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At least 973 records · Page 54Linked to original sources
PubMed1988

A possible role for spinal noradrenaline in the mechanisms of 6-hydroxydopamine against pentylenetetrazol induced convulsions in rats.

The threshold of the generalized clonic convulsions induced by intravenous infusion of pentylenetetrazol (PTZ) was significantly increased by the intraperitoneal administration of noradrenaline (NA) neurotoxin, 6-hydroxydopamine, which produced no changes in the levels of catecholamines in discrete areas of rat brain, but the effect was accompanied by spinal depletion of NA. Moreover, the anticonvulsant effects of phenobarbitone (PB) and diphenylhydantoin (DPH) against PTZ convulsions were also significantly increased in the animals pretreated with 6-OHDA. These results suggest that the observed elevation of PTZ convulsive threshold and the potentiation of anticonvulsant activity of PB and DPH in 6-OHDA treated rats were possibly mediated through spinal cord depletion of NA.

Animals↗
PubMed1989

Blockade of N-methyl-D-aspartate induced convulsions by 1-aminocyclopropanecarboxylates.

1-Aminocyclopropanecarboxylic acid is a potent and selective ligand for the glycine modulatory site on the N-methyl-D-aspartate receptor complex. This compound blocks (ED50 234 mg/kg) the convulsions and deaths produced by N-methyl-D-aspartate (125 mg/kg) in a dose dependent fashion. In contrast, 1-aminocyclopropanecarboxylic acid does not protect mice against convulsions induced by pentylenetetrazole (80 mg/kg), strychnine (2 mg/kg), bicuculline (6 mg/kg), or maximal electroshock (50 mA, 0.2 s), and does not impair motor performance on either a rotarod or horizontal wire at doses of up to 2 g/kg. The methyl- and ethyl- esters of 1-aminocyclopropanecarboxylic acid are 5- and 2.3-fold more potent, respectively, than the parent compound in blocking the convulsant and lethal effects of N-methyl-D-aspartate. However, these esters are several orders of magnitude less potent (IC50 greater than 40 microM) than 1-aminocyclopropanecarboxylic acid as inhibitors of strychnine-insensitive [3H] glycine binding, indicating that conversion to the parent compound may be required to elicit an anticonvulsant action. These findings suggest that 1-aminocyclopropanecarboxylates may be useful in the treatment of neuropathologies associated with excessive activation of N-methyl-D-aspartate receptor coupled cation channels.

Amino Acids↗
PubMed1993

Indomethacin-induced maternal convulsion in the treatment of preterm labour.

A caucasian 28-year-old woman at 25 weeks gestation with a diagnosis of preterm labour suffered a convulsion after the administration of indomethacin. Convulsions are described as an infrequent complication with this therapy in the non-pregnant population. No such convulsion has been described to date in pregnancy.

Adult↗
PubMed1982

Tryptophan availability, central serotonergic function and methionine sulphoximine-induced convulsions.

A convulsant dose (100 mg/kg) of l-methionine-RS-sulphoximine (MSO) produced temporally correlated decreases in central 5-hydroxytryptamine (5-HT) and plasma and brain tryptophan (TRY) concentrations in C57BL/6J mice. In contrast, a subconvulsant dose of MSO (50 mg/kg) had no effect on central 5-HT levels and only decreased brain tryptophan at one time-point after its administration. The pattern of findings suggests that the decrease in central 5-HT levels resulting from a convulsant dose of MSO is related to an impairment in 5-HT synthesis resulting from a restriction of tryptophan availability. Administration of 25 mg/kg and 100 mg/kg doses of l-tryptophan with convulsant doses of MSO significantly increased seizure latency. It is suggested that the central 5-HT system modulates the expression of MSO-induced seizures.

Animals↗
PubMed1987

2-Amino-7-phosphonoheptanoic acid, a selective antagonist of N-methyl-D-aspartate, prevents barbital withdrawal-induced convulsions and the elevation of cerebellar cyclic GMP in dependent rats.

