Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pregnant mice are more susceptible to flurothyl-induced seizures than are non-pregnant controls. The possibility that the well-known increase in beta-endorphin concentration which accompanies pregnancy was involved in this effect was examined by testing whether naloxone administration could block the increased seizure susceptibility. Pregnant female, control female and male C3H mice were treated with 5-50 mg/kg naloxone 5 min before flurothyl seizure testing. Naloxone markedly increased clonic seizure susceptibility in all three groups at a dose of 50 mg/kg, but had little effect at lower doses. In contrast, naloxone had differential effects on myoclonic seizures in pregnant and control female mice, being anticonvulsant in the controls, but proconvulsant in the pregnant mice. A role for endogenous opiates is unlikely in mediating clonic seizures in pregnant mice, but may be involved in myoclonic seizures.
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PMID:The effect of naloxone administration on pregnancy-associated seizures. 371 30

The action of morphine, applied either iontophoretically (40-200 nA balanced current) or systemically (5-10 mg/kg, intraperitoneally) to rat cortical neurons, was investigated in vivo, using intracellular electrodes. Morphine increased the apparent input resistance and increased the number of both spontaneous and evoked action potentials. Several cells, which normally generated single spikes, generated bursting potentials; neurons with bursting activity increased their activity. Naloxone, iontophoretically or systemically applied, did not reverse or prevent the morphine-induced excitation. The iontophoretic administration of cadmium suggested that the effects of morphine were due, at least in part, to a postsynaptic site of action. It is suggested that the increase of cellular excitability induced by morphine could contribute to its production of seizures in cortex.
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PMID:Action of morphine on rat cortical neurons intracellularly recorded in vivo: evidence for an excitatory postsynaptic effect which is naloxone insensitive. 373 58

The present work deals with an EEG and behavioural study of the effect of cyclazocine against the convulsions due to pentylentetrazol (PTZ) in mice, rats and rabbits. In rats, cyclazocine, at the high doses (15-25 mg/kg) prevents the tonic motor convulsions and EEG epileptiform "grand mal" seizure induced by PTZ. In rabbits and mice, cyclazocine inhibits the tonic motor convulsions without modifying either the spike-frequency or the duration of the PTZ-induced EEG seizures. Naloxone, even at high doses, was not able to block the anticonvulsive effects of cyclazocine on PTZ-induced convulsions in the rat. The effects of cyclazocine were compared to those of phencyclidine. These results confirm the multiple behavioural effects of cyclazocine and support the idea that both cyclazocine and phencyclidine, may act on the PCP/sigma receptor identified in binding studies.
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PMID:Phencyclidine-like effect of cyclazocine on pentylentetrazol-induced seizures in laboratory animals. 403 53

Electroconvulsive shock (ECS)-induced seizures present a clear cut diurnal rhythmicity when BALB/c mice are subjected to a light-dark (L/D) schedule. On the contrary, in the absence of external synchronizers no evident fluctuations in epileptic behaviour were evident. Naloxone decreased the threshold of ECS-induced convulsions, thus confirming an involvement of opioids in this type of behaviour. These findings indicate that opioids present a diurnal (L/D) but not circadian (L/L) rhythmicity in BALB/c mice.
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PMID:Diurnal variations in electroconvulsive shock-induced seizures: involvement of endogenous opioids. 404 Oct 21

As more small peptidergic components of the central nervous system are isolated, their role in disease states is being investigated. Several of these neuropeptides, especially the opioidlike peptides, adrenocorticotropic hormone, and some hypothalamic releasing factors, have been found to alter neuronal excitability. This finding has led to the proposal that these peptides may play a role in the pathogenesis of the epilepsies. We tested this hypothesis in a genetic model of epilepsy. At nontoxic doses, several exogenously administered peptides had anticonvulsant properties, while others were proconvulsant. The most potent anticonvulsant was the opioidlike peptide beta-endorphin. Its effect was similar to that of the opioid alkaloids. Using the potent antagonist naloxone hydrochloride to block possible endogenous opioid-like peptides, we found no effects on seizures in naive animals. Naloxone did alter postictal events, however, by partially blocking the postictal refractoriness to further seizures. We speculate that one possible role for the endogenous opioid peptides may be to limit the spread of seizures or to modulate postictal susceptibility to further seizures. Naloxone was effective in this model only after stressful situations occurred that modified the seizures and presumably induced a release of endogenous opioidlike peptides. Support for this hypothesis from other epilepsy models is discussed. Other peptidergic systems may also be active in various epileptic models, and the current understanding of their roles is reviewed.
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PMID:Neuropeptides: a role as endogenous mediators or modulators of epileptic phenomena. 609 40

The convulsant benzodiazepine Ro 5-3663, bicuculline and picrotoxin induced electroencephalographic (EEG) and behavioural convulsions. In rabbits, the EEG modifications consisted, with increasing doses, of three different patterns: slow waves in the optic lead, spike- and wave-complexes in the sensorimotor cortex, and grand-mal generalized seizures. These EEG effects were terminated by administration of diazepam (1 mg/kg) and morphine (0.25-1.0 mg/kg). Naloxone, in doses of 5-10 mg/kg, potentiated the effects of the three convulsant drugs. This potentiating phenomenon was also antagonized by the administration of diazepam and morphine. In membrane preparations, obtained from rat cortex, deprived of endogenous modulators of [3H]GABA binding, naloxone but not morphine, was able to inhibit [3H]GABA binding to its specific recognition sites. These data agree with previous findings indicating a GABA-antagonistic effect of naloxone, and support the hypothesis that the anticonvulsant effect of morphine might be, at least in part, due to an increase in GABAergic activity at the synaptic level.
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PMID:Convulsant and anticonvulsant effects of opioids: relationship to GABA-mediated transmission. 629 71

