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PubMed1978

Increase in vivo of unesterified fatty acids, prostaglandin F2 alpha but not thromboxane B2 in rat brain during drug induced convulsions.

The amount of free arachidonic acid and prostaglandin F2 alpha in rat cerebral hemispheres was increased following convulsions induced by carbachol and metrazol. The level of thromboxane B2 was not affected and prostaglandin endoperoxides could only be "trapped" after a very short convulsive period. Unesterified fatty acid levels at 2 minutes post-mortem were decreased by 50% in the cerebral hemispheres of phenytoin treated rats. Under the same conditions, phenobarbital and diazepam had little effect on the levels of free fatty acids in rat brain.

Animals↗
PubMed1979

Effects of some anti-epileptic, neuroleptic and gabaminergic drugs on convulsions induced by D,L-allylglycine.

The antagonism of various seizure and time-related components of the convulsions resulting after IV injection of D,L-allylglycine into male Wistar rats were assessed in a standard test procedure. Trimethadione and ethosuximide did not antagonize the seizure components, whereas clonazepam, phenobarbital, diphenylhydantoin, primidone, valproate sodium, aminoxyacetic acid, etomidate, acetazolamide, flunarizine, pipamperone and baclofen did. The allylglycine test may thus represent a relatively specific method of differentiating between drugs effective against partial or generalized convulsive seizures from those effective against absence seizures. The neuroleptics haloperidol and pimozide were completely inactive in contrast to their reported antagonism of bicuculine seizures. The spectra of the active substances are discussed with respect to Principal Component and Cluster Analysis. Noteworthy are the similarities between baclofen and etomidate; between aminoxyacetic acid, phenobarbital and valproate sodium; and between diphenylhydantoin and flunarizine.

Allylglycine↗
PubMed1985

Convulsive thresholds and severity and the anticonvulsant effect of phenobarbital and phenytoin in adult rats administered 6-hydroxydopamine or 5,7-dihydroxytryptamine during postnatal development.

Rats were administered intracisternal 6-hydroxydopamine (6-OHDA) or 5,7-dihydroxytryptamine (5,7-DHT) within the first three postnatal days, at several ages centered on the third postnatal week or on postnatal day 180. When the rats were 210-days-old, maximal electroshock convulsive thresholds and responses and the anticonvulsant effect of phenobarbital and phenytoin were determined. All 5,7-DHT treatments resulted in an approximate 21% decrease in the tonic convulsive threshold and increased the incidence of tonic hindlimb extension (HLE). Only the 5,7-DHT treatment at 180 days was associated with a more severe HLE response (shortened onset and prolonged duration). All neonatal 6-OHDA treatments were associated with no change in the tonic threshold, but increased the incidence and severity of HLE. The latter effect depended on the postnatal age of 6-OHDA-treatment: treatment at postnatal days 14 and 15 resulted in the greatest increase in severity (52% decrease in onset and 48% increase in duration). The 6-OHDA treatment to 180-day-old rats increased the incidence and duration of HLE but had no influence on the tonic threshold or onset of extension. The effectiveness of both phenobarbital and phenytoin to block HLE was variably decreased by all neurotoxin treatments. The results suggest that interference with the postnatal maturation of monoaminergic influences on seizure processes can have a long-lasting influence on the ability of the brain to limit the generation and spread of seizure activity and on the effectiveness of anticonvulsant drugs.

5,7-Dihydroxytryptamine↗
PubMed1986

Potentiation of the propunishment, but not the convulsant action of the beta-carboline DMCM by naltrexone.

