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

The influence of electrical and chemical stimulation of nucleus caudatus (NC) on bioelectrical seizure activity of amygdala (Am) was studied in rabbits. The electrical stimulation of NC inhibits seizures in Am induced by the administration of picrotoxin into this nucleus. Dopamine (DA) and cholinomimetics-metacholine and neostygmine-applied into NC inhibit seizures in Am. Noradrenaline (NA) acts biphasically, first potentiating and then inhibiting seizures in Am. Serotonin (5-HT) and glutamic acid (GA) administered to NC do not affect the seizures. In the case of seizures excited by electrical stimulation, DA and neostygmine possessed inhibiting action; NA, too, inhibited seizures without, however, inducing primary stimulation. Similarly as in the case of picrotoxin-stimulated seizures, neither 5-HT nor GA brought about the effects. The present study deals with the correlation of dopaminergic anc cholinergic systems in NC.
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PMID:The influence of neuromediators injected into nucleus caudatus on bioelectrical seizure activity of amygdala. 0 50

The role of brain monoamines in the anticonvulsant effect of imipramine was investigated in albino rats, against maximal electroshock-induced seizures, by using drugs with well-defined effects on brain monoamines. The results suggest a definite role for noradrenaline in imipramine anticonvulsant action. Dopamine and 5-hydroxytryptamine do not appear to be involved in this effect of imipramine.
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PMID:Role of brain monoamines in the anticonvulsant effect of imipramine in albino rats. 19 12

The organophosphate chemical nerve agent, soman, causes convulsions, neuropathology, and, ultimately, death. A major problem in treating soman intoxication is that peripherally acting pharmacological agents which prevent death do not prevent seizures. Although a primary cause of these symptoms is the excess of acetylcholine which follows acetylcholinesterase (AChE) inhibition, centrally acting muscarinic blockers, such as atropine, alleviate, but do not block, the convulsive actions of soman. Moreover, there is a relatively weak relationship between CNS reductions of AChE and the incidence of convulsions. There is evidence suggesting that soman intoxication stimulates the release of norepinephrine (NE) in the brain. Recent evidence has implicated NE in the induction and/or maintenance of seizures. Thus, in the present study the relations among soman-induced convulsions, AChE inhibition, and brain NE and other monoamine changes were examined. The time course of brain NE recovery was also determined. Rats were injected (im) with a single dose (78 micrograms/kg) of soman. At this dose 68% of the injected rats developed convulsions. Both convulsive and nonconvulsive rats were sacrificed between 1 and 96 h following soman injection and NE levels in the rostral forebrain and olfactory bulb were determined by HPLC with electrochemical detection. In all convulsive rats NE levels declined substantially. Forebrain NE levels were decreased by 50% at 1 h and 70% at 2 h following soman injection. Recovery of NE began at 8 h and was complete by 96 h following soman administration. Although nonconvulsive rats showed other signs of intoxication, NE levels in these rats were unchanged. Dopamine (DA) and serotonin (5-HT) levels were not significantly affected in either convulsive or nonconvulsive rats. However, 5-hydroxyindoleacetic acid, the major metabolite of 5-HT, and homovanillic acid and 3,4-dihydroxyphenylacetic acid, the two major metabolites of DA, were increased significantly in the forebrain of convulsive, but not nonconvulsive rats, indicating an increase in 5-HT and DA turnover. However, in contrast to the abrupt decline in NE, these increases in DA and 5-HT metabolites were slow and progressive. Taken together, the present results and other recent findings suggest that rapid, sustained NE release could play a role in the induction and/or maintenance of soman-induced convulsions, whereas increased release of 5-HT and DA may be a consequence of seizures. Further investigation of the role of NE in soman-induced convulsions may lead to improved treatment of soman intoxication and a better understanding of the role of NE in other forms of seizures, including human epilepsy.
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PMID:Brain norepinephrine reductions in soman-intoxicated rats: association with convulsions and AChE inhibition, time course, and relation to other monoamines. 142 25

Dopamine beta-hydroxylase (DBH) deficiency is a genetic disorder in which affected patients cannot synthesize norepinephrine, epinephrine, and octopamine in either the central nervous system or the peripheral autonomic neurons. Dopamine acts as a false neurotransmitter in their noradrenergic neurons. Neonates with DBH deficiency have had episodic hypothermia, hypoglycemia, and hypotension, but survivors sometimes cope relatively well until late childhood when overwhelming orthostatic hypotension profoundly limits their activities. The hypotension may be so severe that clonic seizures supervene. Most currently recognized patients are young or middle-aged adults. The diagnosis is established by the observation of severe orthostatic hypotension in a patient whose plasma norepinephrine/dopamine ratio is much less than one.
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PMID:Dopamine beta-hydroxylase deficiency. A genetic disorder of cardiovascular regulation. 167 40

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.
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PMID:Effect of catecholaminergic drugs on quinolinate- and kynurenine-induced seizures in mice. 214 73

