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)

Intracerebroventricular administration of 10--20 microgram of steroid-O-sulfates induced hypermotility, agitation, salivation, EEG abnormalities, stereotypies, wet dog shakes and seizures. Equivalent effects resulted from 30--200 microgram morphine sulfate (H2SO4 salt), 50 microgram EGTA or 300--400 microgram of sodium sulfate or phosphate, but not chloride, nitrate or acetate. Non-steroid sulfates, steroid glucuronides and steroid phosphates were inactive. Naloxone, previously found to antagonize the excitatory effects of androsterone sulfate, failed to antagonize those of cortisol sulfate, sodium sulfate or EGTA. These findings suggest a role for extracellular calcium ions and for sulfate derived from circulating steroids in central responses to opiates.
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PMID:Opiate-like excitatory effects of steroid sulfates and calcium-complexing agents given cerebroventricularly. 21 60

Naloxone in high doses (60--240 mg/kg i.p.) produced a dose-dependent increase in cerebellar cGMP content of mice. The rise in cGMP content reached its maximum within 5 min and was of short duration. Short-lasting episodes of clonic seizures were noted after 240 mg/kg naloxone. Low doses of naloxone (5--10 mg/kg) had no effect on cerebellar cGMP content, but markedly potentiated the increase in cGMP induced by isoniazid. On the other hand, naloxone (5 mg/kg) partially antagonized the fall in cGMP elicited by diazepam, but had only a slight effect on the action of pentobarbital (30 mg/kg i.p.). These results support the assumption proposed by other authors that naloxone exerts GABA antagonistic effects aside from the potent opiate receptor antagonistic activity.
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PMID:The effect of naloxone on cerebellar cGMP content. A possible GABA-antagonistic action? 22 44

Naloxone antagonized convulsions produced by tail vein infusions of d-propoxyphene, heroin, meperidine, normeperidine and thebaine in mice in a dose-related manner. Pretreatment with naloxone (60 mg/kg i.p.) produced a 200 percent increase of the dose of d-propoxyphene or heroin needed to produce a seizure. A 40 percent increase in the convulsant dose of meperidine was observed after naloxone pretreatment (30 mg/kg i.p.). Naloxone (15 mg/kg i.p.) produced a 30 percent increase in the convulsant dose of normeperidine; however, larger doses of naloxone did not produce any further increase in the convulsant dose of either normeperidine or meperidine. Larger doses of naloxone were needed to antagonize convulsions produced by thebaine. Heroin, d-propoxyphene and meperidine produced nonlethal clonic seizures, whereas normeperidine and thebaine produced tonic-clonic seizures which were followed by death. These data suggest that there may be two mechanisms by which narcotic analgesics and their congeners produce convulsions.
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PMID:Antagonism of the convulsant effects of heroin, d-propoxyphene, meperidine, normeperidine and thebaine by naloxone in mice. 112 Sep 55

Past research has demonstrated brain opioid and GABA release in response to ejaculation. In the present study we evaluated the potential role of these neurotransmitters in the postictal behavioral depression (PBD), after-discharge (AD) duration, and seizure intensity in rats kindled in the medial preoptic area (MPOA) and amygdala (AMG). The PBD, the AD duration and the seizure intensity were measured after a standard kindling stimulus and after a standard kindling stimulus applied 2 min after ejaculation. The PBD was significantly increased when the animals were stimulated 2 min after ejaculation. This increase was found in MPOA- but not in AMG-kindled rats. Ejaculation had no effect on AD duration or seizure intensity. Naloxone administration before the initiation of sexual behavior completely blocked the increase in PBD in MPOA-kindled rats. It is suggested, by indirect evidence, that opioid release during sexual behavior is added to the release associated with kindled seizures, increasing the duration of the PBD. Since sexual behavior lacked effect on AD duration or seizure intensity, no evidence could be found suggesting that functionally relevant amounts of GABA are released during this behavior.
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PMID:Sexual behavior enhances postictal behavioral depression in kindled rats: opioid involvement. 129 97

Electroconvulsive shock-induced seizures elevate seizure thresholds in humans and interfere with kindling in animals; opioids may mediate the anticonvulsant mechanism. In a potential model of acute electroconvulsive shock in hippocampal slices, a high-intensity tetanus via the mossy fibers substantially delayed subsequent in vitro kindling through the Schaffer collaterals. Naloxone blocked this effect, implicating the opioid system in the antiepileptogenic properties of this model.
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PMID:Naloxone blocks antiepileptogenic properties of an in vitro electroconvulsive shock model. 168 76