The ability of naltrexone (NTX) to potentiate the propunishment and convulsant properties of DMCM, a benzodiazepine receptor inverse agonist, was studied in mice. Doses (0.39 and 1.56 mg/kg) of DMCM which were below the threshold for propunishment effects showed a marked ability to enhance the suppressive effects of punishment on locomotor activity in the presence of naltrexone (0.5 or 2.5 mg/kg IP), higher doses of DMCM and NTX (3.13 mg/kg and 10 mg/kg, respectively) had a depressant effect of their own on both punished and unpunished locomotor activity. DMCM given alone induced clonic convulsions (ED50: 5.7 mg/kg IP) but this activity was not changed in the presence of naltrexone. These results suggest an interaction of BZ receptors and opioid systems in the control of anxiety.

Animals↗
PubMed1986

The inhibitory effect of endogenous convulsants quinolinic acid and kynurenine on the pentobarbital stimulation of [3H]flunitrazepam binding.

The metabolites of tryptophan-kynurenines with convulsant action quinolinic acid (QA) and l-kynurenine (l-KYN) antagonized the enhancing effect of pentobarbital (1 mM) on [3H]Flunitrazepam binding. IC50 for l-KYN were 35.9 +/- 14.8 microM and for QA 31.2 +/- 7.2 microM respectively. The inhibitory effect of KYN was stereoselective: IC50 of l-isomer was about two fold lower than IC50 of racemic form, d,l-KYN. Scatchard analysis revealed that inhibitory effect of QA and l-KYN on [3H]Flunitrazepam binding enhanced by pentobarbital is due to the decrease in affinity of benzodiazepine receptors. On the basis of these data it is proposed that QA and l-KYN possess their convulsant action interacting with barbiturate/picrotoxin sensitive sites of GABA-benzodiazepine-barbiturate complex.

Animals↗
PubMed1987

Differential convulsive susceptibility of high-activity and low-activity selected mice in response to GABA antagonists.

Lines of mice selectively-bred for High and Low-Activity in an open-field maze were tested for seizure susceptibility to three analeptics: flurothyl, pentylenetetrazol and bicuculline. The major finding was that two replicate High-Activity lines were more susceptible to myoclonic convulsions but less susceptible to clonic convulsions than their respective replicate Low-Activity lines. The major exception to this finding was that the High and Low-Activity lines did not differ for bicuculline-induced clonus although females tended to conform to the general pattern. These results are interesting because they demonstrate that diametrically opposite susceptibility to myoclonus and clonus is not an isolated phenomenon. Similar seizure susceptibility patterns and activity differences have also been reported for the Long-Sleep and Short-Sleep selectively-bred mouse lines. Further, since the progenitor population of the High-Activity and Low-Activity lines were developed from strains that were also part of the progenitor population of the Long-Sleep and Short-Sleep lines, it is hypothesized that some of the same alleles underwent selection in both selective-breeding programs.

Animals↗
PubMed1988

Prevention of the convulsant and hyperalgesic action of strychnine by intrathecal glycine and related amino acids.

Intrathecal administration of 25 micrograms strychnine induced consistent sensory and motor behavioral events in rats. Sensory events included scratching and biting the lower half of the body, spontaneous vocalizations and skin hyperalgesia, evidenced by vocalization and reflex scratching in response to stimulation with a 5.5 g von Frey fiber. This mild stimulus failed to elicit vocalizations in the preinjection condition. Strychnine induced two types of motor seizures: (1) falling over with tail whipping and (2) convulsions. The effect of equimolar doses of glycine (G) and some related amino acids: beta-alanine (A), taurine (T) and betaine (B) on the strychnine syndrome was tested by administering them (intrathecal route) along with strychnine. T and G but not B significantly decreased most of the sensory events triggered by strychnine. All amino acids significantly decreased the incidence and duration of convulsions; T and B abolished them. A decreased vocalizations and skin hyperalgesia but synergized with strychnine to facilitate scratching and self biting. These results are consistent with findings that G, A and T displace strychnine from its binding sites in the CNS.

Alanine↗
PubMed1989

RO15-4513 but not FG-7142 reverses anticonvulsant effects of ethanol against bicuculline- and picrotoxin-induced convulsions in rats.

