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

The role of opiate mechanisms in the development of tolerance and altered susceptibility to seizures after repeated injections of picrotoxin was investigated. Independent groups of rats were pretreated with naloxone (0.3, 1.0, 3.0, and 10.0 mg/kg) or the saline vehicle and then tested for seizures induced by picrotoxin. The procedure was performed on 3 days at 1-week intervals, for a total of 3 testing days. Latencies to different types of seizures, the duration of postseizure immobility, and the number of focal seizure episodes were scored. In the vehicle-treated group, repeated picrotoxin injections led to an increased susceptibility to myoclonic and focal seizures and to decreased duration of postseizure immobility. Naloxone pretreatment significantly decreased the duration of the postseizure akinetic periods in the 1.0- and 10.0-mg/kg groups across all days, suggesting that endogenous opiates are involved in postseizure immobility and that there are interactions between opiate and picrotoxin mechanisms in some seizure-related behaviors. Naloxone did not alter the development of tolerance or sensitivity, indicating that naloxone-insensitive opiate mechanisms or nonopiate mechanisms may be involved in these processes.
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PMID:Picrotoxin-induced behavioral tolerance and altered susceptibility to seizures: effects of naloxone. 833 23

In modern anaesthesia various antagonists are used. They provide efficient tools to facilitate better control of pharmacological effects and side effects of drugs routinely used in anaesthesia. Naloxone is a competitive antagonist of opioids without any intrinsic activity. It counteracts respiratory depression, pruritus, sedation and analgesia caused by opioids. It is fast-acting with a duration of action of 45 to 90 min. Several investigators have reported severe side effects of naloxone including hypertension, tachyarrhythmias, left heart failure and cardiac arrest, and hence the use of naloxone must be carefully considered in every single patient. Flumazenil is a competitive antagonist of benzodiazepines. It is a remarkably safe drug and very effective to terminate all benzodiazepine effects in anaesthesia and intensive-care patients. Serious complications caused by flumazenil have been reported in patients receiving benzodiazepines in the treatment of seizure disorders and in patients with mixed intoxications. Neostigmine is one of several antagonists of neuromuscular blocking agents. Its side effects include bradycardia, increased bronchial secretions and increased peristalsis. Indication depends on the results of neuromuscular monitoring. Physostigmine is an unspecific antagonist of the central anticholinergic syndrome, an acute psychosis that may be caused by numerous drugs used in anaesthesia. Generally, antagonists should be carefully titrated. In emergency medicine the use of these antagonists is not recommended; the primary goal is to restore vital functions.
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PMID:[Antagonists in anesthesia]. 854 33

The influence of naloxone and naltrexone on the hypnotic and protective efficacy of diazepam, chlordiazepoxide, clonazepam and estazolam against electroshock- and pentylenetetrazole-induced seizures was studied in mice. Naloxone and naltrexone significantly decreased the anticonvulsant effects of diazepam and estazolam, but they did not changed that of chlordiazepoxide and clonazepam in electroshock-induced tonic hindlimb extension. Protective effects of benzodiazepines against pentylenetetrazole-induced seizures were slightly diminished by naloxone and naltrexone (16 mg/kg). Opioid antagonists were able to reduce the duration of benzodiazepines-induced sleep at high dose (32 mg/kg) only. These findings suggest that the endogenous opioid system may participate in antiepileptic effects of benzodiazepines but not in their hypnotic activity.
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PMID:Effects of opioid antagonists on anticonvulsant and hypnotic activity of benzodiazepines. 911 81

