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

In experiments with pentylenetetrazol convulsion model it has been found that L-DOPA in a dose of 50 mg/kg has no influence, while 500 mg/kg potentiate convulsions. Amantadine in a dose of 25 mg/kg and particularly markedly in a dose of 100 mg/kg potentaites convulsive seizures. Amphetamine in a dose of 0.5 mg/kg has no effect, while 5 mg/kg potentiate convulsive seizures, which is particularly pronounced in mice. Apomorphine in doses of 0.5 and 5 mg/kg has no marked effect on convulsions. Haloperidol in doses of 0.2 and 2 mg/kg does not have a pronounced effect on convulsive-seizure reactions and does not influence the effect of L-DOPA and amantadine on these reactions. The results obtained suggested a rather indirect effect of the dopaminergic system on convulsive-seizure reactivity. It is possible that the effects of some of the dopaminergic agents studied are realized through influencing the relationships between the dopaminergic system and other neurotransmitter systems (especially cholinergic, GABA-ergic and serotonin-ergic).
 ...
PMID:On certain effects of dopaminergic agents in pentylenetetrazol convulsions. 75 52

Audiogenic seizures in DBA/2 mice have been studied after administration of drugs believed to act as dopamine agonists. Apomorphine at 0.4 mg/kg delays all phases of the response, the tonic phase is absent after 2.0 mg/kg; the clonic phase is abolished by 10 mg/kg. Ergocornine (0.5-8.0 mg/kg) produces effects on the latency and occurrence of seizure stages similar to those of apomorphine. Piribedil, ET 495 (4-100 mg/kg) is less potent; even after 100 mg/kg clonic and tonic phases occurred in 50% of the mice.
 ...
PMID:Effects of apomorphine, ergocornine and piribedil on audiogenic seizures in DBA/2 mice. 117 46

Investigations were made of the action of ACTH and LH-RH on a number of behavioural paradigms and the possible involvement of neurotransmitters or opiates by pretreatment of receptor blockers in rats and mice. ACTH delayed the extinction of active avoidance behaviour. Atropine and haloperidol blocked this action, whereas phenoxybenzamine and propranolol were ineffective. LH-RH or a highly potent analogue of LH-RH (D-Trp6-LH-RH) decreased the rate of disappearance of dopamine in the hypothalamus following alpha-methyl- paratyrosine inhibition of catecholamine synthesis, and blocked the accumulation of serotonin following MAO inhibition. LH-RH or the analogue attenuated the consolidation of passive avoidance learning. Apomorphine-induced cage-climbing was also inhibited by the LH-RH analogue, but this action was not influenced by naloxone. Open-field activity (ambulation, rearing and grooming) was decreased by the analogue peptide. Naloxone blocked the action on ambulation and rearing, but was ineffective on grooming. The LH-RH analogue caused a dose-dependent increase in cataleptogenic activity. This action could not be blocked with naloxone. The LH-RH analogue suppressed picrotoxin-induced seizures. Naloxone restored the situation to the control level. The data suggested that the effects of some neurohormones are mediated by transmitters or endogenous opiates, and that both peptide-transmitter and peptide-peptide interactions have to be considered in the action of neurohormones.
 ...
PMID:Involvement of neurotransmitter and neuropeptides in behavioural action of some neurohormones. 198 90

Administration of reserpine, trifluperidol, chlorpromazine, haloperidol, spiroperidol, and thioproperazine to adult mice shortened the latency and increased the number of animals with clonic seizures induced by 1-kynurenine sulfate or its metabolite quinolinic acid. Haloperidol dose-dependently intensified kynurenine-induced seizures and did not alter pentylenetetrazole seizures. Dopamine abolished the effect of haloperidol while serotonin was ineffective. Pretreatment with 6-hydroxydopamine potentiated kynurenine-induced seizures, but not quinolinic acid-induced seizures. The seizure thresholds of kynurenine and quinolinic acid were not affected by pretreatments with yohimbine, clonidine, piperoxan, phentolamine and tricyclic antidepressants. Apomorphine and amphetamine (i.p.), noradrenaline and adrenaline (i.c.v.) possess anticonvulsant action against kynurenine and not against quinolinic acid. The data obtained suggest a similarity of kynurenine and known convulsants in the involvement of the catecholaminergic processes in their convulsant action. Quinolinic acid markedly differs from kynurenine in its mechanism of action as indicated by their interactions with numerous endogenous substances.
 ...
PMID:Effect of catecholaminergic drugs on quinolinate- and kynurenine-induced seizures in mice. 214 73