The reversal of anticonvulsant effect of ethanol against chemoconvulsions by RO15-4513 was investigated in rats as this novel imidazobenzodiazepine (ethyl-8 azido-5, 6-dihydro-5-methyl-6-Oxo-4H-imidazo [1,5a] [1,4] benzodiazepine-3-carboxylate) is reported to antagonize the acute behavioral and biochemical effects of ethanol in animals. Reversal of ethanol effects on onset of myoclonic jerks, tonic extensor phase, mortality time and percent protection against mortality were compared with not only other anticonvulsant pentobarbital but also with another inverse agonist FG-7142. Pretreatment with RO15-4513 (4 mg/kg) reversed the protective effect of ethanol against bicuculline-induced tonic extensor phase and mortality (87%). This response was sensitive to reversal by RO15-1788 (10 mg/kg). However, onset of myoclonic jerks and duration of clonus were not significantly altered. It also reversed the effect against picrotoxin but the reversal against mortality was up to 50%. As compared to ethanol, RO15-4513 reversed partially the protective effect of pentobarbital against bicuculline- and picrotoxin-induced convulsions. FG-7142 failed to reverse the protective effect of ethanol and pentobarbital against bicuculline-induced tonic extensor phase although it reversed the effect against onset and mortality. It had no effect on the protective effect against picrotoxin-induced convulsions. Both RO15-4513 and FG-7142 possessed proconvulsant effects against bicuculline but not against picrotoxin. These observations suggest that RO15-4513 has a more preferential action against ethanol effects as compared to the other inverse agonist.

Affinity Labels↗
PubMed1992

Alarm substance induces convulsions in imipramine-treated rats.

Male rats were injected with imipramine (0-30 mg/kg) and subsequently tested in the forced-swim test in either fresh water or water soiled by other rats, which presumably contains an alarm substance. Imipramine did not affect the behavior of rats in fresh water. More than half the animals given the combination of imipramine (30 mg/kg) and stress from alarm substance had clonic convulsions. Adrenalectomy did not affect this relationship. This is the first study demonstrating the potential of an alarm substance for inducing convulsions.

Adrenal Glands↗
PubMed1993

Effects of water immersion stress on convulsions induced by pentylenetetrazol.

Increasing durations of water immersion stress were associated with increased serum corticosterone levels, decreased severity of pentylenetetrazol-induced convulsions, and increased latencies to convulse in rats. The results were interpreted in terms of the effects of stress and pentylenetetrazol's actions on GABAergic mechanisms.

Animals↗
PubMed1993

Effect of an adenosine A1 agonist injected into substantia nigra on kindling of epileptic seizures and convulsion duration.

The substantia nigra pars reticulata (SNr) has been reported to be critically involved in the development and propagation of epileptic seizures, while extracellular adenosine appears to be important for making seizures stop. In the present study, an adenosine A1 receptor agonist [N6-cyclohexyladenosine (CHA); 2.0 nmol/side, or vehicle] was injected bilaterally into the SNr shortly before each of the first five of a series of daily kindling stimuli delivered to the rat amygdala. Injections did not affect the acquisition of kindled afterdischarges or the rate at which seizures developed over subsequent kindling sessions, but convulsions occurring 48-72 h after treatment were significantly shortened. Thus, purinergic mechanisms in the SNr do not appear to be specifically involved in the acquisition of kindled seizures but may contribute to a postictal inhibitory process that shortens the convulsive component.

Adenosine↗
PubMed1985

Effects of morphine and naloxone on pilocarpine-induced convulsions in rats.

