Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

L-Tryptophan, the amino acid precursor of serotonin and several other monoamines, has frequently been employed as an adjunct with tricyclic antidepressants and monoamine oxidase inhibitors to increase their effectiveness in treating affective disorders. Combined use of L-tryptophan with electroconvulsive therapy (ECT) has generally not been successful and, in fact, may actually have a deleterious effect upon treatment. A case of decreased seizure duration due to an L-tryptophan-ECT interaction is presented and its implications discussed.
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PMID:Effect of L-tryptophan on electroconvulsive therapy seizure time. 403 41

We previously reported that 6-methoxy-1,2,3,4-tetrahydro-beta-carboline (6-MeO-THBC) attenuated audiogenic seizures (AGS) in 21-day-old DBA/2J mice and also inhibited brain monoamine oxidase-A (MAO-A) and serotonin (5-hydroxytryptamine, 5-HT) uptake leading to increased brain 5-HT concentration. In this study, the sensitivity of AGS to 5-HT manipulation was evaluated by utilizing drug combinations which paralleled the actions of 6-MeO-THBC and which also have been associated with the production of a serotonergic motor syndrome in rats. Combination of a specific 5-HT uptake inhibitor (fluoxetine or citalopram) with the MAO-A inhibitor clorgyline inhibited AGS more effectively than the individual drugs but combination with the MAO-B inhibitor deprenyl did not. Combined administration of clorgyline plus deprenyl also suppressed AGS. Inhibition of AGS by tryptophan was potentiated by combination with either of the mixed MAO inhibitors nialamide or tranylcypromine. The effects of these drugs individually and in combination on brain MAO-A and MAO-B activity and 5-HT uptake were also determined ex vivo and were consistent with expected mechanisms of action. These results suggest, first of all, that the inhibition of AGS produced by 6-MeO-THBC is a consequence of its combined MAO-A and 5-HT uptake inhibition properties. Secondly, the similarity of results of pharmacological manipulations of the 5-HT system which produce the rat motor syndrome and which inhibit AGS in the mouse suggests that AGS in 21-day-old DBA/2J mice may be a useful system for assessing functional consequences of these serotonergic manipulations.
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PMID:Combined inhibition of serotonin uptake and oxidative deamination attenuates audiogenic seizures in DBA/2J mice. 408 Jul 61

The pharmacology, side effects, and possible drug interactions of metrizamide, a water-solulbe contrast medium for myelography, are reviewed. Metrizamide concentration in the brain reaches maximal levels two to six hour after lumbar injection, depending on dose and patient positioning, and is largely (55-96%) excreted from the body after 24 hours. Its lower neurotoxicity, compared with other water-soluble contrast agents, can be attributed in part to its undissociated, non-ionic nature. Common side effects, which include headache, nausea, and vomiting, occur to the same degree as with other myelographic contrast media. Reported data suggest that convulsions, which have occurred in a very small percentage of patients, are related to the amount of contrast medium reaching the brain which, in turn, is largely a factor of dose and examination technique. Although the risk of seizures is small, it is recommended that drugs that lower the seizure threshold (phenothiazine derivatives, butyrophenones, tricyclic antidepressants, and MAO-inhibitors) should be avoided 48 hours before metrizamide administration (if possible), should not be used to control nausea, and should not be resumed for 24 to 48 hours after the myelographic procedure. The value of premedication (e.g., with diazepam) to prevent seizures has not been established and is not recommended.
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PMID:Metrizamide: a review with emphasis on drug interactions. 610 72

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

In the experiment, rats were trained to discriminate 5 mg/kg cocaine HCl from saline in a two-bar drug discrimination procedure. Stimulus generalization experiments were carried out with six inhibitor drugs of monoamine oxidase. The rank order of absolute potency of these drugs in inducing stimulus generalization with cocaine was: tranylcypromine (ED50 in mg/kg; 1.2)>pheniprazine (3.5)>deprenyl (5)>pargyline (28)>nialamide (approximately 170); at up to 40 mg/kg, clorgyline failed to produce 50% generalization. All six drugs also potentiated tryptamine in producing body tremors and clonic seizures, the rank order of potency being tranylcypromine (0.081)>clorgyline (0.14) greater than or equal to pheniprazine (0.15)>pargyline (1.97)>deprenyl (15.5)>nialamide (18.7). Tryptamine is a common substrate for both type A and type B monoamine oxidase, so that tryptamine potentiation may serve to determine the relative specificity of the doses at which the inhibitor drugs generalized with cocaine. The present data may suggest that endogenous substances which are preferred substrates for type B monoamine oxidase in rat brain can exert control of behavior by virtue of cocaine-like stimulus properties. beta-Phenylethylamine, more so than dopamine, appears to be candidate substance for mediating the discriminative stimulus properties of cocaine and, perhaps, of other central nervous system stimulants.
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PMID:Evidence that a preferred substrate for type B monoamine oxidase mediates stimulus properties of MAO inhibitors: a possible role for beta-phenylethylamine in the cocaine cue. 610 35