The adaptive changes in the effects of the neuropeptide angiotensin II (AT II) on the convulsive-seizure threshold were studied. AT II was injected intracerebroventricularly (i.c.v.) at a dose of 1 micrograms/mouse and convulsive seizures were induced by timed intravenous infusion of pentylenetetrazol (PTZ) in male albino mice. The sensitivity of DA receptors was altered by: repeated (14 days) intraperitoneal (i.p.) injection of the DA receptor antagonist pimozide (1 mg.kg-1) and subsequent withdrawal of the antagonist for 7 or 21 days; and repeated (14 days) subcutaneous (s.c.) injection of the DA receptor agonist apomorphine (0.5 mg.kg-1). The convulsive-seizure-increasing effect of AT II was enhanced after multiple administration of pimozide and particularly after its withdrawal for 21 days. This effect was also enhanced though to a lesser degree by repeated treatment with apomorphine. Apomorphine applied 21 days after withdrawal of pimozide decreased the pimozide-enhanced effect of AT II. All these adaptive changes in the effects of AT II on the PTZ convulsive-seizure threshold might be associated with the altered receptor-receptor (AT II-DA-GABA) interactions in the brain structures participating in the regulation of the convulsive-seizure threshold.
 ...
PMID:Adaptive changes in the effects of angiotensin II on the convulsive-seizure threshold in cases of altered sensitivity of dopamine receptors. 339 46

The anticonvulsant actions of memantine (1,3-dimethyl-5-aminoadamantane) have been evaluated in mice (seizures induced by maximal electroshock, pentylenetetrazol, bicuculline, picrotoxin, 3-mercaptopropionic acid and N-methyl-D,L-aspartic acid) and in photosensitive baboons, Papio Papio (clonic responses to intermittent photic stimulation). Memantine, 5-20 mg/kg, raised the threshold for electroconvulsions and protected mice against the tonic hind limb extension in pentylenetetrazol-, bicuculline-, picrotoxin- and 3-mercaptopropionic acid-induced seizures, but was ineffective against the clonic phase of chemically-induced seizures. In the baboons, no protection against photomyoclonic responses was observed within 5 h after the intravenous administration of memantine, 1-9 mg/kg. Amantadine, 100 mg/kg, reduced the protective effect of memantine against electroconvulsions. Apomorphine, haloperidol, pimozide, spiroperidol and bicuculline did not modify the anticonvulsant activity of memantine in electroconvulsions. These studies demonstrate an anticonvulsant action of memantine in rodents and suggest that dopaminergic mechanisms do not contribute to its mechanism of action.
 ...
PMID:Anticonvulsant action of 1,3-dimethyl-5-aminoadamantane. Pharmacological studies in rodents and baboon, Papio papio. 395 70

Apomorphine (up to 10 mg/kg) and amantadine (up to 100 mg/kg) did not affect pentetrazol-induced convulsions in mice. One of two GABA-ergic agonists tested, baclofen (10 mg/kg), decreased seizure susceptibility (except for the clonic phase) while another, amino-oxyacetic acid (up to 20 mg/kg) had no effect. Combined treatment was most effective in the case of baclofen (5 mg/kg) and amantadine (100 mg/kg) where number of animals with tonic seizures was decreased. Dopaminergic stimulation did not modify the action of some anticonvulsants tested. However, GABA-ergic stimulation resulted in a marked potentiation of the action of carbamazepine (10 mg/kg) and acetazolamide (20 mg/kg), being less pronounced in reference to diazepam (0 . 5 mg/kg) in lefadol (20 mg/kg). On the other hand, combined treatment with GABA-ergic and dopaminergic stimulants was shown to enhance the action of carbamazepine and acetazolamide, but not in the clonic phase. The obtained results suggest effectiveness of GABA-ergic stimulation in the case of all drugs tested and the combined treatment with GABA-ergic and dopaminergic agonists in potentiating the effects of some antiepileptics.
 ...
PMID:Effect of combined GABA-ergic and dopaminergic stimulation on the action of some antiepileptic drugs in pentetrazol-induced convulsions. 626 89