Systemic administration of morphine hydrochloride (MF; 5-80 mg/kg; i.p.) in rats enhanced the epileptogenic potential of pilocarpine hydrochloride (PIL) in a dose-dependent manner. PIL, 100 mg/kg; i.p., which did not result in convulsions by itself, produced sustained limbic seizures and epileptic brain damage in MF-pretreated rats. MF-induced enhancement of PIL neurotoxicity was blocked by naloxone hydrochloride (NAL; 2 and 10 mg/kg; i.p.). Administration of NAL (2-20 mg/kg) prior to PIL in the dose of 380 mg/kg moderately decreased the incidence of convulsions, brain damage and lethal toxicity produced by this agent. These results support the hypothesis that opiate mechanisms are involved in the maintenance of the threshold for propagation of seizure activity within limbic circuits.

Animals↗
PubMed1994

Day-night variations in melatonin secretion by the pineal gland during febrile and epileptic convulsions in children.

The pineal gland is a complex neuroendocrine organ with pronounced effects on central nervous system activity. Because previous studies in animals and humans have suggested an anticonvulsant role for the pineal hormone melatonin, we studied the day-night variations in plasma melatonin in normal children and children with febrile or epileptic convulsions. We found significant changes in day-night melatonin levels during convulsions, consistent with the hypothesis that melatonin has an inhibitory function on central nervous system activity.

Brain↗
PubMed1987

Monosodium L-glutamate lesions reduce susceptibility to hypoglycemic feeding and convulsions.

Lesions of the circumventricular regions of the brain induced by neonatal administration of monosodium L-glutamate (MSG) are associated with chronic hypophagia and deficits in response to a variety of feeding challenges. These deficits occur despite the fact that, at least at high doses, MSG can produce obesity. The cause of the feeding deficits in MSG-treated animals is unknown. However, the circumventricular regions that are damaged by MSG contain high concentrations of insulin binding sites. In order to determine whether the MSG lesion alters responsiveness to circulating insulin, we have investigated the response of non-obese MSG-treated mice to doses of exogenous insulin designed either to stimulate feeding or to induce hypoglycemic convulsions. We report that MSG produces a dose-related decrease in hypoglycemic convulsions and glucoprivic feeding, suggesting that a loss in sensitivity to insulin may contribute to the MSG syndrome.

Animals↗
PubMed1995

Effects of single cyclosporin A pretreatment on pentylenetetrazol-induced convulsion and on TRE-binding activity in the rat brain.

Using electrophoretic mobility-shift assay (EMSA), we examined changes in DNA-binding activities of transcriptional factor-activated protein-1 (AP-1), which is a Fos-Jun protein complex, onto its responsive element TRE in the hippocampus and amygdaloid nucleus of rats stimulated with pentylenetetrazol (PTZ) injection, and also investigated the effects of a single administration of the immunosuppressant cyclosporin A (CsA). In EMSA with nuclear extracts from the rat brain, the TRE-binding activity of AP-1 in the hippocampus and amygdaloid nucleus markedly increased 2 h after the PTZ injection (75 mg/kg, i.p.). These PTZ-induced increases of the TRE-binding protein in these regions were completely suppressed, by pretreatment with CsA (5 mg/kg, s.c.) 1 h before the PTZ injection. In addition, the administration of CsA significantly ameliorated PTZ-induced convulsion. This therapeutic effect of single CsA pretreatment may be based, in part, on the effects on the TRE-binding activity of AP-1 in the brain. Since single pretreatment of CsA in the present study had no effect on the PTZ-induced induction of c-fos mRNA, c-jun mRNA, Fos protein nor Jun protein, the inhibitory effects of single CsA administration on PTZ-induced TRE-binding activity in the brain may be related to the effects of CsA on AP-1 itself. These results suggest that an immune response via activation of transcriptional factor in the brain tissue is involved in the convulsion.

Amygdala↗
PubMed1994

The effect of corticosterone in rats submitted to the elevated plus-maze and to to pentylenetetrazol-induced convulsions.

