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

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

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

1. The running component of audiogenic seizures in mice has been used as the basis of a sequential screening test for the detection of a variety of centrally acting drugs.2. For acceptance by the test, an active compound must completely suppress the running component in a total of sixteen mice at a dose of 1/5 LD50 intraperitoneally.3. Considerable economies in the numbers of animals required for screening have been achieved, the mean number of mice required to reject an inactive compound being 2.0.4. The running component is highly sensitive to anticonvulsants and general central depressants, and insensitive to phenothiazine tranquillizers and morphine. Reserpine caused an increase in the severity of the running component.5. The statistical model used in this test is of general application to screening test situations which use quantal data.
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PMID:A sequential screning test based on the running component of audiogenic seizures in mice, including reference compound PD50 values. 582 29

The authors used the compounds 2-methyl-3)2-phenyl-3-methyl tetrahydroxasino)-propiophenone hydrochloriad (code PsI) and 1-phenoxycarboxy-1-phenyl-2-methyl-3 (2-phenyl-3-methyl-tetrahydroxasino-propan hydrochlorid(code P3) and carried out the following studies: influence of tripamine, corasol and strichnine seizures 1-phenoxycarboxy--1-phenyl-2-methyl--3 (2-phenyl--3-methyl-tetrahydroxasino) propar hydrochlor (Code P8) in white mice, effect on the hypertensive action of reserpine in white rats, investigations on the analeptic action in urethanized cats as well as on the analgetic effect, examined both by the test of "hot plate" and the method of Hendreshot-Forsaith. The examined compounds, administered in a dose of 1/6 of LD50, showed analgetic effect weaker than that of the preparations Morphinum hydrochloricum and Analigin, but their analeptic effect was less manifested that of of corasol. Similar to MAO-inhibitor-oproniazid although in smaller degree the compound PS1 potentiated tripamine seizures and inverted the hypotensive effect of Reserpine into hypertensive.
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PMID:[Pharmacological studies of 2-methyl-3(2-phenyl-3-methyl-tetrahydrooxazino)-propiophenone hydrochloride and 1-phenoxycarboxy-1-phenyl-2-methyl-3(2-phenyl-3-methyl-tetrahydrooxazino)-propane hydrochloride compounds]. 610 91

d-Amphetamine protected young chicks against electroconvulsive seizure (ECS) in a dose-dependent manner in the dose range of 1-10 mg/kg. Reserpine pretreatment reduced ECS threshold and decreased the anticonvulsant effect of d-amphetamine in chicks. FLA-63 protected chicks against ECS and potentiated the anticonvulsant effect of d-amphetamine, whereas the dopamine antagonist pimozide antagonised the protective effect of d-amphetamine against ECS. Both the alpha-adrenoceptor antagonist phentolamine, and the serotonin antagonist cyproheptadine, had no significant influence on the anticonvulsant effect of d-amphetamine. d-Amphetamine significantly increased the levels of 5-hydroxytryptamine, noradrenaline and dopamine in the hyperstriatum, brain stem and optic tectum of the chick respectively. The present data suggests that brain dopamine may be the principal monoamine involved in the protective influence of d-amphetamine against ECS in young chicks.
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PMID:Studies on the pharmacology of d-amphetamine on maximal electroconvulsive seizure in young chicks. 641 41

The effect of alterations in whole brain monoamine content on the plasma lidocaine concentration resulting in seizures was studied in rats. Reductions in brain monoamine content were produced by treatment with one of the following drugs: reserpine, parachlorophenylalanine (PCPA), or alpha methyl paratyrosine (AMPT). Reserpine depleted norepinephrine (NE), and dopamine (DA) by 75 per cent and serotonin (5HT) by 54 per cent; PCPA reduced brain 5HT 56 per cent without changing NE and DA; AMPT reduced brain NE and DA by 54 and 60 per cent, respectively, without altering 5HT content. Treatment with 5-hydroxytryptophan, a serotonin precursor combined with the peripheral decarboxylase inhibitor RO4-4602 increased brain 5HT content by 400 per cent without changes in DA and NE. Whole brain NE concentrations were assayed fluorometrically, DA brain concentrations were assayed by HPLC, and lidocaine concentrations in plasma were determined by gas chromatography. Plasma lidocaine concentrations at the onset of convulsions were found to be elevated significantly only by drugs causing serotonin depletion; increasing to 128 per cent of control with reserpine treatment and 139 per cent of control with PCPA treatment. Depletion of NE and DA had no effect on the lidocaine seizure threshold. Increases in brain 5HT caused a small but not statistically significant decrease to 94 per cent of control in the mean plasma lidocaine concentration at seizure onset.
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PMID:Cerebral monoamines and lidocaine toxicity in rats. 705 26

