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

The effectiveness of haloperidol pretreatment in preventing the toxic effects of high doses of amphetamine and cocaine was studied in rats. In this model, toxic effects were induced by intraperitoneal (i.p.) injection of amphetamine 75 mg/kg (100% death rate) or cocaine 70 mg/kg (82% death rate). Haloperidol failed to prevent amphetamine-induced seizures, but did lower the mortality rate at most doses tested. Haloperidol decreased the incidence of cocaine-induced seizures at the two highest doses, but the lowering of the mortality rate did not reach statistical significance at any dose. These data suggest a protective role for the central dopamine blocker haloperidol against death from high-dose amphetamine exposure without reducing the incidence of seizures. In contrast, haloperidol demonstrated an ability to reduce cocaine-induced seizures without significantly reducing mortality.
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PMID:The effect of haloperidol in cocaine and amphetamine intoxication. 262 24

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

The relationship between wet-dog shaking (WDS) and after-discharge (AD), and the effects of neuroleptics on WDS and AD elicited by hippocampal stimulation, were investigated. AD elicited by hippocampal stimulation consisted of primary and secondary phases. The intensity of the WDS during a 150 sec observation period showed two peaks. The intensity of WDS was reached at the 1st and 2nd peak in the 1st and the 2nd phase of AD, respectively. Haloperidol and chlorpromazine significantly and dose-dependently blocked the appearance of WDS. In particular, the number of WDS decreased during the early 1st phase and the 2nd phase of AD, after hippocampal stimulation. When the hippocampus was stimulated at intervals of 24 hr for 3 successive days a week, the number of WDS during 10-40 sec after stimulation decreased gradually and a small peak appeared during 40-60 sec in the 3rd and 4th week group. This pattern is similar to that seen in the chlorpromazine- and haloperidol-injected group. The possibility that seizure susceptibility, when the hippocampus is stimulated repeatedly, mimicks findings in case of blockage of dopaminergic function by the injection of neuroleptics, has to be considered.
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PMID:Effects of neuroleptics on hippocampal stimulation-induced 'wet-dog shaking' in rats. 286 34

The effects of tiapride on the convulsive seizures induced by pentylenetetrazole, strychnine, picrotoxin and bemegride, and on electric seizure are reported and compared with those of sulpiride, chlorpromazine, haloperidol and reserpine. The number of deaths and intensity of convulsion increased dose-dependently and also with the increase in amplitude of electric shock. Tiapride and a similar compound, sulpiride, did not affect these seizures, whereas chlorpromazine potentiated strychnine-induced and electric seizure. Haloperidol and reserpine potentiated electric seizure, and chlorpromazine and reserpine tended to potentiate bemegride-induced seizure. Reserpine also tended to potentiate pentylenetetrazole-induced seizure. These results suggest that tiapride would be clinically safer than other drugs with anti-dopamine activity, except for sulpiride.
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PMID:Comparative study of tiapride and neuroleptics with anti-dopamine activity on convulsive seizure in mice. 288 32

Using a neuropharmacological approach we studied the dopaminergic influence on the effects of angiotensin II (ATII) in some behavioural reactions. Haloperidol reduced the exploratory behaviour-increasing effect of ATII in the open field. Haloperidol also reduced the apomorphine stereotypy-increasing effect of ATII. Sulpiride tended to overcome the locomotor activity-decreasing effect of ATII. Seven resp. 21 days after withdrawal of pimozide (applied for 14 days) the convulsive-seizure thresholdincreasing effect of ATII was enhanced. Haloperidol impaired the retention-facilitating effect of ATII in rats performing a shuttle-box active avoidance task. The results suggest close interactions between central DA-ergic transmission and ATII in the realization of the ATII effects on behaviour.
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PMID:Dopaminergic influence on the effects of angiotensin II in behavioural reactions. 301 81

Dopamine (DA) receptor supersensitivity was induced in albino rats by haloperidol (5 mg/kg, ip day, for 18 days) and after 48 hr carbamazepine (CBZ) was administered in graded doses. The animals were subjected to Maximal Electroshock Seizures (MES) test, Minimal Electroconvulsive Threshold (MET) test and Pentylenetetrazole (PTZ)-induced convulsions test. Haloperidol pretreatment marginally increased the effect of CBZ against PTZ induced seizures, but not against electrically induced seizures (MES and MET tests).
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PMID:Influence of dopaminergic receptor supersensitivity on anticonvulsant action of carbamazepine. 321 81