Perinatal hypoxia is known as a risk factor for human epilepsies. Previous studies in our laboratory have shown that the rats with postnatal hypoxia show facilitation of the kindling formation and enhanced susceptibility to pentylenetetrazol (PTZ)-induced seizures even after the maturation. In the present study, the effects of postnatal hypoxia (100% N2, for approximately 5 min, at ten days of age) on monoamine and amino acid levels in the brain of adult rats (three months of age) were investigated to clarify the biochemical basis of the enhanced seizure susceptibility. In the hypoxia-treated rats, norepinephrine (NE) was significantly decreased in the pons-medulla (82% of control) and hypothalamus (85%) as compared with controls. Dopamine (DA) was decreased in the pons-medulla (83%). A decrease in DA metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), was also noted in the substantia nigra (71%) and hippocampus (64%), respectively. On the other hand, gamma-aminobutyric acid (GABA) was significantly increased in the striatum (121%). These findings indicate that the enhanced seizure susceptibility in these rats may be attributed to 1) impaired development of noradrenergic and dopaminergic neurons, of which these transmissions are known as inhibitory modulators of seizure discharge in some animal models of epilepsies, and 2) changes of GABAergic and dopaminergic transmissions in the striato-nigral pathway, which is a wellknown regulation system for seizure propagation.
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PMID:[Long-term effects of postnatal hypoxia on monoamine and amino acid levels in the rat brain]. 226 92

Drugs interacting with dopaminergic neurotransmission were studied on a model of genetic petit mal-like seizures in a strain of Wistar rats. Dopamine participates in the control of seizures in this model, as in other models of petit mal or of genetic epilepsy. Mixed dopaminergic D1/D2 agonists: L-DOPA, apomorphine, amphetamine and nomifensine, gave dose-dependent reductions of the duration of spike and wave discharges. Mixed D1/D2 antagonists: haloperidol, flupentixol and pimozide, caused dose-dependent increases of duration of spike and wave discharges. The findings with specific agonists or antagonists of D1 or D2 receptors did not reveal clearly the respective roles of these receptors in controlling the spike and wave discharges. The D2 agonists, lisuride and pergolide, had no effect on spike and wave discharges, except at toxic doses; bromocriptine decreased the duration of the discharges, but without clear-cut dose-dependency. The D2 antagonists: sulpiride and tiapride, had no effect. The D1 agonist SKF 38393 decreased duration of the spike and wave discharges in a dose-dependent manner. The D1 antagonist SCH 23390 had a biphasic effect: increasing the duration of spike and wave discharges at small doses and decreasing it at large doses. These results suggest that the simultaneous stimulation or inhibition of both receptors, D1 and D2, is necessary for influencing spike and wave discharges in this model.
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PMID:Effects of drugs affecting dopaminergic neurotransmission in rats with spontaneous petit mal-like seizures. 283 51

The basal ganglia are involved in the organization of movement and function in the initiation and expression of generalized and limbic seizures. Dopamine is the principal neurotransmitter of the mesencephalic efferent pathways terminating in the mammalian striatum. No function has been ascribed to mesostriatal dopamine in the control of seizure spread in the brain. This work presents evidence that bilateral application of picomole amounts of apomorphine (a dopamine agonist) into the striatum confers protection against seizures produced by pilocarpine (a cholinergic agonist) in rats. The anticonvulsant effect of apomorphine is topographically confined to the caudate-putamen, nucleus accumbens, and olfactory tubercle. Bilateral application of nanomolar amounts of haloperidol (a dopamine antagonist) into the caudate-putamen or systemic application of haloperidol both lower the threshold for pilocarpine-induced seizures. Local application of an excitatory amino acid N-methyl-D-aspartate, into the substantia nigra pars compacta, ventral tegmental area, or retrorubral area, sites of origin of mesostriatal dopaminergic pathways, protects rats against seizures produced by pilocarpine. These results suggest that dopaminergic transmission in the striatum may be operative in complex neuronal networks modulating the seizure threshold.
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PMID:Dopamine-sensitive anticonvulsant site in the rat striatum. 318 11

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

Dopamine agonists with different selectivity for dopamine D-1 and D-2 receptors in the brain were tested for their effects: on thresholds for maximal electroshock seizures in mice and rats and for pentylenetetrazol-induced clonic seizures in mice; on seizures induced by air blast stimulation in gerbils, and on seizures induced by amygdala-kindling in rats. The mixed D-1/D-2 agonist apomorphine exerted anticonvulsant effects in all models except kindling. In gerbils and mice, the anticonvulsant action of apomorphine could be antagonized by the D-2 selective dopamine antagonist sulpiride. When injected alone, sulpiride exerted no significant effect on seizure activity. The preferential D-2 receptor agonists lisuride and (+)-PHNO [+)-4-propyl-9-hydroxynaphthoxazine) differed in their profile of action. Both compounds displayed anticonvulsant efficacy in gerbils, while only lisuride proved capable of reducing kindled seizure severity. (+)-PHNO increased the threshold for electroconvulsions in mice while lisuride was ineffective in this respect or even decreased the threshold. The reverse was obtained in regard to electroshock seizures in rats. The threshold for seizures induced by pentylenetetrazol in mice was increased significantly by lisuride but not by (+)-PHNO. The selective dopamine D-1 receptor agonist SKF 38393-A exerted no anticonvulsant effect in any seizure test except a moderate increase of the electroconvulsive threshold in mice. In contrast, the dopamine precursor L-DOPA (injected after pretreatment with carbidopa) proved capable of reducing seizure activity in all models. In mice, the increase in the threshold for maximal electroshock seizures induced by L-DOPA was significantly reduced by sulpiride, which also attenuated the anticonvulsant effect of L-DOPA in gerbils. Collectively, the data indicate that dopamine D-2 receptors mediate the anticonvulsant effect of dopamine agonist and, at least in part, of L-DOPA whereas D-1 receptors seem not to be involved.
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PMID:Studies on the involvement of dopamine D-1 and D-2 receptors in the anticonvulsant effect of dopamine agonists in various rodent models of epilepsy. 375 88


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