1. In order to examine the effects of corticosterone in the anxiety response, the effect of acute, subchronic and chronic corticosterone (CORT) administration were studied using two animal models to study anxiolytic effects of drugs: the elevated plus-maze and the blockade of pentylenetetrazol (PTZ)-induced clonic convulsion. 2. The results obtained with the plus-maze showed an increase in the percentage of open arm entries and time spent in the open arms after acute treatment with the CORT. These results may be interpreted as an anxiolytic effect of corticosterone. Three days of vehicle treatment followed by an acute CORT administration, produced results that should also indicate anxiolytic effect of the corticosteroid. No effect was seen after 14 days of vehicle treatment followed by an acute CORT injection. Subchronic or chronic CORT treatment did not produce results different from controls. CORT treatment did not affect the PTZ-induced clonic convulsion. 3. In conclusion these results suggest that the acute anxiolytic effect observed in the elevated plus-maze did not occur after repeated CORT administration or mild stressors. Moreover they also suggest that the anxiolytic effect did not involve GABA mechanisms.

Administration, Cutaneous↗
PubMed1991

Effect of tyrosine on the potentiation by aspartame and phenylalanine of metrazol-induced convulsions in rats.

Male rats were treated by oral intubation with tyrosine (Tyr), at doses of 0.5 and 1.0 g/kg body weight, alone or together with 1 g aspartame (APM)/kg body weight, or an equivalent dose of phenylalanine (Phe; 0.5 g/kg body weight); the effects on seizures induced by an effective dose of metrazol (ED50) were observed. Tyr (0.5 g/kg body weight) had a protective effect against the Phe-potentiation of metrazol-induced clonic-tonic convulsions. At the same dose Tyr had no effect on the seizure-promoting activity of APM, but at 1 g/kg it reduced the proconvulsant potential of the sweetener. Analysis of the brain and plasma amino acid concentrations indicated that the Tyr to Phe ratio tended to be enhanced in Tyr-Phe treated rats compared with those treated with Phe alone. This ratio remained essentially constant in the brain of APM-treated rats, compared with those treated with APM plus 1 g Tyr/kg body weight, whereas an increase in this ratio in the plasma was observed. These results confirm that Tyr antagonizes the proconvulsant effect of Phe and APM and they further suggest that no simple relationship exists between the relative brain concentrations of the two amino acids and the response to metrazol convulsions.

Animals↗
PubMed1991

Interspecies and interstrain studies on the increased susceptibility to metrazol-induced convulsions in animals given aspartame.

The ability of aspartame (APM) to increase the susceptibility to metrazol-induced convulsions was studied in two strains of mice (CD1 and DBA/2J) and in guinea-pigs. Rats were included as known positive controls. Plasma and brain levels of phenylalanine (Phe) and tyrosine (Tyr) were measured in CD1 mice and guinea-pigs at various intervals after a dose of 1 g APM/kg body weight (administered orally to mice and ip to guinea-pigs). In mice, peak levels of Phe and Tyr were observed in plasma after 30 min and in brain after 60 min. In guinea-pigs peak plasma levels of Phe and Tyr occurred 30 min after treatment. Phe was at a maximum in guinea-pig brain after 30 min, while Tyr levels reached a peak at 120 min. In further experiments Phe and Tyr levels were measured 1 hr after APM doses of 0.5, 0.75 or 1 g/kg. In CD1 mice, plasma Phe and Tyr levels were increased significantly only at the highest dose, whereas in brain, Tyr concentrations were significantly increased by 0.75 or 1 g APM/kg and Phe was significantly increased by all three doses. In the guinea-pig, plasma Phe and Tyr were increased significantly only by 1 g APM/kg and in brain this dose significantly raised only the Phe levels. Monoamine and metabolite levels were determined in the brain striata of CD1 and DBA/2J mice 1 hr after the oral administration of 1 or 2 g APM/kg body weight; no differences from control values were found in either strain. The studies of potentiation of metrazol-induced convulsions showed that APM, at doses of up to 2 g/kg body weight, had no such effect in mice or guinea-pigs. In contrast, as expected, the potentiation was significant in the rat at 1 g/kg.

Animals↗