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At least 19 recordsLinked to original sources

PubMed1982

Experimental febrile convulsions: long-term effects of hyperthermia-induced convulsions in the developing rat.

The susceptibility of infant rats to experimental febrile convulsions was investigated. Rats were subjected to a single hyperthermia convulsion at 5, 10, 15, or 20 days of age or the a series of convulsions from 5 to 20 days of age. Susceptibility to the experimental febrile convulsion decreased with age in all rats except those subjected to multiple convulsions. In this group, susceptibility tended to increase. This results is discussed in terms of its similarity to the kindling phenomenon and to the incidence of recurrent febrile convulsions in the human infant. Sex differences in susceptibility to the convulsion were examined, but none were found. Mature rats that had been subjected to experimental febrile convulsions as infants were found to be significantly more susceptible to a convulsive dose of pentylenetetrazol than controls. The results of this study indicate that even a single experimental febrile convulsion during infancy can exert a long-lasting, if not permanent, enhancement in seizure susceptibility. The similarities between the present findings and human infantile febrile convulsions are discussed.

Age Factors↗

PubMed1990

Genetic correlations among inbred strain sensitivities to convulsions induced by 9 convulsant drugs.

Inbred mouse strains differed significantly in sensitivity to convulsions induced by 9 convulsant drugs administered using a timed infusion procedure. Some strains (e.g. BALB/cJ, A/J) were generally seizure-susceptible, while some were generally seizure resistant (e.g. C57BL/6J, SWR/J). However, the overall pattern of strain sensitivities was complex, and depended upon drug and convulsant sign. Five of the drugs (bicuculline, DMCM, picrotoxin, TBPS and pentylenetetrazol (PTZ] produce convulsions, at least in part, through their interactions with the GABA receptor, while the other 4 (strychnine, CHEB, 4-aminopyridine and kainic acid) act through independent mechanisms. We predicted that responses to drugs with similar mechanisms of action would be genetically correlated. However, strains sensitive to picrotoxin-induced convulsions were not necessarily sensitive to convulsions elicited by PTZ or TBPS. Furthermore, different convulsant signs produced by a single drug were not always strongly correlated. Instead, genetic correlations were found among inbred strains for sensitivity to similar convulsant signs produced by different drugs. This suggests that genetic variation in sensitivity to these convulsant drugs arises primarily from variation in systems important for the expression of the convulsion.

Animals↗

PubMed1983

Effect of dihydroergotoxine on the susceptibility of rats to convulsions produced by different convulsant agents.

The study was undertaken to test further whether diminished GABAergic transmission might be responsible for the increased susceptibility of rats to picrotoxin-induced convulsions. In rats kept individually in cages in a noise-free room, the time between the intraperitoneal injection of the convulsant agent and the onset of convulsions was measured. Acute and subacute treatment with low doses of dihydroergotoxine (0.01-1.0 mg/kg) increased the occurrence and decreased the latency of picrotoxin-induced convulsions. Acute administration of dihydroergotoxine, 1.0 mg/kg, caused convulsions in animals injected with the subconvulsive dose (3 mg/kg) of bicuculline and of 10.0 mg/kg dihydroergotoxine in animals injected with the subconvulsive dose (1.5 mg/kg) of strychnine. Some of the animals injected with the 100% convulsive dose of strychnine were protected by dihydroergotoxine pretreatment (1.0 mg/kg) as evidenced by the lower occurrence of convulsions and fewer animals dying, as well as by a delay in the appearance of convulsions at 10.0 mg/kg. These results together with the previous findings on the GABA system suggest that dihydroergotoxine potentiates the appearance of picrotoxin and bicuculline-induced convulsions by a diminution of GABAergic transmission.

Animals↗

PubMed1980

Altitude convulsion threshold and time to altitude convulsion in gold thioglucose obese mice.

Gold thioglucose-induced hypothalamic obesity caused a higher altitude convulsion threshold and a decrease in the time to altitude convulsion. The average altitude convulsion threshold for the obese mice was 151 torr (38,500 ft). In contrast, the average value for the controls was 131 torr (41,500 ft). It was also observed that at 206 torr (32,000 ft), the average time until altitude convulsion of the obese mice was 69 s; at 179 torr (35,000 ft), 27 s; at 141 torr (40,000 ft), 17 s; at 111 torr (45,000 ft), 10 s; at 87 torr (50,000 ft), 9 s; and at 69 torr (55,000 ft), 8 s. On the other hand, the average control time until altitude convulsion at the above-mentioned altitudes was 97, 37, 26, 11, 9, and 8 s, respectively. Moreover, the average accumulation of fat between pleura and lungs in obese mice was 154 (Table I) or 181 mg (Table II), while the value of the control group was only 72 to 67 mg. Such an increase of fat accumulation in the thoracic cage could decrease the tidal volume. The altitude convulsion threshold and the time until altitude convulsion might thus be changed. The time until altitude convulsion may be regarded as a convenient objective measure of altitude tolerance in mice.