Female Sprague-Dawley rats were maintained on a diet of barbital for 8 weeks, a period of time previously shown to result in tolerance to and dependence on the drug. After completing this course, the barbital was abruptly withdrawn and the selective antagonist of N-methyl-d-aspartate (NMDA), 2-amino-7-phosphonoheptanoic acid (APH), or saline was infused intracerebroventricularly over 48 hr. Control rats which had not received barbital, were similarly infused with either saline or APH. All animals were observed for 12-48 hr following the withdrawal of the barbital; spontaneous convulsions, previously reported to be numerous and severe after withdrawal of the drug, were counted and graded according to severity. Forty-eight hr after withdrawal of barbital, the rats were killed by focussed microwave irradiation and cerebellae were collected for later determination of levels of cGMP. Nine convulsions occurred in 29 rats withdrawn from barbital and infused intracerebroventricularly with APH, this contrasted markedly with 61 convulsions seen in 29 animals withdrawn from the drug and infused with saline. There was a 3-fold elevation of levels of cGMP in the saline-infused, barbital-withdrawn rats when compared to control rats infused with saline. This evaluation was markedly, although not completely, prevented by the intracerebroventricular infusion of APH. These data provide evidence that dicarboxylic amino acid pathways, specifically those acting through NMDA receptors, are involved in seizure activity seen following abrupt abstinence from barbital.

2-Amino-5-phosphonovalerate↗
PubMed1979

Relationship of some open-field behaviors to amygdaloid kindled convulsions in Wistar rats.

Repeated low-intensity electrical stimulation (kindling) of the amygdala eventually produces convulsive behavior in animals. The present study examined the relationship between behaviors displayed in a novel open-field situation with behavioral characteristics of the kindled clonic convulsion (CC). Wistar rats were given two open-field tests and were subsequently kindled to clonic convulsions. A multiple regression analysis indicated that rats which urinated more often in the open-field tests tended to show longer latencies to CC onset. Thus, open-field urination was a significant predictor of latency to CC onset. It is suggested that an emotionality construct may be related to rate of kindling.

Amygdala↗
PubMed1982

Effects of bipiperidyl mustard (BPM) lesions on insulin hypoglycemic convulsions.

Systemic gold thioglucose (GTG) is well known to produce hyperphagia, resulting in obesity, and histological damage focused relatively selectively in the ventromedial hypothalamus (VMH). Although structurally very different, bipiperidyl mustard (BPM) produces apparently similar effects. However, a proposed mechanism for concentration and hence localization of GTG toxicity depends on its structural similarity to glucose, binding it to glucoreceptors and focusing the cytotoxicity of the gold thio-portion. We recently showed that GTG treatment also produces an early decrease and a later increase in sensitivity to insulin hypoglycemic convulsions. We report here that BPM also produces a similar biphasic change in sensitivity to insulin hypoglucemic convulsions. For both, the differences are in the brain's convulsive response to hypoglycemia, rather than in the degree of hypoglycemia in response to insulin. Thus, GTG and BPM cytotoxic lesions appear similar in this regard as well. BPM is another way of producing a relatively discrete brain lesion which alters the brain's functional adjustment to hypoglycemia. The significance of this control center and its relationship to the control(s) of feeding and systemic metabolism are discussed.

Animals↗
PubMed1985

Lateralized state-dependent learning produced by hippocampal kindled convulsions: effect of split-brain.

In previous experiments, it was demonstrated that convulsions kindled from a ventral hippocampal focus in rats supported state-dependent learning which tended to lateralized to, and asymmetrical in, the right hemisphere. The question of the differential contribution of the left and right hippocampus to the production of state-dependency can best be addressed through confining the seizure to one or the other hemisphere via commissurotomy. In the present investigation, then, commissurally-intact and split-brain rats were implanted with bilateral hippocampal electrodes, then a left or a right focus was kindled. Later behavioral testing in an aversive inhibitory avoidance (IA) paradigm, revealed that intact animals, both left and right kindled groups, displayed good state-dependency. Split-brain animals, however, exhibited differential state-dependent responses to convulsive stimulation. Those kindled in the left hippocampus showed good retention when the conditions of seizure during training and testing were the same (same-state conditions), while showing deficient recall in changed-state conditions (a good state-dependent profile). On the other hand, those kindled in the right hippocampus displayed good retention of the IA experience in both same- and changed-state conditions. Differential recall after a left versus a right hippocampal convulsion in split-brain animals could not be accounted for in terms of differential seizure parameters, laterality of afterdischarge, extent of extracommissural damage or the extent of the actual transection. Possible mechanisms underlying this effect were discussed.