Rats were kindled by repeated injections of pentylenetetrazole (PTZ; 37.5 mg/kg; i.p.) in the presence or absence of the opioid receptor antagonist naloxone. Naloxone (10 mg/kg; i.p.) applied 30 min before each PTZ application had no major effect on the seizure development, although a slight decrease in the seizure expression of fully kindled animals could be observed. In the kindled animals, a pronounced but transient increase in c-fos mRNA level was observed in several brain areas after the injection of PTZ. The magnitude of c-fos induction was related to the seizure stage reached. Detectable c-fos mRNA levels in the cortex were observed in rats showing stage four seizures, whereas the expression of c-fos in the hippocampus required stage five kindled seizures. The induction of c-fos expression in the hippocampus of stage five kindled rats but not in other brain areas was prevented by treatment of naloxone prior to each PTZ application. In contrast, a single injection of naloxone to kindled rats was not sufficient to prevent c-fos mRNA expression in the hippocampus. In addition, a single PTZ application (at the higher dose of 45 mg/kg) to rats that were not kindled also caused c-fos expression in several brain regions, but this was not influenced by naloxone. Assuming that c-fos expression reflects neuronal activity our findings suggest a functional role of endogenous opioid peptides in the development of kindling-induced neuronal excitation in the hippocampus. In addition, the excitation of the hippocampus does not appear to be involved in the seizure activity but may be responsible for the impairment of learning in PTZ-kindled rats which can be prevented by pretreatment with naloxone [A. Becker, G. Grecksch, M. Brosz, Naloxone ameliorates the learning deficit induced by pentylenetetrazole kindling in rats, Eur. J. Neurosci. 6 (1994) 1512-1515].
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PMID:Pentylenetetrazole (PTZ)-induced c-fos expression in the hippocampus of kindled rats is suppressed by concomitant treatment with naloxone. 959 56

The nuclei comprising the neuronal network for audiogenic seizures (AGS) are located primarily in the brainstem. Previous studies suggested a role for the periaqueductal grey (PAG) in the AGS network. The present study evaluated this possibility in genetically-epilepsy prone rats (GEPR-9s) by examining the effects of bilateral focal microinjection of a competitive NMDA receptor antagonist (DL-2-amino-7-phosphonoheptanoic acid (AP7), 1 and 5 nmol/side), a GABA(A) agonist (gaboxedol (THIP), 10 and 15 nmol) or an opioid peptide receptor antagonist (naloxone, 5 nmol) into PAG, based on the proposed role of these receptors in PAG neurotransmission. Blockade of NMDA receptors by AP7 (both doses) or activation of GABA(A) receptors with THIP (15 nmol/side) in the PAG suppressed AGS susceptibility. Naloxone displayed a seizure-suppressant effect that was delayed and incomplete. The seizure suppressant effect of AP7 or naloxone, unlike THIP, was observed at doses that did not produce motor quiescence. These data suggest that the PAG is a requisite nucleus in the neuronal network for AGS in GEPR-9s and that GABA(A), opioid peptide and NMDA receptors in the PAG modulate AGS propagation.
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PMID:The periaqueductal grey is a critical site in the neuronal network for audiogenic seizures: modulation by GABA(A), NMDA and opioid receptors. 1023 93

Preconditioning is defined as an adaptive mechanism produced by short periods of hypoxia/ischemia, resulting in protection against subsequent ischemic insult, and development of seizures. Results of the present study demonstrate that an episode of normobar hypoxia reduces the susceptibility to convulsions induced by pentylenetetrazol (PTZ) 30 min, 24 h, as well as 4 and 7 days later. Administration of morphine showed similar effects after 24 h. Naloxone, given before ischemic preconditioning, as well as morphine, blocked the development of the protection. Administration of D-Ala-Met-enkephalin-Gly-ol (DAMGO - a selective mu-opioid receptor agonist), as well as trans-3, 4-dichloro-N-methyl-N-[7-(1-pyrrolidinyl) cycloexilbenzeneacetamide ethane sulfonate] (U-69,593 - a selective kappa-opioid receptor agonist), mimicked the effects of hypoxic preconditioning (HPC). (-)-N-(Cyclopropylmethyl)-4,14-dimethoxymorphinan-6-one (cyprodime - a selective mu-opioid receptor antagonist, as well as nor-binaltorphimine dihydrochloride (nor-BNI - selective kappa-opioid receptors antagonist), given before HPC as well as before respective opioid receptor agonists, blocked the development of the protection. This study provides evidence that mu- and kappa-opioid receptors are involved in HPC against seizures in the brain.
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PMID:The role of opioid receptors in hypoxic preconditioning against seizures in brain. 1111 85