Altitude↗

PubMed1987

Binding of [3H]muscimol to calf cerebrocortical synaptic membranes and the effects of sulphur-containing convulsant and non-convulsant compounds.

Endogenous and xenobiotic sulphur-containing convulsant and non-convulsant compounds containing structural moieties of, or bearing a structural resemblance to, GABA and homocysteine were tested in binding studies for their potency in displacing the GABA-mimetic [3H]muscimol from specific, high-affinity sites (Kd = 3.6 nM; Bmax = 3.94 pmol/mg protein) on freeze-thawed, Triton-treated calf-brain synaptic membranes. The xenobiotic convulsants, 4-mercaptobutyric acid (MBA), 3-mercaptopropionic acid (3-MPA) and 2-mercaptopropionic acid (2-MPA) were found to be two-site competitive inhibitors exhibiting apparent inhibition affinity constants (Kiapp) of 5000 microM, 3750 microM, and 4800 microM, respectively; while homocysteic acid (Kiapp = 4800 microM) was shown to be a one-site partial competitive inhibitor. Intermediary metabolites of methionine: S-adenosyl-L-homocysteine, L-cysteine, the convulsant L-homocysteine, and its non-convulsant disulphide oxidation product, homocystine, were found to be one-site partial competitive inhibitors exhibiting Kiapp values of 5750 microM, 8350 microM, 5000 microM, and 510 microM, respectively. The endogenous anticonvulsant neuroeffector, taurine, and the tripeptide, reduced glutathione (GSH) were shown to be, respectively, one-site (Ki = 20 microM) and two-site (Kiapp = 4300 microM) competitive inhibitors of [3H]muscimol binding. These findings are discussed with regard to a previously proposed mechanism for the convulsant action of homocysteine.

Animals↗

PubMed1978

Febrile convulsions followed by nonfebrile convulsions: analysis based on a maximum likelihood method and discriminant function.

Two hundred sixty-two nontreated patients with febrile convulsions only and 107 with later nonfebrile convulsions were analyzed based on a maximum likelihood method and discriminant function. The formula for discrimination is as follows: y = 2.9193 x (basic EEG abnormality at the first examination) + 2.2134 x (more than 20 minutes in duration of convulsion) + 1.7358 (fever under 38.4 degrees C before convulsion) + 1.7005 x (specific EEG abnormality at the first examination) + 1.6703 x (more than 5 recurrences) + 1.5610 x (over 4 years of age at the last convulsion) + 1.4921 x (exogenous causes) + 0.3741 x (family histroy of febrile convulsions among second or third relatives)--3.0397. If an item is positive, coefficient x 1 is to be used, and if it is negative, coefficient x 0 is to be applied. When one classifies patients with y greater than 0 as the FCC group, and those with y less than 0 as the FC group, misclassification may be theoretically expected in 18.9% of cases (accuracy in 81.1%).

Age Factors↗

PubMed1977

Febrile convulsions followed by nonfebrile convulsions. A clinical, electroencephalographic and follow-up study.

103 patients with febrile convulsions followed by nonfebrile convulsions and 512 patients with febrile convulsions only (FC group) under 5 years of age at the first examination were analyzed from many aspects. A trimodal curve in distribution by age at onset of nonfebrile convulsions was seen: 2--3 years of age with occasional grand mal, 5--6 years of age with absence, and 12 years of age with awakening grand mal. Specific EEG abnormality was observed in 40% at the first examination (29% in FC group). Typical or atypical spike-and-wave complex, polyspikes, or continuous EEG abnormality were characteristic (slow wave burst with spike for FC group). Development from febrile convulsions into nonfebrile convulsions was detected in 17% among male and female patients. To identify an effective sign for the prediction of this development, the ratio between correct and incorrect prediction rates was analyzed. Specific paroxysmal EEG abnormality was increased over 3 years of age. EEG change due to aging and the significance of EEG reexamination were indicated.

Age Factors↗

PubMed1992

Effects of malaoxon on phosphatidylinositol signaling in convulsing and non-convulsing non-pregnant and pregnant female rats and their offspring.

