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PubMed1987

Cerebellar metabolism of phosphatidylethanolamine and its water-soluble precursors during bicuculline-induced convulsive seizures.

The incorporation of labeled ethanolamine into phosphatidylethanolamine (PE) and its water-soluble precursors, phosphoethanolamine and CDP-ethanolamine, is measured in rat cerebella during the course of bicuculline-induced convulsive seizures. The labeling of CDP-ethanolamine and phosphoethanolamine diminishes 6 min after the administration of both bicuculline and radioactive ethanolamine whereas that of PE is unaffected in these conditions. Time is very important to this effect; indeed, no differences of the labeling of PE water-soluble precursors can be found in rat cerebellum of normal and convulsing animals 12 min after the administration. The cerebellar pool of CDP-ethanolamine doubles after 6 min of convulsions, which means that unlabeled CDP-ethanolamine forms from a non-radioactive source, such as lipid, may be through the reversal of the ethanolamine phosphotransferase reaction. This effect disappears 12 min after the injection of the convulsant.

Animals↗
PubMed1987

Inhibition of sound-induced convulsions by metoprine in the audiogenic seizure susceptible rat.

Metoprine which increases brain histamine by blocking its methylation, was recently demonstrated to inhibit electrically induced tonic convulsions in rats. Its effect was now tested on audiogenic convulsions in genetically audiogenic seizure sensitive rats. Metoprine (20 mg/kg, i.p.) reduced the severity of seizures significantly 4 and 28 h after drug administration. Also the duration of convulsions was significantly decreased. These results agree with an involvement of histaminergic neurons in convulsive phenomena perhaps as a part of an anticonvulsive inhibitory transmitter system.

Acoustic Stimulation↗
PubMed2002

Zinc in CSF of patients with febrile convulsion.

OBJECTIVE: This prospective study was carried out from July-December 1999 to see the status of zinc in CSF of children with febrile convulsion and to compare this to that of control. METHODS: Forty-two cases of febrile convulsion and 30 controls (fever without convulsion) were enrolled into the study. CSF zinc was estimated by atomic absorption spectrophotometry (AAS) in Atomic Energy Center, Dhaka and compared between the two groups. RESULTS: The mean zinc level in CSF in the study sample was 40.19mgm/L and that in control was 74.98mgm/L. This difference was statistically significant (p<0.001). CONCLUSION: The study concludes that a significantly lower of zinc exists in CSF of children with febrile. However no relationship was found between CSF zinc status with age, sex, degree & duration of fever and time of lumbar puncture after convulsion.

Age Distribution↗
PubMed2005

Extremely low frequency magnetic fields modulate bicuculline-induced-convulsion in rats.

The effect of extremely low frequency (ELF, 60 Hz) magnetic fields (MFs) on convulsions was investigated in rats. We determined the onset and duration of convulsions induced by bicuculline alone or by co-exposure to MFs and bicuculline. In addition, we measured the GABA concentrations in the rat brains using HPLC-ECD. MFs strengthened the convulsion induced by bicuculline (0.3, 1, and 3 microg, i.c.v.), with a shortening of the onset time, but lengthening of the duration time. Co-exposure to MFs and bicuculline decreased the GABA levels in the cortex, hippocampus and hypothalamus, whereas MFs alone reduced the level of GABA only in the hippocampus. These results suggest that the exposure to MFs may modulate bicuculline-induced convulsions due to GABA neurotransmissions in rat brains.

Animals↗
PubMed1983

The effect of naloxone and morphine on convulsions in mice following withdrawal from nitrous oxide.