Investigations were made of the action of ACTH and LH-RH on a number of behavioural paradigms and the possible involvement of neurotransmitters or opiates by pretreatment of receptor blockers in rats and mice. ACTH delayed the extinction of active avoidance behaviour. Atropine and haloperidol blocked this action, whereas phenoxybenzamine and propranolol were ineffective. LH-RH or a highly potent analogue of LH-RH (D-Trp6-LH-RH) decreased the rate of disappearance of dopamine in the hypothalamus following alpha-methyl- paratyrosine inhibition of catecholamine synthesis, and blocked the accumulation of serotonin following MAO inhibition. LH-RH or the analogue attenuated the consolidation of passive avoidance learning. Apomorphine-induced cage-climbing was also inhibited by the LH-RH analogue, but this action was not influenced by naloxone. Open-field activity (ambulation, rearing and grooming) was decreased by the analogue peptide. Naloxone blocked the action on ambulation and rearing, but was ineffective on grooming. The LH-RH analogue caused a dose-dependent increase in cataleptogenic activity. This action could not be blocked with naloxone. The LH-RH analogue suppressed picrotoxin-induced seizures. Naloxone restored the situation to the control level. The data suggested that the effects of some neurohormones are mediated by transmitters or endogenous opiates, and that both peptide-transmitter and peptide-peptide interactions have to be considered in the action of neurohormones.
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PMID:Involvement of neurotransmitter and neuropeptides in behavioural action of some neurohormones. 198 90

To evaluate the safety and possible efficacy of high-dose naloxone for the treatment of acute cerebral ischemia, 38 patients received a loading dose of 160 mg/m2 over 15 minutes followed by a 24-hour infusion at the rate of 80 mg/m2/hr. Nausea and/or vomiting were common side effects. Naloxone was discontinued in seven patients (because of hypotension in one, bradycardia and hypotension in two, myoclonus in one, focal seizures in two, and hypertension in one); all seven patients responded to treatment and no permanent sequelae to naloxone were noted. Twelve of the 38 patients showed early neurologic improvement (by completion of the naloxone loading dose). However, there was no correlation between such a loading dose response and clinical outcome at 3 months. Our experience suggests that naloxone is safe at the dose used, but data for efficacy are inconclusive.
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PMID:High-dose intravenous naloxone for the treatment of acute ischemic stroke. 233 51

The effects of a selective kappa-agonist, U-50,488H, on systemic kainic acid-induced behavioral and histological changes were studied in rats. U-50,488H inhibited kainic acid-induced wet dog shakes in a naloxone reversible manner; however, U-50,488H did not protect rats against kainic acid-evoked behavioral seizures. As revealed by histological analysis, kainic acid caused edema and severe neuronal damage in several brain regions, notably in CA1 but also in the CA3 fields of both hippocampi. Pretreatment of rats with U-50,488H markedly protected hippocampal neurons, especially those in CA1, against kainic acid-induced neurotoxicity. Naloxone by itself had little effect on kainic acid-induced seizures or hippocampal neuron loss. Naloxone plus U-50,488H resulted in less severe seizures and, consequently, less hippocampal cell loss than after kainic acid alone. These data indicate that U-50,488H can markedly attenuate the neurotoxic and behavioral consequences of systemic kainic acid administration. However, the mechanism of these effects requires further study with more specific opioid antagonists.
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PMID:The interaction between kappa-opioid agonist, U-50, 488H, and kainic acid: behavioral and histological assessments. 253 86

The development of tolerance to analgesic effects of ethanol and ketamine, development of cross-tolerance between those drugs, and the effects of ketamine on the symptoms of ethanol abstinence were investigated in mice and rats. The analgesic action of ethanol (2.8 g/kg in rats, 5 g/kg in mice) was significantly reduced in the animals chronically treated with ethanol. Chronic treatment with ketamine (100 mg/kg in rats, 160 mg/kg in mice twice daily for 7 days) resulted in development of tolerance to the analgesic effects of ketamine. Cross-tolerance developed to the analgesic action of ketamine in mice and rats receiving ethanol chronically. A chronic treatment with ketamine resulted in development of significant cross-tolerance to the antinociceptive action of ethanol. Ketamine significantly attenuated the symptoms of ethanol abstinence (head shakes) in mice (20 mg/kg) and rats (25 mg/kg). Naloxone pretreatment (2 mg/kg) antagonized the inhibitory action of ketamine on the ethanol abstinence in rats. Doses of 12.5-75 mg/kg of ketamine abolished or significantly inhibited the ethanol abstinence symptoms (audiogenic seizures) in rats. The results demonstrate some similarities of the action of ketamine and ethanol and suggest a possibility that the endogenous opioid system participates in the mechanisms of action of the investigated compounds.
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PMID:Interaction between ketamine and ethanol in rats and mice. 258 34

The relationship between wet-dog shaking (WDS) and afterdischarge (AD) elicited by dorsal hippocampal stimulation was investigated. The number of the WDS during a 150-s observation period was 9.6 +/- 2.0 (mean +/- SEM) and no WDS was seen during the non-seizure period. The effects of morphine and neuroleptics on WDS and AD were also investigated. Morphine significantly inhibited the number of WDS elicited by hippocampal stimulation. Naloxone significantly antagonized the inhibitory effect of morphine. Haloperidol and chlorpromazine significantly and dose-dependently inhibited the number of WDS at very small doses. The inhibitory effect of chlorpromazine on WDS was not antagonized by pretreatment with naloxone. The present results suggest that central dopaminergic mechanisms may be important in WDS elicited by hippocampal stimulation. The effect of morphine on WDS is probably mediated via an opioid receptor having a modulating effect on central dopaminergic mechanisms.
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PMID:Effects of morphine and neuroleptics on wet-dog shaking behavior elicited by hippocampal stimulation in rats. 286 Jun 86


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