Phosphatidylinositol (PI) signaling during organophosphate (OP) induced convulsions and tissue Ca2+ changes in 10 weeks old male, and 14 weeks old non-pregnant and pregnant female rats, and the offspring of the latter were explored. Brain inositol and inositol-1-phosphate (Ins1P) served as indices of alterations in brain PI signaling, and brain tissue Ca2+ as an index of early neuronal injury. A dose of malaoxon OP, which produced convulsions in about 60% of the exposed rats in different rat groups, was 39.2 for male, and 8.2 mg/kg for pregnant female rats, respectively. Malaoxon (8.2 mg/kg) did not produce convulsions in non-pregnant female rats. All the rats were followed for 1 or 4 hr subsequent to malaoxon. Malaoxon decreased cerebral inositol in both male and female rats, and the decrease was similar in spite of the dose difference. The decrease was larger in the convulsing than in the non-convulsing rats. A tendency towards a decrease of brain inositol also occurred in the offspring. Ins1P levels were markedly increased in male, and also in non-pregnant female rats, but not in the brains of pregnant female rats. Ins1P was not markedly changed in the brains of the offspring. Malaoxon elevated brain tissue Ca2+ in male but not in female rats or their offspring. Cholinergic systems and PI signaling in the brain seem to be associated with OP-induced convulsions both in male and female rats; females seem to be more sensitive than males. Malaoxon may also have slightly modified PI signaling in the offspring brain. Hormonal factors are likely to modify OP CNS toxicity and cholinergic stimulation of brain PI signaling.

Animals↗

PubMed1983

Comparison of folate levels in convulsing and non-convulsing febrile children.

The relationship between folic acid levels and occurrence of convulsion in febrile subjects was studied in thirty-two children aged 8 months to 5 years. Both the serum and red cell folate levels were significantly higher in the febrile children who convulsed than in those who did not convulse. When the period of convulsion was more than thirty minutes, there was a significant rise in the red cell folate. These results suggest that the accumulation of folate in the serum and red cell may be causally related to the development of the convulsing state in febrile children.

Body Temperature↗

PubMed1984

Effect of convulsions of the synthesis of heterogeneous nuclear RNA associated with polyadenylate and oligoadenylate sequences from El mouse brain as a convulsive strain.

Animals from the El (susceptible to seizures) and ddy (nonsusceptible) mouse strains were subjected to vestibular stimulation by tossing. After convulsions in the El mice, both the stimulated El mice and ddY mice were intracranially injected with [14C]- and [3H]adenosine, respectively. In the control experiment, nonstimulated El and ddY mice received radioactive adenosines in the same manner. The rate of incorporation of adenosine into brain nuclear RNA, expressed as a percentage of the 3H; 14C ratio, was reduced to an average of 68% at 15 min after convulsions, then increased and reached a control value at 5 h. This reduction in nuclear RNA synthesis was not due to alteration of the adenosine triphosphate pool. Gel electrophoresis of RNA revealed no obvious differences in the labeling distribution between El and ddY mice, but the synthesis of RNA species larger than 35S in heterogeneous nuclear RNA (HnRNA) was impaired in convulsed El mice. Nuclear resistant segments of HnRNA with both T1 RNase and RNase A, were chromatographed with poly(U)-Sepharose followed by urea-polyacrylamide gel electrophoresis. The ologo(A) and poly(A) segments consisted of 29, 19, and 11, and 203, 135, and 69 nucleotides, respectively. The convulsions of El mice reduced the incorporation of radioactive adenosines into oligo(A) and poly(A) segments, suggesting that they inhibited transcription as well as polyadenylation within HnRNA.

Adenine Nucleotides↗

PubMed1984

Amino acid metabolism in the brain with convulsive disorders. Part I: Free amino acid patterns in the brain of E1 mouse with convulsive seizure.

To clarify the biochemical mechanism of convulsions from a view point of the amino acid metabolism, the free amino acid patterns in brains of El mice were investigated. The free amino acid levels in the brain excluding the cerebellum were measured by an amino acid autoanalyzer. 1) In the convulsion group, the free aspartic acid and serine levels in brains increased compared to the preconvulsion group. 2) In the postconvulsion group, an increase of glutamine and alanine levels in brains and a decrease of cystathionine level were found compared to the convulsion group. 3) It was found that in the preconvulsion group, the cystathionine and ornithine levels were high and the serine, alanine and GABA levels were low compared to the postconvulsion group. These results suggest that the free amino acid balance in the brain of this mouse should play an important role in the inducing mechanism of convulsions.