To assess the appropriateness of hippocampal low-frequency kindling as an experimental model of epilepsy, we stimulated, bipolarly, left ventral hippocampus of 8 cats with 2 mA biphasic square wave pulses (1 msec duration) once a day. The pulse-interval was set at 300 msec. Recording electrodes were inserted in right ventral hippocampus, bilateral amygdaloid and bilateral globus pallidus. EEG was monitored before, during and after the delivery of stimulation. If the triggering of epileptic afterdischarge was observed on EEG monitoring, the delivery of stimulation was stopped immediately. Generalized convulsive seizures developed in all subjects within a mean of 26.2 days. In all seizures self-sustained epileptic afterdischarge, defined as epileptiform spikes three times the base line amplitude with a frequency greater than the stimulating pulse-interval (300 msec) in the stimulated hippocampus lead, was triggered abruptly. Therefore we could measure the number of stimulating pulses required for the triggering of epileptic afterdischarge, defined as pulse-number threshold, definitely in all cases. At the completion of kindling the pulse-number threshold was measured at 12.3 +/- 0.9 (+/- SE). After five generalized convulsions were induced we tested the stability of the pulse-number threshold and the duration of triggered epileptic afterdischarge. Both the two measures did not change statistically at the interstimulation interval from 24 hrs to 96 hrs. In addition we carried out testing with antiepileptic and antipsychotic drugs. Phenobarbital (10 mg/kg, i.p.) increased the pulse-number threshold and the after discharge duration simultaneously. Haloperidol (3 mg/kg, i.p.), oppositely, decreased the pulse number threshold and the after discharge duration.
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PMID:[Reliable induction of generalized seizures in hippocampal kindling triggered with low-frequency electrical stimulations]. 340 8

We assessed the acute effects of some psychotropic drugs on amygdaloid-kindled seizures produced by low-frequency stimulation. We used the number of stimulating pulses required for the induction of epileptic afterdischarge (pulse-number threshold, PNT) as an indicator for the seizure-generating threshold, and the duration of the epileptic afterdischarge (AD duration, ADD) as an indicator for the duration of the induced seizures. Methamphetamine and atropine elevated the PNT and reduced the ADD. Haloperidol reduced the PNT at all tested doses and reduced the ADD at high dosage. Imipramine elevated the PNT at low doses and reduced the PNT at high dosage. Imipramine also reduced the ADD. Reserpine at high dose elevated the PNT without affecting the ADD.
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PMID:Acute effect of some psychotropic drugs on low-frequency amygdaloid kindled seizures. 367 71

Caerulein, cholecystokinin octapeptide (CCK-8) and diazepam delayed the onset of seizures produced by harman and thiosemicarbazide (TSC). Caerulein had the potency of diazepam, whereas CCK-8 was less active by a factor of four. The convulsions induced by isoniazid (INH) were very resistant to both caerulein and diazepam; CCK-8 was not tested against isoniazid. Haloperidol did not influence the effect of TSC; it enhanced isoniazid-induced seizures, and antagonized the convulsant effect of harman.
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PMID:Anticonvulsant effects of caerulein, cholecystokinin octapeptide (CCK-8) and diazepam against seizures produced in mice by harman, thiosemicarbazide and isoniazid. 626 41

The effects of levodopa, apomorphine and 3,4-dihydroxyphenylserine (DOPS) on tonic seizures elicited by strychnine were investigated in mice. Levodopa (6.25-100 mg/kg), apomorphine (0.2-0.8 mg/kg) and FLA-63 (12.5 mg/kg) profoundly delayed the onset and reduced the incidence of strychnine seizures. In addition, these drugs decreased strychnine-induced mortality. DOPS (1-16 mg/kg) apparently shortened the onset of strychnine seizures and altered strychnine-induced mortality in a dose-dependent manner; low doses (1-2 mg/kg) enhanced while moderate doses (4-8 mg/kg) reduced the mortality rate. FLA-63 (12.5 mg/kg) potentiated the anticonvulsant effect of low doses of levodopa (6.25-12.5 mg/kg) while it had no significant influence on the anticonvulsant effect of higher doses (25-100 mg/kg) of levodopa. In addition, the onset of strychnine seizure was further delayed by FLA-63. Haloperidol (0.5 mg/kg) potentiated the convulsant effect of strychnine (1 mg/kg) as well as strychnine-induced mortality. It also antagonised the protective effect of levodopa (12.5 and 100 mg/kg) against strychnine (1 mg/kg). Phentolamine (5 mg/kg) and +/- propranolol (1 mg/kg) antagonised strychnine seizures. Strychnine-induced mortality was also reduced by these drugs. In addition, the effects of DOPS (2 mg/kg) on strychnine seizures were antagonised by phentolamine and propranolol. These results indicate that enhancement of dopaminergic and noradrenergic neurotransmission respectively attenuate and potentiate strychnine seizures in mice.
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PMID:Influence of levodopa, apomorphine and 3,4-dihydroxyphenylserine (DOPS) on strychnine-induced seizures in mice. 642 68


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