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

Two experiments were conducted to investigate the effects of naloxone hydrochloride on seizure thresholds seizure afterdischarges (thresholds and durations) and on post-ictal depression. Experiment 1 examined the effects of naloxone dosage and interstimulation interval (ISI) on kindled seizures. Eight male hooded rats were exposed to a factorial combination of two ISIs (30 and 60 s) and 3 naloxone doses (2, 10 mg/kg and a saline control) during a threshold testing procedure. Naloxone was found to significantly shorten motor seizure duration and post-ictal depression. Experiment 2 examined the effects of naloxone on a subsequent suprathreshold-stimulation-induced seizure following an initial suprathreshold stimulation. A factorial combination of 3 naloxone doses (2, 5 and 10 mg/kg) and a saline control and two ISIs (2 and 6 min) separating the two stimulations was employed. While no main effects for either naloxone or ISI were found in the subsequent seizure activity, there was a significant interaction between naloxone and ISI for the subsequent motor seizure duration. It was concluded from the results of the present experiments that the direction and consistency of naloxone's effects on kindled seizures were present but not very strong. However, the effects of ISI on seizure activity were found to be consistent with the previous literature.
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PMID:The effects of naloxone and interstimulation interval on post-ictal depression in kindled seizures. 636 73

Naloxone, an opiate antagonist, has recently been reported to temporarily reverse neurologic deficits associated with subarachnoid hemorrhage. To determine if this unexpected effect of naloxone might also occur in other forms of cerebrovascular diseases, 13 patients who presented with acute neurologic deficits were administered intravenous naloxone. In 3 of these patients, coincidental improvement in neurologic status was seen. In one patient the improvement was permanent. Ten of the 11 patients with non fatal neurologic damage improved later in their hospital course--7 of them to their pre-admission state. The only side effect noted was the temporally related onset of a single focal seizure in an ethanol intoxicated patient with an intracerebral hemorrhage.
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PMID:Naloxone administration to patients with acute stroke. 636 63

The influence of centrally administered meperidine, normeperidine and pentazocine on the excitability of brain was studied by measuring the threshold for flurothyl-induced convulsions in rats. All three opioids are reported to lower seizure thresholds when given subcutaneously to rats in this test. Dose-and time-dependent changes in the seizure threshold occurred after intracerebroventricular injection of pentazocine (10-160 micrograms), meperidine (25-150 micrograms) and normeperidine (50-150 micrograms). Rapid increases in the seizure threshold were associated with pentazocine and meperidine, whereas a slowly developing decrease in the threshold was caused by normeperidine. Naloxone (10 mg/kg, s.c.) antagonized the anticonvulsant effect of meperidine (but not that of pentazocine) and enhanced the proconvulsant effect of normeperidine. Thebaine (25-150 micrograms), which had no marked influence on the seizure threshold when given intracerebroventricularly, lowered the threshold after subcutaneous injection of 12.5 and 25 mg/kg. This effect was not altered by injection of naloxone. These results show that centrally administered opioids can act on excitatory or inhibitory systems that regulate seizure mechanisms in the rat brain. Furthermore both naloxone-sensitive and naloxone-insensitive components are involved. Meperidine, pentazocine and thebaine have different actions on the seizure threshold after intracerebroventricular, as opposed to subcutaneous, administration. This work has, therefore, identified the route of administration as a critical variable in the effect of opioids on the seizure threshold in rats.
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PMID:Studies on the excitatory and inhibitory influence of intracerebroventricularly injected opioids on seizure thresholds in rats. 647 79

Albino rats received 10 s of sub-seizure electrical stimulation applied to the dentate gyrus granule cells immediately after acquisition of information on trial 1 of a 2-trial radial maze spatial memory task. Granule cell stimulation selectively reduced the probability of accessing information held in declarative memory ('knowing that' a particular maze location contains food) while leaving procedural memory intact ('knowing how' to search for food in the maze). This specific memory impairment was prevented by pretreatment with the opiate antagonist naloxone. Naloxone also improved memory performance when given to non-stimulated subjects.
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PMID:Selective impairment of declarative memory following stimulation of dentate gyrus granule cells: a naloxone-sensitive effect. 648 30

