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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

Selective treatments which alter the catecholamine content of discrete areas of the brain were tested for their effect on electroshock seizure intensity in the rat. The data indicate that depletion of noradrenaline and dopamine in near ventricular areas by the intracerebroventricular administration of the benzoquinolizine, Ro 4-1284, enhances electroshock seizure intensity. The enhancement of seizure produced by systemic Ro 4-1284 was antagonized by the intracerebroventricular injection of noradrenaline or dopamine which do not appear to penetrate more than 1 mm into the brain. Further, pretreatment with systemic iproniazid and L-dopa completely antagonized the increased seizure intensity produced by intracerebroventricular Ro 4-1284 and repleted brain catecholamines in both near and far ventricular areas. Thus, the effects of both noradrenaline and dopamine in attenuating electroshock seizure intensity appear to be exerted principally through periventricular structures.
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PMID:Brain areas involved in the catecholamine mediated regulation of electroshock seizure intensity. 1 93

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

Methyl-2 (2 Naphtyl) Aziridine (MNA) is a new agent which has been demonstrated to have effects on paradoxical sleep (PS) and on the levels of cerebral noradrenaline (Yamamoto, 1975). It has been tried on a experimental model of epilepsy, the kindling effect, produced in the cat by repetitive stimulation of the amygdala. The results obtained in the cat confirmed blockage of paradoxical sleep (PS) and revealed a marked reduction in the number of stimuli required to produce the effect. The shortening of the time before the first generalised seizure did not seem attributable to privation of paradoxical sleep. The role of cerebral catecholamine reduction, however, is discussed.
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PMID:[Preliminary study of the comparative action of 1 methyl-2 (2 naphtyl) aziridine on kindling effect and on paradoxical sleep (author's transl)]. 20 79

Brain levels of tyrosine, dopamine (DA), noradrenaline (NA), tryptophan, 5-hydroxytryptamine (5-HT), and 5-hydroxyindoleacetic acid (5-HIAA) were measured after 30, 60 and 120 min of sustained seizure activity, induced in paralyzed, artificially ventilated and anaesthetized (70% N2O) rats by administration of bicuculline (1.2 mg/kg i.v.). In separate animals the rates of accumulation of DOPA and 5-hydroxytryptophan (5-HTP) were estimated in three different brain regions after blockage of the aromatic L-amino acid decarboxylase with NSD 1015 (100 mg/kg). The tissue level of NA was markedly reduced at 30 min and remained low during 120 min of sustained epileptic seizures. In contrast, the DA concentration, being essentially unaffected at 30 min, continuously increased during the following 90 min. 5-HT decreased significantly after 30 min but returned to control levels following 60 and 120 min of seizure activity. The 5-HIAA concentration progressively increased. In all three brain regions (striatum, limbic forebrain and hemispheres) the rate of tyrosine hydroxylation increased. Tryptophan hydroxylation showed a significant increase only in the limbic forebrain. The results suggest that bicuculline-induced seizures lead to an increased functional activity in NA neurons and, at least initially, also in 5-HT neurons. In contrast, DA neurons appear to be inhibited.
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PMID:Monoamine metabolism during bicuculline-induced epileptic seizures in the rat. 30 80

Severe depletion of brain noradrenaline and separately of brain dopamine was induced in rats by intracerebral injection of the selective neurotoxin 6-hydroxydopamine, and the susceptibility of the treated animals to various seizure-inducing manipulations was examined. A significant potentiation of the seizures induced both by Metrazol and by electroconvulsive shock was found in animals depleted of brain noradrenaline, but no alteration was seen after depletion of brain dopamine on either measure. The catecholaminergic drug cocaine also induced seizures, but these were found not to depend on either brain noradrenaline or dopamine as they continued to occur in the virtual absence of either catecholamine. It is concluded that cocaine induces seizures by a non-specific toxic mechanism and that noradrenaline, but not dopamine, is involved in reducing the suceptibility of the central nervous system to the several distinct forms of seizure induction examined.
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PMID:Catecholamines and convulsions. 46 25