The incidence of withdrawal convulsions was determined in mice following removal from a 70 per cent nitrous oxide environment. Groups of 20 mice received saline (control), naloxone or morphine subcutaneous injections five minutes prior to withdrawal. The observer was blind to the treatments. In comparison to the control group, the proportion convulsing was significantly (p less than 0.05) increased following naloxone 0.125 mg (n = 40), 0.25 mg, but not 0.5 mg. The proportion convulsing was significantly decreased following morphine 0.4 mg. Overall proportions of mice convulsing was 0.55 for the saline control group; 0.73 for naloxone 0.125 mg; 0.80 for naloxone 0.25 mg; 0.60 for naloxone 0.50 mg; and 0.38 for morphine 0.4 mg. Modification of this phenomenon by both an opiate antagonist and agonist suggests endorphin withdrawal as a possible mechanism. However, this should be regarded as indirect evidence pending further study of this area.

Animals↗
PubMed2005

Electroconvulsive shock induces neuron death in the mouse hippocampus: correlation of neurodegeneration with convulsive activity.

The relationship between convulsive activity evoked by repeated electric shocks and structural changes in the hippocampus of Balb/C mice was studied. Brains were fixed two and seven days after the completion of electric shocks, and sections were stained by the Nissl method and immunohistochemically for apoptotic nuclei (the TUNEL method). In addition, the activity of caspase-3, the key enzyme of apoptosis, was measured in brain areas immediately after completion of electric shocks. The number of neurons decreased significantly in field CA1 and the dentate fascia, but not in hippocampal field CA3. The numbers of cells in CA1 and CA3 were inversely correlated with the intensity of convulsions. Signs of apoptotic neuron death were not seen, while caspase-3 activity was significantly decreased in the hippocampus after electric shocks. These data support the notion that functional changes affect neurons after electric shock and deepen our understanding of this view, providing direct evidence that there are moderate (up to 10%) but significant levels of neuron death in defined areas of the hippocampus. Inverse correlations of the numbers of cells with the extent of convulsive activity suggest that the main cause of neuron death is convulsions evoked by electric shocks.

Animals↗
PubMed1985

Blood manganese levels in children with convulsive disorder.

Manganese deficiency syndromes have been well described in animals and include among a wide variety of metabolic aberrations the heightened susceptibility to convulsions induced by electroshock or drugs. We have measured manganese blood levels in two populations of children: (1) a reference group of 120 ambulatory patients without neurologic disease, (2) 197 patients with convulsive disorder. Blood manganese was found to be age related in infants under 1 year of age. Highly significant was the lower mean blood manganese found in the convulsive disorder group as compared to the reference group. There was also a slight trend in the convulsive group for blood manganese to decrease from 1 to 22 years of age. No significant differences in manganese levels were found related to sex, type of seizure disorder, type of anticonvulsant drug therapy, or serum level of drug. Although this study does not demonstrate a causal relation between manganese and seizure disorder, and cannot be used as the basis for altering current approaches to therapy, it provides insight into the potentially important role of previously unrecognized factors in the pathophysiology of this syndrome.

Adolescent↗
PubMed1990

Proposals for the mechanism of action of convulsive therapy: a synthesis.

The convulsive therapies have been powerful additions to somatic treatment in psychiatry and have enjoyed widespread application for the benefit of many. A number of theories have been advanced in efforts to account for therapeutic efficacy but none has been comprehensive. These theories can be distinguished by whether they posit a central therapeutic role for stimulation, inhibition, psychological effects, or mixed processes induced by treatment. After critically reviewing extant theories, we propose a model for the effects of the convulsive therapies: Convulsive therapy is essentially nonspecific; "nonphysiological" depolarizations are distinctly important for the restoration of aberrant intravesicular transmitter ratios with resultant therapeusis. We present this model as a working hypothesis that may contribute to the guidance of research in the mechanism of action of convulsive treatment and offer several testable hypotheses in this regard.

Brain↗
PubMed1987

Evidence for increased activity of mouse brain fatty acid cyclooxygenase following drug-induced convulsions.