An investigation was made of the effect of morphine dependence on the characteristics of seizures induced in mice by convulsant drugs with differing mechanisms of action. Morphine dependence was induced in 90-day-old mice (weighing 29 to 32 g) by a 6-day schedule of twice daily i.p. injections of increasing doses of morphine (5, 32.5, 58, 82.5, 100, and 135 mg kg-1). Thirty minutes after the last morphine administration, convulsant drugs (4-aminopyridine 8 mg kg-1, pentylenetetrazol 50 mg kg-1, bicuculline 2.5 mg kg-1, strychnine 2.0 mg kg-1, and beta-mercaptopropionic acid 50 mg kg-1) were injected. 4-Aminopyridine (4-AP) and pentylenetetrazol (PTZ) increased both the number of animals with convulsions and death and in the case of 4-AP the period of convulsion latency was also increased. Naloxone at 1.0 mg kg-1 blocked the 4-AP effects, indicating that this action was mediated through an opioid receptor. Strychnine and beta-mercaptopropionic acid had an effect opposite 4-AP and PTZ in the number of animals with convulsions and death. On the other hand bicuculline had an effect more like 4-AP and PTZ than other inhibitory synapse-blocking drugs. We conclude that chronic morphine treatment modified the response of convulsant drugs depending on their mechanisms of action.
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PMID:Effect of different convulsant drugs on some seizure parameters in morphine-dependent mice. 630 71

The effects of repeated infusion of small, initially subconvulsive amounts of beta-endorphin, met-enkephalin or morphine sulfate into the amygdala and hippocampus were investigated. beta-endorphin and met-enkephalin evoked epileptiform spiking when infused into the posterior amygdala or ventral hippocampus. Morphine evoked epileptiform spiking when infused into the anterior amygdala. Naloxone blocked or terminated the spiking. Repetition of the infusions led to the gradual development of bilateral generalized convulsions by beta-endorphin and met-enkephalin and to the development of tolerance to morphine. An unexpected observation was that handling, immobilization or conspecific threat potentiated the epileptiform effects of beta-endorphin and morphine in many cases. These results suggest that endogenous opiate mechanisms might play a role in convulsive seizures and that stressful stimuli can exacerbate opiate seizures.
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PMID:Intracerebral beta-endorphin, met-enkephalin and morphine: kindling of seizures and handling-induced potentiation of epileptiform effects. 632 69

Opioid agonists were used to investigate the modulation of seizures mediated by mu, kappa and delta opiate receptors in the seizure-sensitive Mongolian gerbil. Morphine (1.0-25 mg/kg, s.c.) were used as prototypic agonists for mu, kappa and delta opiate receptors. Each opioid decreased the incidence and severity of the seizure as compared to control values. The anticonvulsant effects of morphine (10 mg/kg, s.c.) and ketocyclazocine (0.5 mg/kg, s.c.) were reversed by naloxone (1.0 mg/kg, s.c.), while the anticonvulsant effects of N-allylnormetazocine (2 mg/kg, s.c.) were not significantly changed by naloxone. Additionally, abnormal behavior was observed following administration of the opioids. Morphine (10 mg/kg, s.c.) produced excitation and hyperresponsiveness with intermittent cataleptic-like states. Ketocyclazocine (10 mg/kg, s.c.) predominantly produced a stuporous, immobile state, accompanied by some loss of posture. N-allylnormetazocine (10 mg/kg, s.c.) produced ataxia and stereotypic side-to-side head nodding . Naloxone was able to reverse the behavioral effects produced by morphine and ketocyclazocine but not those produced by N-allylnormetazocine. The data presented are consistent with earlier studies which demonstrated the anticonvulsant effects of beta-endorphin in the gerbil. This study further suggests that opioids have a protective role against seizure activity in the gerbil and the opioid anticonvulsant effect is not specific to one type of opioid agonist.
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PMID:Similar anticonvulsant, but unique, behavioural effects of opioid agonists in the seizure-sensitive Mongolian gerbil. 633 Jun 6

Rats ranging in postnatal age from 6 hours to 28 days were implanted with cortical and depth electrodes as well as an indwelling cannula in the lateral ventricle. We then administered varying amounts of the opiate peptides leucine-enkephalin and beta-endorphin intracerebroventricularly with continuous electroencephalographic monitoring. Leucine-enkephalin produced electrical seizure activity in rats as young as 2 days. beta-Endorphin administration was associated with seizures at the fifth postnatal day, with a high incidence of apnea resulting in death in animals as young as 6 hours. An adult seizure response to beta-endorphin and leucine-enkephalin was seen at 15 and 28 days of age, respectively. Naloxone blocked the seizure produced by these opiate peptides in all age groups. The data indicate that the opiate peptides are potent epileptogenic compounds in developing brain, that seizures induced by leucine-enkephalin differ from those caused by beta-endorphin, and that petit mal-like seizure activity can be an adult response in the rodent.
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PMID:The ontogeny of seizures induced by leucine-enkephalin and beta-endorphin. 633 Dec 81


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