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Query: UMLS:C0036572 (seizures)
80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Morphine, beta-endorphin and [D-Ala2, D-Leu5] enkephalin administered intracerebroventricularly exerted a protective effect on electroconvulsive shock (ECS)-induced seizures in mice. This effect was reversed by intraperitoneal injections of naltrexone. The role of mu and delta receptors in ECS-induced convulsions is discussed.
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PMID:Opioid antagonism of electroshock-induced seizures. 633 Jul 66

The chemoconvulsant pentylenetetrazol (PTZ) was administered by a variety of routes to rats pretreated with morphine (10-50 mg/kg s.c.). In a naloxone-reversible, dose-dependent manner, morphine decreased the threshold for seizures induced by the slow intravenous infusion of PTZ. In addition, morphine increased the severity of seizures induced by the intravenous, intraperitoneal, and subcutaneous routes of administration of PTZ. Morphine also caused an increased incidence of multiple seizures following subcutaneous administration of PTZ. These results demonstrate that morphine has a proconvulsant effect on PTZ-induced seizures in the rat.
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PMID:Proconvulsant effect of morphine on seizures induced by pentylenetetrazol in the rat. 648 46

Post-decapitation seizures (PDR) are a spinal reflex which seems regulated by some monoaminergic neurons present in the spinal cord (S.C.). In order to better characterize the role of dopaminergic neurons in PDR, we studied the effect of treatment with opiates, which are known to increase dopamine (DA) and serotonin (5HT) metabolism in the brain, on the duration of PDR and on the metabolism of DA and 5HT in S.C. Morphine, given either IP or ICV, reduced the duration of PDR and increased DA metabolism. Both effects were more evident after systemic administration. [D-Ala2]Met5 enkephalin amide acted similarly to ICV administered morphine. Biochemical and behavioral effects were significantly correlated.
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PMID:The effect of opiate treatment on the postdecapitation reflex and monoamine metabolism in the rat spinal cord. 663 93

In several species, larger doses of systemically-administered morphine induce seizures while smaller doses potentiate chemically-induced convulsions. However, it is generally considered that morphine acts as an anticonvulsant in the rat. In the present study, the effects of pretreatment with morphine on both electrical and motor manifestations of pentylenetetrazol (PTZ)-induced seizures in the rat were examined. Morphine (60 and 120 mg/kg) significantly delayed the onset of motor seizures induced by pentylenetetrazol but also induced a significantly greater number of motor seizures, a greater percentage of deaths and a lowering of the chemoconvulsive threshold for pentylenetetrazol. Recordings from animals with chronically-implanted supracortical electrodes showed that pretreatment with morphine (60 mg/kg) both altered the onset pattern of CNS excitation induced by pentylenetetrazol and delayed the onset of electrical seizure activity. These recorded electrocortical effects were similar to the behavioral effects observed in the non-implanted animals. Larger doses of morphine (175 and 250 mg/kg) by themselves produced both motor and electrocortical seizures in rats with chronically-implanted electrodes.
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PMID:Effect of morphine pretreatment on pentylenetetrazol-induced seizures in the rat. 664 54

In a naloxone-reversible, dose-dependent manner, morphine (10-50 mg/kg i.p.) protected against seizures induced by maximal electroshock and increased the incidence and severity of seizures induced by bicuculline, in rats. Morphine also potentiated seizures induced by isoniazid and by picrotoxin. Thus, opiate activity influences the expression of seizures in contrasting ways depending upon the mode of seizure induction. Since morphine consistently potentiated seizures induced by interference with GABA transmission, it appears that GABAergic systems may be of particular significance for the elucidation of the varied effects of morphine on seizure susceptibility.
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PMID:Morphine potentiates seizures induced by GABA antagonists and attenuates seizures induced by electroshock in the rat. 665 73

