 3 patients were found to have prior neurodevelopmental deficits. The other 14 patients did not have such risk factors (group B) and had normal brain CT scans. Despite the small size of the study, the results are unequivocal, and it can be concluded that brain CT scan is not indicated in the management of simple or complex febrile convulsions. Brain CT may be justifiable, but may not be clinically useful in the management of febrile convulsion patients with prior neurodevelopmental deficits.

Brain↗
PubMed1989

Interaction between GABAergic anticonvulsants and the NMDA receptor antagonist MK 801 against MES- and picrotoxin-induced convulsions in rats.

The interaction between GABAergic (barbiturates, diazepam, ethanol) and other (phenytoin) anticonvulsants and the N-methyl-D-aspartate (NMDA) receptor antagonist MK 801 in protecting rats against maximal electroshock (MES)- and picrotoxin-induced (10 mg/kg) convulsions was studied. MK 801 (0.1 to 5 mg/kg) showed anticonvulsant responses against MES-induced convulsions in a dose dependent manner, higher doses showing severe muscle relaxation, motor incoordination, and anticonvulsant action. It also produced stereotypic head movement, circling behavior, and affected locomotion. When subanticonvulsant dose (1 mg/kg) of MK 801 was simultaneously administered with subprotective doses of GABAergic anticonvulsants, it significantly potentiated the effects of barbiturates, as compared to other agents. At 1 mg/kg, MK 801 did not offer protection against tonic convulsions though protected (100%) the animals from mortality due to picrotoxin-induced convulsions. It potentiated the effect of a subprotective dose (5 mg/kg) of pentobarbital, but not of diazepam, against tonic convulsions. However, no mortality was observed in either group. The antiglutamate action of barbiturates, particularly that of pentobarbital, may contribute to the observed potentiating response between pentobarbital and MK 801.

Animals↗
PubMed1995

PK 11195 reduces the brain availability of lindane in rats and the convulsions induced by this neurotoxic agent.

The effect of pretreatment with PK 11195, a ligand of the 'peripheral-type' benzodiazepine receptor (PBR), on convulsions induced by lindane (gamma-hexachlorocyclohexane, gamma-HCH) in rats was examined, to determine whether the mechanism of this convulsant activity may be mediated through the PBR. PK 11195 elicited a protective effect against the convulsant activity of orally administered lindane. It reduced the frequency of animals exhibiting convulsions and delayed the time to onset of these seizures. The concentration of lindane in the brain was found to be significantly lower in PK 11195 pretreated rats and a high correlation between blood and brain lindane concentrations was obtained. When similar experiments were repeated with alpha-HCH, a non-convulsant isomer of HCH, brain and blood concentrations were again found to be significantly reduced in PK 11195 pretreated animals. We conclude that the 'anticonvulsant' action of PK 11195 was not due to an interaction of PK 11195 and lindane on common CNS target sites, but by an action of PK 11195 on the gastrointestinal tract of the animal, delaying the absorption of lindane into the bloodstream.

Animals↗
PubMed1979

Possible involvement of brainstem norepinephrine in pentylenetetrazol convulsions in rats.

The thresholds of twitch and clonic convulsion induced by intravenous infusion of pentylenetetrazol (PTZ) were measured in rats treated with 6-hydroxydopamine (6-OHDA). In adult rats, intraventricularly applied 6-OHDA increased susceptibility to PTZ convulsions and decreased norepinephrine (NE) contents of the cortex, hypothalamus and brainstem. When 6-OHDA was applied intraventricularly at 8 days after birth, PTZ convulsion susceptibility was slightly decreased and brainstem NE content was significantly increased. However, the effects of 6-OHDA given at 20 days after birth were similar to those observed in adults. Significant decrease of cortical and hypothalamic NE contents, but no change in PTZ convulsion susceptibility, occurred following 6-OHDA injections into the dorsal and ventral NE bundles. These results suggest that the brainstem NE neurons play an inhibitory role on the development of PTZ convulsions.

Animals↗
PubMed1982

Dissociation between behavioral and electrocortical manifestations of electroshock convulsions during the action of an anticonvulsive drug.