Animals↗
PubMed1977

Activity pattern and convulsions in the abstinence period after barbital treatment in the rat.

Barbital solution was given as the only drinking fluid to male rats for 50 weeks (daily dose around 200 mg/kg). During the treatment and in the abstinence period activity and convulsive episodes were recorded with jiggle cages. Sensitivity to hexobarbital was tested with a threshold method. A 12:12 HR L:D schedule was used. During the barbital treatment the activity of the treated rats started earlier (prior to light off) and ended earlier (prior to light on) compared with controls. A clear 24-hr pattern remained and the total activity was same as in the controls. In the first part of the abstinence period there was a large increase in activity with loss of the 24-hr pattern. Later in the abstinence period the activity was still increased both during light and darkness but a 24-hr pattern influenced by the L:D cycle was re-established. The changes in activity seemed to occur in a least two phases with the second phase lasting between abstinent Days 20-60. A similar two phase pattern was seen also in the changes of the hexobarbital thresholds. The convulsive episodes had several maxima during the abstinence period. The first one occurred around abstinent Days 3--4 and the second one was seen around Day 12. After Day 37 no convulsions were seen. All recorded changes can tentatively be explained by a common increased excitation in the central nervous system.

Animals↗
PubMed1983

Inhibition of pentylenetetrazol induced genetically-determined stereotypic convulsions in tottering mutant mice by diazepam.

Genetically-determined stereotypic behavioral convulsions (GDSC) resulting from the autosomal recessive mutation tottering (tg) were studied in C57BL/6J mice. GDSC was found to be reliably induced in (tg/tg) homozygotes with 30 mg/kg pentylenetetrazol (PTZ), a dose that is significantly below the threshold for induction of generalized clonic convulsions in (tg/+) heterozygotes and (+/+) wild type C57BL/6J mice. The effects of anticonvulsant drugs on GDSC were studied in (tg/tg) mice induced by 30 mg/kg PTZ. Ethosuximide (250 mg/kg), phenytoin (25 and 50 mg/kg), sodium phenobarbital (25 and 50 mg/kg), naloxone (6 mg/kg), valproic acid (150 mg/kg), sodium valproate (200 mg/kg) and aminooxyacetic acid (25 mg/kg) were all without effect on PTZ induced GDSC. In contrast to its usual anticonvulsant action, phenytoin caused GDSC in (tg/tg) mice. Diazepam (4 mg/kg) was completely effective in blocking GDSC 2 hr post administration. Ethosuximide (250 mg/kg), which did not protect (tg/tg) mice against GDSC, was able to protect both (tg/tg) and (tg/+) mice against generalized clonic-tonic convulsions induced by 85 mg/kg PTZ. These results suggest a novel mechanism of action for the induction of GDSC by 30 mg/kg PTZ in (tg/tg) mice which may involve benzodiazepine receptors.

Animals↗
PubMed1988

Benzodiazepines increase tonic component of postdecapitation convulsions in mice.

The effects of benzodiazepines (BDZs) and GABA system on tonic and clonic component of postdecapitation convulsion (PDC) were studied in mice. Mice decapitated at the occipito-cervical junction, exerted biphasic convulsions, i.e., initially tonic and subsequently clonic convulsions. BDZs such as diazepam or clonazepam increased tonic and clonic components of PDC. These effects were not antagonized by Ro 15-1788, a benzodiazepine receptor antagonist. The increased tonic component was antagonized by the GABA receptor antagonists, bicuculline and picrotoxin, whereas the clonic component was augmented by them. Aminooxyacetic acid, which increases the endogenous GABA content by inhibiting the GABA-transaminase, increased the tonic component significantly; this increase was antagonized by both bicuculline and picrotoxin. Muscimol, a GABA agonist, however did not affect the tonic components but rather augmented the clonic component. Bicuculline and picrotoxin did not antagonize this effect of muscimol. These results indicate that endogenous GABA may play a crucial role in mediating the tonic component of PDC and the facilitation of this component by BDZs may also be due to the activation of GABA in the spinal cord. Furthermore, the mechanisms of the tonic component may be different from that of the clonic component.