1. The effects of some noradrenergic agents on seizures induced by strychnine were investigated in mice. 2. Strychnine (0.5-4 mg/kg, i.p.) dose-dependently produced tonic seizures. 3. DOPS (4-8 mg/kg, i.p.) significantly shortened the latency of seizures elicited by strychnine (2 mg/kg, i.p.). Similarly, DOPS (4 mg/kg, i.p.) effectively increased the incidence and significantly shortened the latency of seizures induced by strychnine (1 mg/kg, i.p.). 4. Imipramine (20-40 mg/kg, i.p.) and pargyline (200 mg/kg, i.p.) significantly shortened the latency of strychnine (2 mg/kg, i.p.)-induced seizures. 5. Phentolamine (5-20 mg/kg, i.p.) effectively antagonised the seizures elicited by strychnine (2 mg/kg, i.p.). Furthermore, phentolamine (10 mg/kg, i.p.) attenuated the seizure-potentiating effect of DOPS (4 mg/kg, i.p.). 6. Propranolol (0.5-2 mg/kg, i.p.) and prazosin (1-2 mg/kg, i.p.) reduced the incidence and significantly delayed the latency of seizures induced by strychnine (2 mg/kg, i.p.). 7. Reserpine (5-10 mg/kg, i.p.) significantly prolonged the latency of strychnine (2 mg/kg, i.p.)-induced seizures. 8. Clonidine (0.25-1 mg/kg, i.p.) dose-dependently and significantly antagonised strychnine (2 mg/kg, i.p.)-induced seizures. 9. Idazoxan (1-4 mg/kg, i.p.) in a dose related manner significantly shortened the latency of seizures induced by strychnine (2 mg/kg, i.p.). Similarly, idazoxan (2 mg/kg, i.p.) profoundly potentiated seizures elicited by strychnine (1 mg/kg, i.p.). Idazoxan (4 mg/kg, i.p.) significantly antagonised the protective effect of clonidine (1 mg/kg, i.p.) against strychnine (2 mg/kg, i.p.)-induced seizures. 10. Disulfiram (3 x 25 - 3 x 100 mg/kg, i.p.) significantly attenuated strychnine (2 mg/kg, i.p.)-induced seizures. DOPS (4 mg/kg, i.p.) significantly potentiated strychnine seizures in disulfiram (3 x 100 mg/kg, i.p.)-pretreated animals. 11. These results indicate that enhancement of noradrenergic neurotransmission potentiates strychnine seizures in mice.
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PMID:Strychnine-induced seizures in mice: the role of noradrenaline. 793 64

Dopamine agonists and antagonists with different affinities for D1 and D2 receptors in the brain were assessed for their ability to affect clonic seizures in mice induced by chemoconvulsants. The dopamine D2 antagonists remoxipride (5-20 mg/kg) and raclopride (5-20 mg/kg), haloperidol (2.5 and 5 mg/kg) and the D1 antagonist SCH 23390 (0.3, 1.5 mg/kg) did not markedly modify seizures induced by pentylenetetrazole, picrotoxin or bicuculline. The dopamine D2 agonist quinpirole only weakly blocked the action of pentylenetetrazole while the D1 agonist SKF 38393 (1-10 mg/kg subcutaneously) caused a dose-dependent blockade of pentylenetetrazole-induced seizures. The D1/D2 agonist apomorphine given at "postsynaptic" doses (1 and 2 mg/kg) blocked pentylenetetrazole-induced seizures. The protection afforded by apomorphine against pentylenetetrazole seizures appeared to be associated with its activation of both D1 and D2 receptors since both raclopride and SCH 23390 blocked the action of apomorphine. Reserpine and the two partial dopamine autoreceptor agonists, (-)3-PPP and HW-165, at high (non-autoreceptor selective) doses induced seizures in animals treated with the subconvulsive dose of pentylenetetrazole. The overall results suggest that dopamine receptor blockade has a minor or limited effect on seizures caused by GABA inhibition. The anticonvulsant effect of dopamine agonists such as apomorphine appears to be mediated by postsynaptic dopamine D1 and D2 receptors. Stimulation of dopamine D1 receptors can reduce seizure activity caused by GABA receptor blockade possibly by facilitation of GABA transmission in the striatum and substantia nigra.
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PMID:Effects of dopamine D1 and D2 receptor agonists and antagonists on seizures induced by chemoconvulsants in mice. 810 21


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