It was shown that 5-OH-5-ethyl-5-phenyl-butyramide (formerly called 5-ethyl-5-phenyl-2-pyrrolidinone) significantly reduces convulsions induced by electroshock in rats, and by drugs in mice. We are reporting a dissociation between the effects of this drug on the behavioral manifestations of electroshock and on the electrocortical afterdischarges. At 50 mg/kg, the drug reduced greatly the duration of the tonic phase of muscular convulsions, but had little or no effect on their total duration or on the electrocortical afterdischarges. At 100-150 mg/kg, the effect on the tonic phase was only slightly larger, but the total duration of behavioral convulsions and the intensity of electrocortical afterdischarges were substantially reduced, while the duration of the latter was either slightly reduce or increased. Only 200 mg/kg, which had clear depressant effects, produced a complete disappearance of all manifestations of electroshock convulsions. It can be concluded that this drug acts more strongly on subcortical structures that transmit cortical convulsions to the muscles, than on the cortical mechanisms that generate electrocortical afterdischarges.

Animals↗
PubMed1982

Age-dependent reduction in maximum electroshock convulsive threshold associated with decreased concentrations of brain monoamines.

This study investigated modification of the tonic convulsive threshold to maximum electroshock in 15- and 30 day old rats treated with drugs which reduce steady-state concentrations of monoamines. On postnatal day 15, reduction of central catecholamine concentrations by 6-hydroxydopamine or of central serotonin concentrations by 5,7-dihydroxytryptamine or p-chloroamphetamine did not alter the tonic convulsive threshold. However, simultaneous depletion of catecholamines and serotonin by tetrabenazine was associated with a significant decrease in the tonic threshold. This effect could be reversed partially by simultaneous administration of the catecholamine and serotonin precursors, L-dihydroxyphenylalanine and 5-hydroxytryptophan, respectively. On postnatal day 30, reduction of brain serotonin concentration, but not catecholamine concentrations, was associated with a significant decrease of the tonic convulsive threshold. In a previous study, in which 7-8 day old rats were used, a tetrabenazine-induced decrease in the tonic convulsive threshold prevented by L-dihydroxyphenylalanine but not 5-hydroxytryptophan. Furthermore, intracisternal 6-hydroxydopamine, but not 5,7-dihydroxyhyptamine, decreased the threshold on postnatal day 8. Therefore, the results of the present day study involving 15- and 30 day old rats, together with the earlier findings in 7-8 day old rats, [28] suggest an apparent developmental transition from catecholaminergic to serotonergic dominance in regulation of the tonic convulsive threshold during the first postnatal month.

5,7-Dihydroxytryptamine↗
PubMed1986

Nicotine-induced convulsions in cats and central nicotinic receptors.

The effects were investigated of intracerebroventricular (ICV) injections in the cat of ganglionic blocking agents, antimuscarinic drugs, alpha and beta adrenergic blocking substances, dopamine antagonists, an antihistamine, reserpine and a 5-hydroxytryptamine antagonist as well as the inhibitors of catecholamines, 5-hydroxytryptamine and acetylcholine synthesis upon convulsions produced by nicotine, which was similarly injected. Mecamylamine and hexamethonium but not atropine, scopolamine, yohimbine, phenoxybenzamine, tolazoline, propranolol, practolol, chlorpromazine, haloperidol, antazoline and methysergide abolished the convulsions evoked by nicotine. Furthermore, reserpine, but not 6-hydroxydopamine, as well as 5,6-dihydroxytryptamine and hemicholinium blocked the convulsions caused by nicotine. It appears, therefore, that the convulsions produced by nicotine are mediated through central nicotinic receptors. However, the depressed catecholaminergic, 5-hydroxytryptaminergic and histaminergic mechanisms induced by reserpine can also suppress the convulsions evoked by nicotine.

5,6-Dihydroxytryptamine↗
PubMed1987

Effect of pentylenetetrazol-induced convulsions on the development and expression of limbic kindled seizures.

Male Long-Evans rats experienced three convulsions induced by intravenously administered pentylenetetrazol (PTZ) and were then kindled by electrical stimulation of the olfactory bulb or amygdala. Pretreatment with PTZ did not alter the rate of kindling in either site but did enhance the expression of kindled seizures once generalization had occurred (PTZ-treated animals had significantly longer motor seizures, measured by clonus duration, than did saline-treated controls). This suggests that PTZ-induced convulsions have selective effects on areas of the brain that are involved in the expression of the motor seizure. In addition, rats treated with PTZ after kindling had convulsions that were significantly longer in duration than any of their three pre-kindling convulsions, indicating that kindling produced an increased sensitivity to PTZ's convulsant effects. Comparison of this experiment with previous research suggests that the ability of a drug treatment to generate a kindling-like effect is related to the pattern of seizure activity that it produces.