Animals↗
PubMed1994

Influence of chronic aminophylline on antielectroshock activity of diazepam and aminophylline-induced convulsions in mice.

The effects of chronic administration of aminophylline (AMPH; 50 mg/kg, twice daily for 14 consecutive days) were studied on both antielectroshock efficacy of diazepam (DZP) and convulsive activity of AMPH in mice. AMPH injected acutely at a dose of 50 mg/kg significantly reduced anticonvulsant action of DZP elevating ED50 from 10.9 (control) to 15.9 mg/kg (p < 0.01). After the administration of AMPH for 3 days, ED50 value was still higher compared with control. Chronic treatment with AMPH resulted in further increase of ED50 of DZP, which was 20.2 mg/kg, and this elevation was significant not only when compared with saline-treated animals, but also with acute and 3-day administration of the xanthine (p < 0.01, 0.05, and 0.001, respectively). Therefore, no tolerance to this AMPH-mediated effect was found, and even an enhancing influence was observed. On the other hand, chronic treatment with AMPH decreased convulsive activity of AMPH elevating ED50 for induction of clonic seizures from 218 to 252 mg/kg (p < 0.01). The remaining seizure parameters were unaffected. Furthermore, in both cases pharmacokinetic interactions were excluded, at least in terms of total plasma levels of the drugs. The results suggest that the mechanisms governing AMPH-induced reversal of the anticonvulsant efficacy of DZP qualitatively differ from those underlying AMPH-induced convulsions. Moreover, these data support the claim that AMPH should be avoided in patients suffering from different types of epilepsy.

Aminophylline↗
PubMed1986

Somatostatin-like immunoreactivity and somatostatin receptor binding in rat brain before and after pentylenetetrazol-induced convulsion.

Wistar rats were injected with a convulsant doze of pentylenetetrazol (PTZ) (50 mg/kg, i.p.). Somatostatin-like immunoreactivity (SLI) and 125I-Tyr11-somatostatin binding were measured in various brain areas immediately after PTZ injection, after the first head twitches, and 15 minutes, 1 h, 4 h, and 24 h after generalized tonic-clonic convulsions. SLI tended to decrease in the striatum (p less than 0.02), frontal cortex, hippocampus, and hypothalamus 1 hour after convulsion. Specific somatostatin binding remained stable. According to our results, somatostatin is not connected to initiation or spread of seizure but may play some role in depressing seizures.

Animals↗
PubMed1985

A single neonatal pentylenetetrazol or hyperthermia convulsion increases kindling susceptibility in the adult rat.

Convulsions were induced in young rats (1-21 days) with pentylenetetrazol or hyperthermia. As adults, these animals were kindled electrically in the basolateral or cortical amygdala, the hippocampus, or the pyriform cortex. Fewer amygdala stimulations were required to evoke major motor seizures in subjects treated at 1, but not at 10 or 21 days of age. No further facilitation in kindling rate was observed in subjects receiving 3 convulsions on days 1, 3 and 5 or 1, 5 and 9. This facilitation of electrical kindling was limited to the amygdaloid sites. The results could not be attributed to gross brain damage or differential convulsion histories. This age-limited, structure-specific effect suggests that the amygdala may represent a unique seizure-generating system in the brain that is sensitive to neural alteration at particular times during development.

Amygdala↗
PubMed1985

Altered postnatal ontogeny of alpha 1- and alpha 2-adrenoceptor binding sites in the brain of a convulsive mutant mouse (quaking).

