EFFECT OF MORPHINE AND NALOXONE ON PRIMING‐INDUCED AUDIOGENIC SEIZURES IN BALB/c MICE

Chen, C.S.; Gates, G. Richard; Reynoldson, J.A.

doi:10.1111/j.1476-5381.1976.tb08618.x

Cited by 29 publications

(6 citation statements)

References 14 publications

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“…As a potent antagonist for opioid receptors, the influence of naloxone on seizure activity has been investigated broadly and the results could be epileptogenic (Hardy et al., 1980; Snyder et al., 1980), anticonvulsive (Turski et al., 1985; Puig et al., 1986), or inactive (Chen et al., 1976; Meldrum et al., 1979), depending on different models, naloxone doses, and delivery methods used in previous studies. In our preliminary experiment, naloxone infusion at all four dose levels did not provoke any seizure activity in normal rats, and there was no spontaneous recurrent seizure in untreated and naloxone‐treated P15 SE rats after P15 SE until P60, possibly due to the low doses we used here.…”

Section: Discussionmentioning

confidence: 99%

Protective effects of naloxone in two‐hit seizure model

Yang

et al. 2010

Epilepsia

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SUMMARYPurpose: Early life status epilepticus (SE) could enhance the vulnerability of the immature brain to a second SE in adulthood (two-hit seizure model). Naloxone has been proved to possess inflammation inhibitory effects in nervous system. This study was designed to evaluate the dosedependent protective effects of naloxone in kainic acid (KA)-induced two-hit seizure model. Methods: After KA-induced SE at postnatal day 15 (P15), Sprague-Dawley rats were infused with either saline or different doses (1.92, 3.84, 5.76, and 7.68 mg/kg) of naloxone continuously for 12 h. De novo synthesis of cytokines (interleukin-1b [IL-1b], S100B) was assessed by real-time polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay (ELISA) at 12 h after P15 SE. Glial activation states were analyzed by western blotting of glial markers (glial fibrillary acidic protein[GFAP], S100B, Iba1) both at 12 h after P15 SE and at P45. After a second SE at P45, cognitive deteriorations were evaluated by Morris water tests and neuron injuries were evaluated by TdTmediated dUTP nick end labeling (TUNEL) assays. Results: Naloxone reduced IL-1b synthesis and microglial activation most potently at a dose of 3.84 mg/kg. Attenuation of S100B synthesis and astrocyte activation were achieved most dramatically by naloxone at a dose of 5.76 mg/kg, which is equal to the most powerful dose in ameliorating cognitive injuries and neuron apoptosis after second SE. Conclusions: Naloxone treatment immediately after early life SE could dose-dependently reduce cytokine production, glial activation, and further lower the vulnerability of immature brains to a second hit in adulthood.

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Section: Discussionmentioning

confidence: 99%

Protective effects of naloxone in two‐hit seizure model

Yang

et al. 2010

Epilepsia

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“…and opioid peptides may act as endogenous anticonvulsants in maximum electroconvulsive shock (Tortella and Long, 1985). In some genetically epileptic animals, exogenous opioid peptides act as anticonvulsants (Chen et al, 1976;Meldrum et al, 1979;Bajorek and Lomax, 1982). The mechanism and relationship of the pro-and anticonvulsant effects of the opioid system are not known.…”

Section: Discussionmentioning

confidence: 99%

“…Both pro-and anticonvulsant actions of morphine and endogenous opioids have been reported (Urca and Frenk, 1980;Frenk, 1983). In genetically epileptic animals, such as audiogenic mice (Chen et al, 1976), mongolian gerbils (Bajorek and Lomax, 1982), and Papio pcipio (Meldrum et al, 1979), exogenous morphine and opioid peptides are thought to influence the manifestations of seizures and the electroencephalogram. In electrically induced seizures (Hong et al, 1979;Vindrola et al, 1981;Sarne et al, 1982) and in chemically induced seizures (Hong et al, 1980;Vindrola et al, 19831, the enkephalin content rose after the seizures.…”

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confidence: 99%

Immunoreactive Leucine‐Enkephalin Content in Brains of Epileptic E1 Mice

et al. 1988

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The immunoreactive leucine-enkephalin (IR Leu-E) content in the brains of epileptic E1 mice was determined. E1 mice are mutants from the dd strain of mice and are susceptible to convulsions. Seizures were elicited in E1 mice by repeated postural stimulations. As controls, ddY strain (nonconvulsive) mice and nonstimulated E1 mice (which had not developed convulsions) were used. IR Leu-E content was measured by radioimmuno-assay. Before the convulsion, the IR Leu-E content in the striatum of E1 mice was 60% of the content in the controls. In the hypothalamus, IR Leu-E levels were increased by 85% 45 min after a convulsion. IR Leu-E was also increased in the striatum (176% of preconvulsive state), cortex (121%), medulla oblongata + pons (132%), hypothalamus (180%), and midbrain (159%) 48 h after a convulsion.

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“…The dose of naloxone used was the same as that used by Coimbra et al (18). Using the same kind of seizures in BALB/c mice, Chen et al (19) reported that naloxone reversed the anticonvulsant effect of morphine.…”

Section: Discussionmentioning

confidence: 99%

Do endogenous opioids and nitric oxide participate in the anticonvulsant action of dipyrone?

Reis

Doretto

Duarte

et al. 2003

Braz J Med Biol Res

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It was previously reported that systemic administration of dipyrone inhibited the tonic component of generalized tonic-clonic seizures in both the electroshock and the audiogenic seizure models. The aim of the present study was to investigate the mechanisms involved in the anticonvulsant action of dipyrone by assessing the role of nitric oxide and opioids in the electroshock (female 60-to 90-day-old Wistar rats, N = 5-11) and audiogenic seizure (female 60-to 90-day-old Wistar audiogenic rats, N = 5-11) models of epilepsy. Naloxone (5 mg/kg, sc) significantly reversed the anticonvulsant effect of dipyrone in rats submitted to the induction of audiogenic seizures (ANOVA/Bonferroni's test), suggesting the involvement of opioid peptides in this action. In the electroshock model no reversal of the anticonvulsant effect of dipyrone by naloxone (5 mg/kg, sc) was demonstrable. The acute (120 mg/kg, ip) and chronic (25 mg/kg, ip, twice a day/4 days) administration of L-NOARG did not reverse the anticonvulsant action of dipyrone in the audiogenic seizure model, suggesting that the nitric oxide pathway does not participate in such effect. Indomethacin (10, 20 and 30 mg/kg, ip) used for comparison had no anticonvulsant effect in the audiogenic seizure model. In conclusion, opioid peptides but not nitric oxide seem to be involved in the anticonvulsant action of dipyrone in audiogenic seizures. Correspondence

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EFFECT OF MORPHINE AND NALOXONE ON PRIMING‐INDUCED AUDIOGENIC SEIZURES IN BALB/c MICE

Cited by 29 publications

References 14 publications

Protective effects of naloxone in two‐hit seizure model

Protective effects of naloxone in two‐hit seizure model

Immunoreactive Leucine‐Enkephalin Content in Brains of Epileptic E1 Mice

Do endogenous opioids and nitric oxide participate in the anticonvulsant action of dipyrone?

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