Amygdala↗
PubMed1991

The effect of ofloxacin and ciprofloxacin on pentylenetetrazol-induced convulsions in mice.

There have been several reports that convulsions, although rare, occur in patients who received fluoroquinolones. In this study, conducted for the evaluation of the convulsant action of fluoroquinolones, the effect of ofloxacin and ciprofloxacin on pentylenetetrazol-induced convulsions were investigated in mice. Mice were pretreated intraperitoneally (IP) with saline, ofloxacin (20 or 80 mg/kg) or ciprofloxacin (20 or 80 mg/kg) 30 minutes before subcutaneous (SC) administration of pentylenetetrazol (40 or 60 mg/kg). In another experiment, diazepam (5 mg/kg) was injected (IP) in mice alone or in combination with ofloxacin (80 mg/kg) 30 minutes before pentylenetetrazol (40 mg/kg) administration (SC). In each experiment mice were observed over the following hour for the incidence and onset of clonic convulsions. Results showed that both doses of ofloxacin increased the incidence of clonic convulsions induced by 40 mg/kg pentylenetetrazol. This effect, however was only significant in the higher dose and inhibited by diazepam. On the other hand, a similar proconvulsant effect by ciprofloxacin could not be demonstrated.

Animals↗
PubMed1987

Effect of pentylenetetrazol-induced convulsions on somatostatin-like immunoreactivity in rat cerebrospinal fluid.

Somatostatin is a neuropeptide that in several experimental models of epilepsy has been suggested to modulate epileptic activity. The purpose of the present study was to investigate the role of somatostatin in seizure phenomena. We measured the somatostatin-like immunoreactivity (SLI) by radioimmunoassay of the cisternal CSF of rats. A polyethylene cannula had before-hand been inserted into the cisterna magna. Thereafter seizures were induced by pentylenetetrazol (PTZ). The nonconvulsive group of rats received a single subconvulsive dose of PTZ (30 mg/kg, i.p.). This group of rats exhibited only clonic jerks but not generalized clonic-tonic convulsion (GC). The CSF samples were taken 2 and 10 minutes after the jerks began. The convulsive group of rats received a single convulsive dose of PTZ (50 mg/kg, i.p.), and each of those animals had GC. From those rats the CSF samples were collected 5, 30, and 60 minutes and 4 and 24 h after the GC began. The values were compared with the SLI levels in controls, from which CSF was collected 10 minutes after injection of 0.9% NaCl. In the convulsion group the SLI levels increased 241% (p less than 0.01) five minutes after GC and returned to control level in 30 minutes. In the nonconvulsion group, where the rats expressed only jerks but not GC, SLI levels remained constant. These data suggest that somatostatin is released into CSF after the generalized clonic-tonic phase of the PTZ-induced convulsion.

Animals↗
PubMed1980

A theory of convulsive therapy in endogenous depression: significance of hypothalamic functions.

The repeated induction of seizures (convulsive therapy) relieves the symptoms of severe depressive mood disorders, particularly those accompanied by vegetative symptoms. Neuroendocrine abnormalities characterize patients with endogenous depression, and the abnormalities are reversed by convulsive therapy. Tests of neuroendocrine functions provide criteria for the classification of such cases, and probably will be useful in defining suitable cases for convulsive therapy. We postulate that the antidepressant efficacy of convulsive therapy results from the increased release and more widespread cerebral distribution of hypothalamic peptides with behavioral effects. Such a hypothesis provides a basis for clinical trials of centrally active peptides in cases of endogenous depression, and for studies of neuroendocrine functions as predictors of outcome in convulsive therapy.

Adrenocorticotropic Hormone↗
PubMed1990

Protection against cyanide-induced convulsions with alpha-ketoglutarate.