Neurological side effects associated with neuroleptic drugs result from a complex interaction of multiple neurotransmitters. To clarify the etiology of neuroleptic-induced acute dystonic reactions, monkeys (Cercopithecus aethiops) were treated with haloperidol at doses sufficient to evoke dystonia, and the effects of agents that influenced dopaminergic, cholinergic, or GABAergic neurotransmitters were evaluated. Apomorphine, a dopamine (DA) agonist, and biperiden, an acetylcholine (ACh) antagonist, decreased acute dystonia, whereas alpha-methyl-p-tyrosine (AMPT), an inhibitor of DA synthesis, and physostigmine, an ACh agonist, agonist, increased the symptoms. Muscimol, a GABA agonist, increased the dystonias in a dose-dependent way, and GABA inhibition with picrotoxin also aggravated dystonia, complicated by systemic intoxication and seizures. The reciprocal interaction between DA and ACh influences is consistent with clinical findings and animal models of dyskinesias. Dystonia may also be modulated by GABAergic substrates, but the results suggest complex interactions among DA, ACh, and GABA neurotransmission. Symptoms involving the orofacial, limb, and trunk regions, and purposeless overactivity are discussed in comparison with acute and tardive neuroleptic-induced movement disorders.
 ...
PMID:Dopamine, acetylcholine, and GABA effects in acute dystonia in primates. 677 41

Apomorphine, an agonist of dopamine receptors, blocks or significantly reduces photically induced seizures in the baboon (Papio papio). We therefore studied the effect of subcutaneously administered apomorphine in 11 patients with generalized photosensitive epilepsy. Visual evoked potentials were not altered by apomorphine, but in nine patients apomorphine transiently blocked the epileptic photosensitivity for an average of 45 minutes. Therefore, dopaminergic mechanisms play a role in the pathophysiology of human generalized photosensitive epilepsy.
 ...
PMID:Transient abolition of generalized photosensitive epileptic discharge in humans by apomorphine, a dopamine-receptor agonist. 719 13

1. The effects of some GABAergic and dopaminergic agents on pyrimethamine-induced tonic seizures were investigated in mice. 2. Pyrimethamine dose dependently induced seizures in mice. 3. Muscimol, AOAA and DABA significantly protected mice against pyrimethamine-induced seizures. 4. Bicuculline and picrotoxin effectively potentiated seizures elicited by pyrimethamine and significantly antagonized the protective effect of muscimol against the seizures. 5. Diazepam and phenobarbitone effectively protected mice against seizures elicited by pyrimethamine. 6. L-Dopa significantly potentiated pyrimethamine-induced seizures. 7. Apomorphine and pargyline significantly reduced the latency of seizures induced by pyrimethamine. 8. Haloperidol and pimozide effectively protected mice against pyrimethamine-elicited seizures and also significantly antagonized the potentiating effects of apomorphine and L-dopa on the seizures. 9. Disulfiram significantly potentiated seizures induced by pyrimethamine and also significantly enhanced the seizure-potentiating effect of L-dopa. 10. alpha-Methyl-p-tyrosine effectively protected against seizures induced by pyrimethamine. However, L-dopa significantly potentiated the seizures in alpha-methyl-p-tyrosine-pretreated animals. 11. Muscimol significantly attenuated the potentiating effect of L-dopa on pyrimethamine-induced seizures while bicuculline significantly enhanced the effect of L-dopa. Furthermore, haloperidol significantly potentiated the protective effect of muscimol against pyrimethamine-induced seizures. 12. These results suggest that both GABA and dopamine might be involved in the mechanism(s) of pyrimethamine seizures in mice.
 ...
PMID:GABAergic and dopaminergic systems may be involved in seizures induced by pyrimethamine in mice. 787 56


1 2 Next >>