The anticonvulsive activity of nociceptin, endogenous OP4 receptors agonist was investigated in pentylenetetrazole (PTZ), N-methyl D-aspartic acid (NMDA), bicucculine (BCC) and electrically evoked seizure models of experimental epilepsy. Nociceptin, at the dose of 10 nmol, suppressed the clonic seizures induced by PTZ, NMDA and BCC. [Phe1(psi)(CH2-NH)Gly2]nociceptin-(1-13)-NH2 which has been proposed to be selective antagonist OP4 receptors, did not prevent the action of nociceptin. The effect of [Phe1(psi)(CH2-NH)Gly2]nociceptin-(1-13)-NH2 on seizures induced by PTZ, NMDA and BCC was very similar to that of nociceptin. These data support the hypothesis that it possesses agonistic properties. Naloxone did not reverse the anticonvulsive action of nociceptin as well as [Phe1(psi)(CH2-NH)Gly2]nociceptin-(1-13)-NH2 which excludes the participation of opioid receptor in this action. On the other hand in the electroconvulsive model of generalized seizures, nociceptin as well as [Phe1(psi)(CH2-NH)Gly2]nociceptin-(1-13)-NH2 influenced neither the electroconvulsive threshold nor the maximal electroshock test. The data suggest that nociceptin and [Phe1(psi)(CH2-NH)Gly2]nociceptin-(1-13)-NH2 can exert anticonvulsive action. These properties depend on OP4 but not opioid receptors activation.
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PMID:Nociceptin, OP4 receptor ligand in different models of experimental epilepsy. 1183 99

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.
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PMID:Do endogenous opioids and nitric oxide participate in the anticonvulsant action of dipyrone? 1293 95

The role of endogenous opioid peptides in impairment of spatial performance due to epileptogenesis was examined. Animals were kindled by repeated injections of pentylenetetrazol (PTZ) (40 mg/kg, i.p.) in the presence or absence of the opioid receptor antagonist naloxone. Naloxone in different doses (1, 5 and 10 mg/kg, i.p.) was applied 30 min before each PTZ injection. Behavioral testing was assessed 24 h and 10 days after the last injection in separate groups of animals using Morris water maze. Our results showed that PTZ-induced kindling produced a significant impairment of spatial learning and memory as compared with controls and this effect was not due to the aftereffect of repeated seizures. Naloxone pretreatment in the course of kindling had no effect on seizures development, however it caused an improvement of spatial learning and memory performance in kindled rats. It is likely that the long-lasting changes in neuronal responsiveness associated with kindling led to a defect in the processing of spatial information. These data suggest that endogenous opioid peptides released in the hippocampus during kindling are at least in part responsible for impairment of spatial performance in kindled animals.
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PMID:Naloxone improves impairment of spatial performance induced by pentylenetetrazol kindling in rats. 1728 74

A 60-year-old man without comorbidity underwent a totally extraperitoneal repair of bilateral inguinal hernias under general anesthesia. Forty minutes after the procedure he developed a slow, shallow respiratory pattern with a respiratory rate of 5/min and a self-limiting grand mal seizure lasting 30 seconds. Arterial blood gas analysis indicated significant hypercarbia and acidosis. The total dose of morphine administered was 20 mg intravenously. Naloxone was administered and the respiratory rate improved. The patient was discharged after 24 hours after making a good recovery and has had no further seizures a year after surgery. Although hypercarbia is a well-known complication of laparoscopic surgery when CO2 is used for insufflation, this, to the best of our knowledge, is the first reported case of a patient sustaining a grand mal seizure resulting from CO2 narcosis after laparoscopic surgery. The possible mechanisms are discussed.
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PMID:Carbon dioxide narcosis and grand mal seizure complicating laparoscopic herniorrhaphy. 1731 57


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