Alanine↗

PubMed1990

[Involvements of neuropeptides in pentylenetetrazol-induced convulsion in rats and effects of TRH and ceruletide on the convulsion].

To study the possible involvements of neuropeptides in the occurrence of convulsion, pentylenetetrazol (PTZ) was given to male Wistar rats weighing 250-350 g, and the concentration of neurotensin (NT), and the maximal number of binding sites (Bmax) and dissociation constant (Kd) of NT receptor in the frontal cortex were measured. The effect of the pretreatment of thyrotropin-releasing hormone (TRH) or ceruletide (CER) on the convulsion was also studied. NT was extracted from the homogenates of rat frontal cortex by boiling, and measured by radioimmunoassay. Membrane fractions were incubated with increasing concentrations of 125I-NT. Nonspecific binding was determined in the presence of unlabeled NT and subtracted from total binding to obtain the specific binding. The Bmax and Kd were calculated by Scatchard analysis. Generalized convulsion appeared after intraperitoneal administration of 50 mg/kg PTZ with a latency of 68.2 +/- 4.4 sec. One hour after the administration, neurotensin-like immunoreactivity (NTLI) concentration was reduced from 4.7 +/- 0.6 to 2.3 +/- 0.1 ng/g wet wt (p less than 0.01) and the Bmax of NT receptor from 17.2 +/- 2.8 to 10.8 +/- 1.1 fmol/mg protein (p less than 0.01). However no significant changes were observed in somatostatin-like immunoreactivity (SSLI) concentration and the Bmax and Kd of SS receptor. These facts indicate that PTZ stimulates the release of NT resulting in down regulation of NT receptor. Pretreatment with intracerebroventricular (icv) administration of 30 micrograms/10 microliters NT 30 min before the 50 mg/kg PTZ administration shortened the duration of the convulsion from 135.0 +/- 42.8 to 11.5 +/- 11.9 sec (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

Regional changes in brain 2-14C-deoxyglucose uptake induced by convulsant and non-convulsant doses of lindane.

Lindane-induced dose- and time-related changes in regional 2-14C-deoxyglucose (2-DG) uptake were examined in 59 discrete rat brain structures using the 2-DG autoradiographic technique. At different times (0.5-144 hr) after administration of a seizure-inducing single dose of lindane (60 mg/kg), 2-DG uptake was significantly increased in 18 cortical and subcortical regions mainly related to the limbic system (e.g., Ammon's horn, dentate gyrus, septal nuclei, nucleus accumbens, olfactory cortex) and extrapyramidal and sensory-motor areas (e.g., cerebellar cortex, red nucleus, medial vestibular nucleus). There was also a significant increase in superior colliculus layer II. In addition, significant decreases occurred in a group of 6 regions (e.g., auditory and motor cortices). Non-convulsing animals treated with the same dose of lindane showed a regional pattern of 2-DG uptake less modified than the convulsant group. A non-convulsant single dose of lindane (30 mg/kg) also modified significantly the 2-DG uptake (0.5-24 hr) in some brain areas. Although the various single doses of lindane tested produced different altered patterns of brain 2-DG uptake, some structures showed a similar trend in their modification (e.g., superior colliculi and accumbens, raphe and red nuclei). Repeated non-convulsant doses of lindane produced defined and long-lasting significant elevations of 2-DG uptake in some subcortical structures (e.g., dorsal cochlear nucleus, dentate gyrus). Considering the treated groups all together, 2-DG uptake increased significantly in 26 of the 59 regions examined but only decreased significantly in 9 of them during the course of lindane effects. This fact can be related to the stimulant action described for this neurotoxic agent. The observed pattern provides a descriptive approach to the functional alterations occurring in vivo during the course of lindane intoxication. These results may be linked to the proposed mechanism of lindane neurotoxicity postulating an initial action on the GABAA receptor-chloride channel sites.

Animals↗

PubMed1985

Pro- and anti-convulsant drug effects in combination with the convulsant benzodiazepine Ro 5-4864.