To learn more about postictal behaviors and their underlying mechanisms, five behaviors and EEG recordings were studied following fully generalized, kindled seizures in rats. The behaviors included bar pressing for food; tail withdrawal, squeak, and multiple squeak responses to painful tail shocks; consumption of freely available food; clinging to a vertical grid; and locomotion. Latencies from the end of a seizure afterdischarge until each behavior recovered were compared and were found to cluster in three distinct pairs. Locomotion and grid clinging recovered most quickly; consumption of freely available food and EEG postictal depression recovered next; and bar pressing for food and the multiple squeak response recovered most slowly. Naloxone pretreatment (10 mg/kg but not 1 mg/kg) shortened recovery to multiple squeak responses, grid clinging, and locomotion, without affecting recovery of bar pressing, food consumption, or EEG postictal depression. These results suggest that complex behaviors recover more slowly following a seizure than simple behaviors. It also appears that opioids are released by a kindled seizure and mediate certain postictal changes in motor- and pain-related behaviors.
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PMID:Changes in simple and complex behaviors following kindled seizures in rats: opioid and nonopioid medication. 661 85

Electrically induced seizures were followed by temporary elevations in serum prolactin over baseline in rats, while electrical irritation made no change. Naloxone 4 mg/kg i.p. pretreatment preserved this pattern but attenuated all levels including baseline by about 50%. While atropine 0.1 mg/kg s.c. did not change baseline levels, the prolactin levels after electrical irritation without seizure were about the same as those following a genuine seizure; atropine apparently facilitated stress-induced prolactin release. Seizures did not raise post-haloperidol prolactin levels above their high baseline levels.
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PMID:Postictal prolactin elevations in rats. 665 33

Opioids and opioid peptides influence the threshold to a seizure which is a model of petit mal epilepsy (Cowan, Geller and Adler, 1979). The present authors investigated representative opioid compounds in a model of a grand mal seizure, maximal electroshock (MES). Although all of the opioids and opioid peptides tested blocked tonic hindlimb extension, they divided into two groups, based on their ability to decrease the total length of the tonic component of the maximal electroshock seizure and their sensitivity to blockade by naloxone. The first group contained morphine, meperidine, methadone, ethylketocyclazocine (EK), D-ala2-met-enkephalinamide, D-ala2-leu5-enkephalin and beta-endorphin. The compounds in this group caused a decrease in the length of the tonic component that was dose-related, with the maximum decrease amounting to approx. 40%. The effect was blocked by the prior administration of 1 mg/kg of naloxone. The second group contained the partial agonists, pentazocine and cyclazocine. These opioids also caused a dose-related decrease in the length of the tonic component and, in the largest doses, the tonic component of the convulsion was completely blocked. Naloxone, in doses as large as 10 mg/kg, did not appreciably reverse the action of either drug.
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PMID:The anticonvulsant effect of opioids and opioid peptides against maximal electroshock seizures in rats. 672 28

Naloxone, at subconvulsive dose levels, from 1 to 15 mg/kg were administered to conscious rats. Significant increases in photically evoked afterdischarge occurrence were seen at naloxone dose levels above 5 mg/kg with no clinical evidence of seizure activity being observed. Typically photically evoked afterdischarge augmentation is only observed following the administration of convulsive drugs.
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PMID:Naloxone-induced augmentation of the photically evoked afterdischarge in conscious rats. 673 46

Electrographic seizure activity was recorded shortly following naxolone injections in artificially ventilated, methadone-treated stump-tailed macaques. Plasma-methadone concentrations prior to seizure activity were many times higher than those that have produced respiratory depression and death in nonventilated monkeys. The duration of seizure activity was clearly related to the dose of naloxone. Naloxone was without epileptogenic properties in animals that had not been pretreated with methadone. The results suggest that methadone and naloxone have additive epileptogenic properties when high blood levels of methadone are achieved in the artificially ventilated primate. Naloxone was devoid of antagonistic properties with respect to opiate-induced electroencephalographic spiking activity.
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PMID:Naloxone-induced electrographic seizures in the primate. 677 Mar 98

The postictal immobility syndrome was examined in five experimental grand mal epilepsy models in an attempt to analyze separately the behavioral and underlying neurochemical aspects of the rigid-catatonic and flaccid-cataleptic states. Catalepsy and analgesia were found in varying degrees after maximal electroshock (MES), metrazol, picrotoxin, and Ro 5-3663 activated seizures. Signs of rigidity were noticed after the MES and picrotoxin seizures. Kindled seizures were followed by explosive behavior without signs of rigidity, catalepsy, and analgesia. Naloxone reduced the duration but not the score (intensity) of catalepsy and failed to selectively antagonize analgesia. The relative representation of the tonic stage of convulsions seemed to be the major determinant of the development of catatonic-cataleptic symptomatology. It is suggested that more than a single neurotransmitter system is involved in the postictal immobility syndrome and each epilepsy model has its unique neurochemical profile.
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PMID:Convulsant-specific architecture of the postictal behavior syndrome in the rat. 679 53


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