Enzymatic production of prostaglandins (PGs) from exogenous arachidonic acid was studied in brain microsomal fractions prepared from mice following pentylenetetrazol (PTZ)-induced convulsions. Prostaglandin E2 (PGE2) and prostaglandin F2 alpha (PGF2 alpha) measured either by radioimmunoassay or after incubation with [1-14C]arachidonic acid (AA) was significantly increased in microsomes from the convulsed animals. Pretreatment of the mice with the anticonvulsant ethosuximide prevented the enhanced PG production. The increased PG synthesis could not be attributed to an increased substrate availability nor to an activated phospholipase nor to a direct effect of the convulsant on the fatty acid cyclooxygenase. Evidence that a modification of the cyclooxygenase had occurred with seizure activity was obtained from kinetic analysis; the apparent Km for the AA was lowered from 30 +/- 3 microM in the controls to 12 +/- 1 microM in the PTZ-treated mice. Further evidence for a modification of the fatty acid cyclooxygenase was obtained from incubations of the microsomes with catalase to reduce peroxide formation. Limiting peroxide levels did not decrease the microsomal cyclooxygenase activity in the PTZ-treated mice to control levels. Seizure activity induced by picrotoxin and strychnine also increased the microsomal capacity of the convulsed animals to synthesize PGs. The increased brain fatty acid cyclooxygenase activity may result from a biochemical modification of the enzyme induced by seizure activity.

Animals↗
PubMed1988

Paradoxical convulsant action of a novel non-competitive N-methyl-D-aspartate (NMDA) antagonist, tiletamine.

Intracerebroventricular (i.c.v.) injection of tiletamine, 0.001 mumol, a presumed non-competitive antagonist of N-methyl-D-aspartate (NMDA) receptors, protected mice from convulsions induced by NMDA and quinolinate, but not from those induced by excitatory amino acids interacting preferentially with non-NMDA receptors. At higher doses, however, tiletamine induced convulsions by itself. Tiletamine-induced convulsions were antagonized by the broad spectrum excitatory amino acid antagonist, gamma-D-glutamylamino-methylsulphonate (gamma-D-GAMS), and were potentiated by the competitive NMDA antagonist, 2-amino-7-phosphonohepatanoate (AP7). Intrathecal (i.t.) injection of tiletamine, 0.01-1.0 mumol, dose-dependently suppressed spinal flexor reflexes. Tiletamine, 0.01 and 0.1 mumol, failed to affect spinal Hoffman- (H-) reflexes, whereas tiletamine, 1.0 mumol, led to a 50% increase of the H-reflex amplitude. It is concluded that the anticonvulsant and reflex suppressant action of tiletamine are due to antagonism of NMDA receptor-mediated excitation. The convulsant effect of tiletamine and its excitatory effect on spinal H-reflexes at higher doses, however, appear to be mediated by non-NMDA receptors.

Animals↗
PubMed1995

Effect of unilateral claustral lesion on intermittent light stimulation-induced convulsive response in D,L-allylglycine treated cats.

The effect of unilateral lesions of the claustrum was examined in cats treated with D,L-allylglycine. Prior to the lesion, intermittent light stimulation (ILS) induced (a) myoclonic jerking associated with generalized spike, or polyspike and wave discharge, maximal in the subcortical structures monitored and the cortical visual area, and (b) bisymmetrical generalized-onset tonic-clonic convulsions associated with sustained spike discharge in the motor cortex bilaterally. Subsequent to a unilateral lesion of the claustrum, ILS-induced electro-clinical manifestations of myoclonic jerking remained unchanged. However, the bisymmetrical convulsive pattern transformed into a partial onset secondarily generalized convulsive pattern beginning in the intact hemisphere. It is concluded that the claustrum plays an important role for access of visual afferents to the motor mechanism responsible for ILS-induced convulsive seizure.

Allylglycine↗
PubMed1978

Naloxone as a GABA antagonist: evidence from iontophoretic, receptor binding and convulsant studies.