The effects of several compounds believed to act at the GABA-benzodiazepine receptor complex and which have anticonvulsant or proconvulsant properties when administered in combination with picrotoxin and pentetrazol (leptazol, pentylenetetrazole) were investigated in combination with the convulsant benzodiazepine Ro 5-4864. Tracazolate (25-100 mg kg-1) failed to affect convulsions induced by Ro 5-4864; however, they were prevented by treatment with CL 218,872 (20 mg kg-1). Compounds having proconvulsant activity in combination with a subthreshold dose of Ro 5-4864 were: CL 218,872 (5 mg kg-1), and CGS 8216 (20 mg kg-1) and FG 7142 (40 mg kg-1), two compounds characterized as 'inverse agonists' at benzodiazepine receptors. The phenylquinolines PK 8165 and PK 9084, originally believed to have anxiolytic properties, had no significant effect in combination with Ro 5-4864 (25-100 mg kg-1). The convulsant profile of Ro 5-4864 is compared with that of picrotoxin and pentetrazol.

Animals↗

PubMed2001

Linkage of benign familial infantile convulsions to chromosome 16p12-q12 suggests allelism to the infantile convulsions and choreoathetosis syndrome.

The syndrome of benign familial infantile convulsions (BFIC) is an autosomal dominant epileptic disorder that is characterized by convulsions, with onset at age 3-12 mo and a favorable outcome. BFIC had been linked to chromosome 19q, whereas the infantile convulsions and choreoathetosis (ICCA) syndrome, in which BFIC is associated with paroxysmal dyskinesias, had been linked to chromosome 16p12-q12. BFIC appears to be frequently associated with paroxysmal dyskinesias, because many additional families from diverse ethnic backgrounds have similar syndromes that have been linked to the chromosome 16 ICCA region. Moreover, one large pedigree with paroxysmal kinesigenic dyskinesias only, has also been linked to the same genomic area. This raised the possibility that families with pure BFIC may be linked to chromosome 16 as well. We identified and studied seven families with BFIC inherited as an autosomal dominant trait. Genotyping was performed with markers at chromosome 19q and 16p12-q12. Although chromosome 19q could be excluded, evidence for linkage in the ICCA region was found, with a maximum two-point LOD score of 3.32 for markers D16S3131 and SPN. This result proves that human chromosome 16p12-q12 is a major genetic locus underlying both BFIC and paroxysmal dyskinesias. The unusual phenotype displayed by one homozygous patient suggests that variability of the ICCA syndrome could be sustained by genetic modifiers.

Age of Onset↗

PubMedDate not supplied

[Effect of serotoninergic and antiserotoninergic preparations on convulsions induced by the endogenous convulsants kynurenine and quinolinic acid].

Serotoninergic drugs DL-5-hydroxytryptophan, 5-methoxytryptamine (mexamine) and 5-hydroxytryptamine (serotonin) were found to reduce clonic convulsions induced by intracerebroventricular administration of DL-kynurenine sulfate in mice. Serotonin antagonist deseril weakened the antikynurenine effect of DL-5-hydroxytryptophan and mexamine. Quinolinic acid-induced convulsions could be attenuated only by DL-5-hydroxytryptophan. Deseril and metergoline and destruction of the cerebral serotoninergic neurons by 5,6-dihydroxytryptamine potentiated the convulsant effect of quinolinic acid but not kynurenine. The serotoninergic protective anticonvulsant mechanism is probably better developed against kynurenine rather than quinolinic acid.

Animals↗

PubMedDate not supplied

[The role of mediators in the genesis of convulsive activity. Biogenic monoamine content of the brain of rats with various predispositions to audiogenic convulsions].

Content of serotonin, tryptophane, adrenaline, noradrenaline, dopamine, DOPA and tyrosine in was studied in cerebellum, truncus cerebri, hypothalamus and brain hemispheres of rats with various predisposition to audiogenic convulsions. Distinct decrease in content of brain serotonin, noradrenaline and increase in dopamine content was noted in rats with high level of audiogenic convulsive activity. The data obtained suggest that the increase in dopamine and decrease in serotonin and noradrenaline content in brain tissue may be among the factors responsible for elevation of potential convulsive activity of central nervous system.

Acoustic Stimulation↗

PubMed1977

[Influence of convulsive and pre-convulsive components of an audiogenic seizure on the process of consolidation of temporary connections].

In comparing the seizures of different severity in rats an amnestic effect of the convulsive phases of the audiogenic attacks on the short-term (in difference from the long-term) memory and the process of consolidation of temporary associations was revealed. Without behavioristic seizures the audiogenic attacks almost failed to derange the short-term memory. The results obtained confirmed the authors' results obtained earlier on different nature of the convulsive and preconvulsive phases of the motor activity during the audiogenic attack in rats. The preconvulsive phase is regarded only as a peculiar motor aura of the audiogenic attack without any convulsive components.

Acoustic Stimulation↗