Rats were pretreated either with saline or with various doses of morphine. Thirty minutes following this pretreatment animals received an injection of either naltrexone (5 mg/kg) or saline. Motility was measured following the second injection. All animals then received 40 mg/kg pentamethylenetetrazol (PTZ). Morphine, but not naltrexone, showed anticonvulsant action by increasing the latencies to the first preclonic jerk and seizure onset. In addition, morphine tended to shorten seizure duration, whereas naltrexone tended to lengthen it. However, at the most effective anticonvulsant dose morphine-treated animals showed significantly more covulsive seizures than did the saline-treated controls. The continuation of these multiple seizures was blocked by naltrexone. At doses which did not lower preseizure motility but rather increased it, morphine significantly embraced the duration of the behavioral post-ictal depression (PID). Naltrexone, though effecting preseizure motility when administered after morphine, did not effect PID. These results are taken as evidence, that morphine possesses both pro- and anticonvulsant properties, depending on the prior occurrence of a PTZ-induced seizure. The possibility that seizures cause increased sensitivity of the organism to morphine is discussed.
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PMID:Pro- and anticonvulsant action of morphine in rats. 742 89

Propofol (i.v. and i.p.) exhibited anticonvulsant activity in three models of seizure in the mouse, induced by bicuculline, kainic acid and N-methyl-DL-aspartic acid (NMDLA). Morphine, pethidine and fentanyl, which showed a biphasic dose-response relationship with respect to seizure modulation, abolished the anticonvulsant activity of propofol to exhibit their own intrinsic activity in proconvulsant doses. This occurred with very low doses of fentanyl and pethidine (15 micrograms kg-1 and 0.5 mg kg-1, respectively) in the NMDLA model. Thus it appears that propofol has anticonvulsant activity only when a convulsion is elicited directly; it does not prevent the actions of compounds that lower seizure threshold to convulsant stimuli. The anticonvulsant doses of morphine and fentanyl did not summate with the anticonvulsant activity of propofol. However, there was some evidence of summation of anticonvulsant activity between pethidine and propofol in the NMDLA model.
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PMID:Interactions between opioid drugs and propofol in laboratory models of seizures. 771 78

Recent studies have suggested that cholecystokinin may have a role in modulating the effects of the endogenous opioid system in physiological functions such as thermoregulation and pain control. However, the possible interaction of cholecystokinin and morphine in epileptogenesis is unknown. We studied the effect of subcutaneous morphine and intracerebroventricularly administered cholecystokinin octapeptide sulphate ester and receptor antagonists CCK-A (MK 329) and CCK-B (L 365,260) on seizures provoked by maximal electroshock in male Sprague-Dawley rats. Seizures were induced through electrode-gel-coated ear clip electrodes by a high voltage, high internal resistance constant current generator, 30 minutes after morphine administration and 10 minutes after cholecystokinin-8-SE, CCK-A and CCK-B infusion. Morphine decreased the length of the tonic component of the seizure and cholecystokinin potentiated this decrease. Cholecystokinin antagonists blocked the effects of both cholecystokinin and morphine. The results suggest that cholecystokinin acts as an endogenous agonist with opioids in the regulation of seizure susceptibility through both CCK-A and B receptors and may be responsible for part of the anticonvulsant action of morphine.
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PMID:Cholecystokinin potentiates morphine anticonvulsant action through both CCK-A and CCK-B receptors. 774 54

Morphine, fentanyl and pethidine exhibited a biphasic dose response relationship with respect to their effects on seizure thresholds to bicuculline, pentylenetetrazole, N-methyl-DL-aspartate (NMDLA) and kainic acid in mice. The usual pattern was for low doses to be anticonvulsant and higher doses to be proconvulsant. However this pattern was reversed for fentanyl and pethidine when NMDLA was used to induce seizures. The low dose effects of all three opioid drugs was sensitive to 1 mg kg-1 naloxone in all seizure models. The responses to high doses of pethidine were unaffected or enhanced by this dose of naloxone. Naloxone reversed the effects of the higher doses of morphine and fentanyl in all models except bicuculline induced seizures.
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PMID:The activity of opioid analgesics in seizure models utilizing N-methyl-DL-aspartic acid, kainic acid, bicuculline and pentylenetetrazole. 791 38


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