From the following three lines of evidence, it is proposed that at least part of the convulsant activity of naloxone is a result of GABA receptor blockade. Firstly, iontophoretic naloxone reversibly antagonized GABA-evoked depression of firing rate in 21 of 27 neurons tested in the rat olfactory tubercle-nucleus accumbens region, without blocking inhibition evoked in the same cells by glycine (15 cells) or morphine (6 cells). Secondly, i.p. naloxone in high doses caused convulsions in mice, and potentiated the convulsant activity of bicuculline, but not that of strychnine. Diazepam, which protected mice against convulsions elicited by bicuculline, but not by strychnine, also protected mice against naloxone. Thirdly, naloxone, morphine, levorphanol and its non-analgesic enantiomer dextrorphan displaced 3H-GABA from GABA receptor sites in homogenates of human cerebellum, all with comparable low potencies (IC50 = 250--400 micron). There was no correlation with affinities at the stereospecific receptor sites that mediate opiate-induced analgesia, since the potent opiates etorphine and diprenorphine were relatively inactive (IC50 greater than 3 mM). In addition naloxone displaced 3H-GABA from receptor sites in rate forebrain and cerebellum, with similar low potency.

Action Potentials↗
PubMed1981

Lowering of the convulsive threshold by non-steroidal anti-inflammatory drugs.

Administration of convulsant doses of pentetrazole induced an increase of PGF2 alpha, PGE2 and TXB2 immuno-reactive material in mouse brain in vivo. The non-steroidal anti-inflammatory drugs indomethacin, flurbiprofen and diclofenac in equipotent doses inhibited the convulsion-induced increase of prostaglandins and thromboxane B2 (P less than 0.01). The same drugs also lowered the LD50 of pentetrazole (P less than 0.05) and accelerated the onset of tonic seizures evoked by pentetrazole (P less than 0.05). Ibuprofen in a submaximal centrally effective dose acted in the same way on cerebral PG and TXB2 synthesis and on the LD50 of pentetrazole but failed to influence significantly the latency time to the onset of pentetrazole-induced tonic seizures. Aspirin (100 mg/kg) and paracetamol (30 mg/kg), which were without effect on cerebral PG and TXB2 concentrations following pentetrazole-induced seizures, were also ineffective in lowering the convulsive threshold and the LD50 of pentetrazole. It is concluded that non-steroidal anti-inflammatory drugs act on the convulsive threshold by inhibition of cerebral prostaglandin and/or thromboxane synthesis.

Animals↗
PubMed1985

Antagonism of N-methyl-D,L-aspartic acid-induced convulsions by antiepileptic drugs and other agents.

The effects of common antiepileptics, GABAmimetic drugs, excitatory amino acid antagonists as well as of clonidine, corynanthine, chlorpromazine and atropine were studied against clonic convulsions induced in mice by N-methyl-D,L-aspartic acid (NMDLA) after subcutaneous (340 mg/kg; ED97) and intravenous (105 mg/kg; ED97) administration. Among the antiepileptics studied, valproate (ED50: 340 mg/kg after subcutaneous injection of NMDLA) and diazepam (ED50: 0.78 mg/kg after intravenous and 14 mg/kg after subcutaneous injection of NMDLA) antagonized NMDLA-induced convulsions, whereas phenobarbital (up to 80 mg/kg), diphenylhydantoin (up to 50 mg/kg) and ethosuximide (500 mg/kg) were totally ineffective. Moreover, 2-amino-5-phosphonopentanoic acid and 2-amino-7-phosphonoheptanoic acid (but not glutamic acid diethyl ester), aminooxyacetic acid, cetyl GABA and clonidine protected strongly against the convulsant whereas progabide was only weakly active. THIP showed a higher activity against intravenous than against subcutaneous NMDLA. Baclofen and atropine even increased mortality and the remaining agents exerted no significant protective action. The data suggest that NMDLA-induced convulsions can be blocked effectively by direct antagonism of NMDLA-produced excitation, enhancement of GABA-mediated inhibition, and activation of central alpha 2-adrenoceptors. The possible efficacy of valproate in cases of epilepsy with a distinct rise in plasma excitatory amino acid levels should be carefully considered.

Animals↗
PubMed1994

Clobenpropit (VUF-9153), a new histamine H3 receptor antagonist, inhibits electrically induced convulsions in mice.