The ethanol withdrawal syndrome in man and animals is characterized by signs of CNS hyperactivity although a direct measurement of a physiological variable reflecting this CNS hyperactivity has never been performed in untreated man or in animals. We induced ethanol dependence in the rat by means of intragastric intubation with a 20% w/v ethanol solution, thus keeping the animals in a state of continuous severe intoxication for 3--4 days; during the subsequent state of withdrawal characterized by tremor, rigidity, stereotyped movements and general seizures a 25% increase in cerebral oxygen consumption (CMRO2) could be measured; this increase was not due to catecholamines originating from adrenal medulla as adrenomedullectomized animals showed a similar increase in CMRO2 (28%); the withdrawing animals showed a corresponding cerebral blood flow (CBF) increase. The elevated CMRO2 and CBF could be reduced to normal by administration of a beta-adrenergic receptor blocker (propranolol 2 mg/kg i.v.), and hence the increased CMRO2 during ethanol withdrawal could be related to catecholaminergic systems in the brain, e.g. the noradrenergic locus coeruleus system which is anatomically well suited as a general activating system. This interpretation is supported by the earlier neurochemical finding of an increased cerebral noradrenaline turnover during ethanol withdrawal. The exact mechanism underlying the increased cerebral oxygen consumption during ethanol withdrawal and the effect of propranolol on cerebral function during this condition remains to be clarified.
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PMID:Cerebral blood flow and oxygen consumption during ethanol withdrawal in the rat. 57 52

We have investigated the relationship between catecholamine turnover and susceptibility to audiogenic seizures (AGS) in the developing DBA/2J mouse. Turnover of dopamine and norepinephrine was determined after administration of alphamethylparatyrosine at 3 weeks of age when nearly all mice (94%) exhibited AGS, at 6 weeks when only 30% were susceptible, and at 12 weeks when none developed seizures. Turnover of brain dopamine increased progressively from 236 ng/g/hr at 3 weeks to 389 ng/g/hr by 12 weeks of age. Norepinephrine turnover increased significantly between 3 and 6 weeks of age, then remained stable thereafter. Turnover times for each catecholamine did not change appreciably with maturation. Our results support the notion that susceptibility to AGS may be mediated in part by brain catecholaminergic mechanisms.
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PMID:Ontogeny of brain catecholamine turnover and susceptibility to audiogenic seizures in DBA/2J mice. 65 4

The mutant, sex-linked recessive px (paroxysm) gene, expressed in female White Leghorn chicks (Gallus domesticus), causes seizures beginning on approximately day 9 after hatching. In an attempt to determine possible central nervous system involvement in the seizures, brain levels of the putative transmitter noradrenaline were assayed. Brains of px chicks and controls (normal female siblings) were removed at 7, 14, and 21 days, weighed, and frozen immediately in liquid nitrogen for later analysis by the alumina-trihydroxyindoleamine method. Noradrenaline was assayed in whole brain and in 4 brain parts: optic lobes, brainstem, cerebral hemispheres, and cerebellum. No differences between px and controls were found in whole brain or optic lobe levels. Brainstem levels of noradrenaline increased significantly with time in both groups, though px increases were more rapid. Px chicks at 21 days of age had significantly higher levels or noradrenaline in the cerebral hemispheres, while cerebellar levels were significantly lower at the same age. The differences found in brainstem, cerebral, and cerebellar noradrenaline are of interest as possible explanations for the lowered body temperature, hyperexcitability, and lack of motor coordination seen in the px chicks.
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PMID:Brain noradrenaline concentration in seizure-prone chicks, Gallus domesticus. 67 64

Acute plumbism include recurrent seizures, cerebral palsy and mental retardations. The impairment of the central nervous system (CNS) with increased lead absorption is of paramount concern which remains unsolved because of the lack of specific and sensitive neurochemical/biochemical indicators of the effect of lead on the CNS. In our experimental acute lead-zinc poisoning, significant increase in noradrenaline and slight decrease in dopamine have been found in the brains of rats, which suggest that there is change in neurotransmitter metabolism in lead poisoning.
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PMID:Dopamine and noradrenaline levels in the brains of lead and zinc poisoned rats. 67 13


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