Protection against convulsions induced by cyanide was observed after treatment with alpha-ketoglutarate, either alone or in combination with sodium thiosulfate, a classical antagonist for cyanide intoxication. However, sodium thiosulfate alone did not protect against cyanide (30 mg/kg)-induced convulsions. gamma-Aminobutyric acid (GABA) levels in brain were decreased by 31% in KCN-treated mice exhibiting convulsions. The combined administration of alpha-ketoglutarate and sodium thiosulfate completely abolished the decrease of GABA levels induced by cyanide. Furthermore, sodium thiosulfate alone also completely abolished the decrease of GABA levels. These results suggest that the depletion of brain GABA levels may not directly contribute to the development of convulsions induced by cyanide. On the other hand, cyanide increased calcium levels by 32% in brain crude mitochondrial fractions in mice with convulsions. The increased calcium levels were completely abolished by the combined administration of alpha-ketoglutarate and sodium thiosulfate, but not affected by sodium thiosulfate alone. These findings support the hypothesis proposed by Johnson et al. (Toxicol. Appl. Pharmacol., 84 (1986) 464) and Robinson et al. (Toxicology, 35 (1985) 59) that calcium may play an important role in mediating cyanide neurotoxicity.

Animals↗
PubMed1992

Protective effect of NG-nitro-L-arginine (N5-[imino(nitroamino)methyl]-L-ornithine) against cyanide-induced convulsions in mice.

The effects of NG-nitro-L-arginine (NNA; an inhibitor of the oxidative L-arginine pathway) on convulsions induced by cyanide were investigated in mice. NNA prevented cyanide-induced convulsions in a dose-dependent manner. Furthermore, the inhibitory effect against convulsions induced by cyanide with NNA was abolished by pretreatment of L-arginine. However, NNA did not change blood cyanide levels in mice 5 min after injection of potassium cyanide. Since NNA prevents against oxidative L-arginine pathway-dependent guanylate cyclase activation in intact cells, it was suggested that the protection against cyanide-induced convulsions with NNA may be due to the inhibition of guanylate cyclase. In support, methylene blue, an inhibitor of guanylate cyclase, elicited a similar inhibition against convulsions induced by cyanide.

Animals↗
PubMed1990

Noradrenergic involvement in pinealectomy induced convulsions in gerbils.

Gerbils treated with various noradrenergic compounds were pinealectomized (PINX) or sham-operated (SHAM) and observed for convulsive activity. Although declines in cortical and hypothalamic norepinephrine content were found after alpha-methylparatyrosine (alpha MPT) or PINX, treatment with alpha MPT did not produce convulsions in SHAM gerbils or in gerbils which were PINX one week earlier. Likewise, alpha MPT did not increase the number or severity of convulsions observed in acutely PINX gerbils. Treatment with propranolol or isoproterenol did not have any effect on convulsive activity of PINX gerbils, except that isoproterenol increased the excitability of all the gerbils. In conclusion, reducing catecholamine content or modifying beta-noradrenergic receptor activity was not able to alter the convulsive activity which occurs after acute PINX.

Animals↗
PubMed1984

Brain cyclic nucleotides and the development of convulsion, with reference to the anticonvulsant activity of diazepam.

Dibutyryl cyclic GMP (DbcGMP) or dibutyryl cyclic AMP (DbcAMP) given to mice intracerebroventricularly in a dose of 200 or 400 nmol/head produced electroencephalographic and electromyographic changes corresponding to twitches, and clonic and tonic convulsions. Lower doses of DbcGMP or DbcAMP facilitated the pentylenetetrazol-induced clonic and tonic convulsions. Diazepam given intraperitoneally in a dose of 0.5 mg/kg suppressed clonic and tonic convulsions induced by DbcGMP and DbcAMP, but the twitches were not suppressed. These results suggest that these nucleotides lower the threshold for electrical discharges related to convulsion and facilitate the propagation of convulsion. Diazepam suppresses this facilitation.

Animals↗
PubMed1984

Monosodium-L-glutamate-induced convulsions--I. Differences in seizure pattern and duration of effect as a function of age in rats.

Convulsive activity in 3, 10, 60 and 180-day old Sprague-Dawley rats was studied following the i.p. administration of 4 mg g-1 of commercial MSG. The latency period increased with the age of the animals while the duration of the convulsive period was longer in younger animals and shorter in 60-day old rats. Convulsions were predominantly tonic in 3 and 10-day old rats, tonic-clonic in 60-day old rats, and predominantly clonic in 180-day old animals. The severity of the convulsions and death incidence increased progressively with age. Animals injected either with sodium chloride equimolar to MSG or physiological saline solution showed no convulsive activity. The effects of MSG without trace metals were no different from those produced by commercial MSG.

Aging↗