The effect of clobenpropit (VUF-9153), a new histamine H3 receptor antagonist, on electrically induced convulsions was studied in mice. Clobenpropit significantly and dose dependently decreased the duration of each convulsive phase. Its anticonvulsant effects were prevented by pretreatment with (R)-alpha-methylhistamine and imetit (VUF-8325), histamine H3 receptor agonists. These findings suggest that the effect of clobenpropit on electrically induced convulsions is due to an increase in endogenous histamine release in the brain, which is consistent with biochemical results that clobenpropit increased brain histidine decarboxylase activity dose dependently. The anticonvulsive effect of clobenpropit was antagonized by mepyramine, a histamine H1 receptor antagonist, but not by zolantidine, a histamine H2 receptor antagonist, indicating that histamine released by the anticonvulsant effect of clobenpropit interacts with histamine H1 receptors of postsynaptic neurons. The present findings of the effect of clobenpropit on electrically induced convulsions are fully consistent with those of thioperamide as described previously (Yokoyama et al., 1993, Eur. J. Pharmacol. 234, 129), supporting the hypothesis that the central histaminergic neuron system is involved in the inhibition of seizures.

Animals↗
PubMed1987

Modulation of postdecapitation convulsions in rats by alpha-adrenergic and 5-hydroxytryptamine1A agents.

Postdecapitation convulsions were analyzed in rats after the administration of a variety of adrenergic and serotonergic agents. Drugs were selected on the basis of their relative affinities for 5-hydroxytryptamine1A, alpha 2-adrenergic and/or alpha 1-adrenergic receptors. The 5-hydroxytryptamine1A-selective agonists, 8-hydroxy-N,N-dipropyl-2-aminotetralin and buspirone, significantly increased the duration of the convulsions. The alpha 2-adrenergic antagonists, yohimbine and corynanthine, had no affect on either the latency or duration of the convulsions. By contrast, each of the three alpha 1-adrenergic agents increased the latency and decreased their duration. However, the order of potency was WB 4101 greater than ipsapirone greater than prazosin and this rank order did not correlate with drug potencies for the alpha 1-adrenergic receptor as determined by radioligand binding studies. The high potency of both ipsapirone and WB 4101 in inhibiting the postdecapitation convulsions may relate to the combined effects of the drugs at both alpha 1-adrenergic and 5-hydroxytryptamine1A receptors.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1989

Effects of GABA-ergic agents on spontaneous non-convulsive epilepsy, EEG and behaviour, in the WAG/RIJ inbred strain of rats.

The effects of GABAergic agents on non-convulsive epilepsy were studied by intracerebroventricular injections of muscimol and bicuculline in WAG/Rij rats. The WAG/Rij rat strain is recognized as an animal model for human absence epilepsy. EEG registrations and behavioural observations showed that muscimol dose-dependently increased the non-convulsive absence epilepsy. Besides this, it induced EEG spikes and body twitches. Bicuculline induced spikes and body twitches as well but decreased the non-convulsive epilepsy. All effects of muscimol can be blocked by bicuculline and vice versa, which suggests that the observed effects are genuine GABAA effects. These results implicate that non-convulsive epilepsy can be caused by a GABAergic hyperfunction.

Animals↗
PubMed1982

The effect of anticonvulsant drugs on convulsions triggered by direct stimulation of the brainstem.

Brainstem-triggered convulsions are generalized convulsive seizures produced by direct electrical stimulation of the mesencephalic reticular formation. Four anticonvulsant drugs, phenobarbital, phenytoin, trimethadione, and ethosuximide, were tested against brainstem-triggered convulsions in the rat using a standard pharmacological dose-response paradigm. All four drugs proved to be active in small, subtoxic doses, producing a response profile similar to that previously reported for maximal pentylenetetrazol seizures. These results appear consistent with the hypotheses that: (1) the brainstem plays an important role in the production of generalized convulsions; and (2) that anticonvulsant drugs exert major therapeutic effects at the brainstem level.

Animals↗