Binding assays of [3H]dihydroalprenolol ([3H]DHA), [3H]prazosin and [3H]clonidine have been performed on whole brain (minus cerebellum) homogenates of the convulsive mutant mice quaking (qk) and the controls of the same strain (C57BL/6J:B6). In 70-day-old mutants (which fully exhibit the qk convulsive phenotype), the binding of [3H]DHA to beta-adrenoceptor binding sites was not different from the controls, whereas the binding capacities of [3H]prazosin and [3H]clonidine to alpha 1-and alpha 2-adrenoceptor sites, respectively, were greatly enhanced. The biphasic ontogenic pattern of alpha 2-adrenoceptors had a greater amplitude in the brain of 30- to 90-day-old mutants than in the corresponding B6 controls. In mutants younger than 30 days or older than 90 days, the number of alpha 2-adrenoceptor sites was not modified. The number of alpha 1-adrenoceptor binding sites was increased in the brain of the mutants, only in animals older than 70 days. In younger mice, the postnatal modulation of alpha 1-adrenoceptor sites was identical to the controls. Regional studies were performed in 70-day-old mice. [3H]clonidine binding was increased in the brainstem of the mutants, and to a lesser extent in the cerebral cortex, while it was slightly diminished in the hypothalamic area. [3H]prazosin binding was also increased in the brainstem of the mutants, and decreased in the olfactory bulbs. Our results suggest that the convulsions of the qk mutants are selectively associated with modifications of alpha- and not beta-adrenoceptor binding sites.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

The role of the middle ear and tonsil in the etiology of febrile convulsions.

The middle ear and tonsil are thought to be important sources of infection in children with febrile seizures. However, these patients are rarely examined by an otolaryngologist in the acute phase and we are unaware of any previous studies where otolaryngologists have documented the presence of acute suppurative otitis media (ASOM) and tonsillitis in a series of children with febrile convulsions. We carried out a prospective study on 47 children admitted to two Dublin hospitals with a diagnosis of simple febrile convulsion. All children were examined by an otolaryngology resident within 6 h of admission. Nine children were noted to have ASOM and 18 had acute tonsillitis. The otolaryngology resident's opinion of the condition of the ears and throat often differed from that of the admitting pediatric resident, as documented in the clinical records. We review the recent literature on febrile convulsions and discuss the possible role of the otolaryngologist in the prevention of seizure recurrence.

Child, Preschool↗
PubMed1989

Computer-assisted predictive mathematical relationship among electroshock voltage and duration and occurrence of convulsion in mice.

A microcomputer program in BASIC for predicting percentage of occurrence of electroshock-induced convulsion in mice was designed. A formula published by the author to express the mathematical relationship among the drug dose, the time, and the biological response was used in this program. Analysis of the actual, and the computer-assisted predicted percentages of occurrence of convulsion has shown that the program is fairly accurate in expressing convulsion response of mice as a function of the voltage and the duration.

Animals↗
PubMed1995

In vivo modification of GABAA receptor with a high dose of pyridoxal phosphate induces tonic-clonic convulsion in immature mice.

The biologic cofactor, pyridoxal-5'-phosphate (PLP), is responsible for tonic-clonic convulsion in immature mice. The mechanisms underlying such convulsive fits induced by administration of a single high dose of PLP were studied. The administration of PLP resulted in a 13% increase of PLP in the P2 fraction compared to control P2, and the calculated data suggested that membrane bound PLP increased over 31% (approximately 1 microM). The P2 fraction of administered mice was treated with [3H]NaBH4 and analyzed by SDS-polyacrylamide gel electrophoresis. The radioactivity was mainly incorporated into a 52 kDa protein which corresponded to a GABAA receptor subunit. The addition of PLP in vitro competitively inhibited [3H]GABA binding as well as [3H]flunitrazepam binding to synaptic membranes in a concentration-dependent manner, and 50% inhibition was achieved with 1 mM PLP. The results obtained in the present study demonstrate that PLP was rapidly permeable into the brain through the immature blood-brain barrier and then bound directly to GABAA receptor. It is probable that specific amino groups of lysine residues on the GABAA receptor react in vivo with PLP to form Schiff bases, and that the in vivo modification of the receptor produces a degeneration of GABAergic neurotransmission leading to the onset of a convulsive fit.

Animals↗