Inbred E1 mice are highly susceptible to convulsive seizures upon "throwing" stimulation. The strain is known to have an abnormal 5-hydroxytryptamine (5-HT) metabolism. In the study here 5-HT level, [14C]5-hydroxytryptophan (5-HTP) metabolism, MAO activity and [3H]5-HT receptor binding were examined in the cortex, brainstem and cerebellum. In the interictal period cortical and brainstem 5-HT level and [3H]5-HT receptor binding were significantly lower. In the same period cortical biosynthesized [14C]5-HT from [14C]5-HTP taken up was higher, and MAO activity was not changed. L-DOPA with MK486 induced a low threshold of seizures and decreased cortical 5-HT level. Abnormally functioning 5-HT neurones may exist in the E1 mouse cortex.
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PMID:Brain 5-hydroxytryptamine level, metabolism, and binding in E1 mice. 641 6

Pharmacological exploration of the central nervous system carried out by means of a series of tests confirms the affinity of 3-(2,2-dibromovinyl)-2,2-dimethylcyclopropanecarboxylic acid alpha-cyano-3-phenoxybenzyl ester (delta-methrin) for the nervous system and reveals the following activities of deltamethrin: Deltamethrin has no neuroleptic or sedative action. It inhibits motility, sense of balance and inquisitiveness of treated animals. It potentiates chloral-induced hypnotic action but not that of pentobarbital. Not only does it have no antagonistic action on convulsivant agents: electric shock, pentetrazol, strychnine, but it stimulates their toxicity and prolongs the convulsive seizures. The fact that deltamethrin acts on different convulsivant agents (i.e. pentetrazol and strychnine) with various sites of action suggests that its activity is located in both the cortical and the medullary centres. Deltamethrin reveals the latent toxicity of tryptamine used in the non-toxic dose range; this predicts that deltamethrin might have an IMAO (inhibitor of monoamine oxidase) activity. Experiments carried out under the conditions adopted showed that deltamethrin acts on various sites.
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PMID:Pharmacological effects of deltamethrin on the central nervous system. 653 10

1 Evidence concerning the convulsant effects of non-monoamine oxidase inhibitor antidepressant drugs has been reviewed. 2 Mianserin is convulsant in therapeutic doses but seizures have not been reported following overdose. 3 The convulsant effects of mianserin are probably no greater than for other non-monoamine oxidase inhibitor antidepressant drugs. 4 Enzyme-inducing anti-epileptic drugs can reduce the peak plasma concentration of mianserin and shorten its elimination half-life, probably by inducing its metabolism.
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PMID:Antidepressant drugs, convulsions and epilepsy. 682 60

The uptake of [3H]dopamine by synaptosomes from rat brain striatum was biphasic, the rapid phase requiring less than 1 min for completion and the slower phase occurring over a few minutes. This uptake of labeled dopamine was enhanced by prior exposure of the synaptosomes to Fe2+, which gives rise to peroxidation of the synaptosomal lipids. Both lipid peroxidation and enhancement of dopamine uptake were unaffected by the presence of inhibitors of monoamine oxidase but were blocked by inclusion of omicron-phenanthroline in the preincubation medium. It is concluded that lipid peroxidation may be involved in certain neuropsychiatric disorders such as seizures evoked by exposure to high oxygen pressures.
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PMID:Dopamine uptake in striatal synaptosomes exposed to peroxidation "in vitro". 683 Jun 9

Several 1,3,4-oxadiazol-thiones were synthesised and characterized by their melting points elemental analysis and I.R. spectra. All the oxadiazol-thiones possessed anticonvulsant activity which was reflected by protection upto 80% against pentylenetetrazole induced seizures and 40% protection against maximal electroshock induced seizures. Substantiations at position-3 of oxadiazol-thiones have shown marked effect on MAO inhibitory activity. No definite correlation between monoamine oxidase inhibitory and anticonvulsant activity could be established. It was observed that by the substitution of one, two and three methyl groups in the phenyl ring of 2-arylamino methyl side chain anticonvulsant activity against both maximal electroshock induced convulsions and pentylenetetrazol induced convulsions decreases i.e. the order of activity was found to be unsubstituted greater than monomethyl greater than dimethyl greater than trimethyl.
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PMID:Anticonvulsant and monoamine oxidase inhibitory activity of substituted oxadiazol-thiones. 714 16


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