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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

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

Norepinephrine (NE) concentrations were measured in 15 discrete areas of the central nervous system of two types of genetically epilepsy-prone rats (GEPRs) and in nonepileptic controls. Both moderate-seizure (GEPR-3) and severe-seizure (GEPR-9) animals had extensive abnormalities in brain NE concentration. Deficits of equal magnitude in GEPR-3s and GEPR-9s were found in the spinal cord, midbrain minus the inferior colliculus, inferior colliculus, hypothalamus, amygdala, hippocampus, occipital + parietal cortex, frontal cortex, and olfactory septum. Because both types of GEPRs share these deficits and share seizure susceptibility, we hypothesize that these areas are candidates for regulation of seizure susceptibility in GEPRs. In addition, because GEPR-9s have more severe seizures than GEPR-3s and because GEPR-9s had greater NE deficits in several brain areas (cerebellum, pons-medulla, thalamus, and possibly the temporal cortex and olfactory bulbs), we hypothesize that these areas may be important in regulation of seizure severity in GEPRs. All animals used in these experiments had been protected from seizure-provoking stimuli and were naive to seizures. Because the abnormalities in NE concentration were present in seizure-predisposed animals that were protected from seizures, we conclude that these abnormalities are important components of the seizure-predisposition characteristic of GEPRs and do not result from seizure experience.
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PMID:Noradrenergic abnormalities in the central nervous system of seizure-naive genetically epilepsy-prone rats. 200 21

Norepinephrine concentrations and tyrosine hydroxylase activity were determined in the brains of moderate-seizure and severe-seizure genetically epilepsy-prone rats (GEPRs) and in nonepileptic control rats. Both moderate-seizure (GEPR-3) and severe-seizure (GEPR-9) animals had widespread abnormalities in brain norepinephrine concentrations. Abnormalities in tyrosine hydroxylase activity were restricted to the midbrain. The state of abnormal seizure susceptibility, but not severity, in the GEPR may be determined by noradrenergic deficits in the hypothalamus/thalamus. Both seizure severity and susceptibility may be determined by noradrenergic deficits in the telencephalon, midbrain, and pons-medulla. Seizure severity but not susceptibility may be determined by noradrenergic abnormalities in the cerebellum.
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PMID:Indices of noradrenergic function in the central nervous system of seizure-naive genetically epilepsy-prone rats. 287 67

Norepinephrine depletion of the central nervous system by peripheral N-(2-chloroethyl)-N-ethyl bromobenzylamine administration accelerates the development of seizures kindled by repeated stimulation of the amygdala. These data, in conjunction with previous 6-hydroxydopamine data, demonstrate the robustness of this phenomenon and emphasize the importance of noradrenergic innervation originating from the locus ceruleus in the suppression of seizure development.
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PMID:DSP-4 treatment accelerates kindling. 378 Sep 25

Young adult Louis rats were implanted for chronic sleep recording to test the effect of diethyldithiocarbamate (DDC) on sleep. Recordings of EEG and EMG were done continuously for 12 h during the 12 consecutive days. There were 2 days of baseline recording, 3 days of recording with a single daily injection of placebo, 3 days of recording with a single daily injection of DDC (500 mg/kg i.p.), and 3 days of DDC withdrawal recording with placebo injection. Placebo injections did not change the proportion of time spent in different behavioural states. With daily injection of DDC there was an increase in wakefulness, no change in slow-wave sleep and elimination or drastic reduction in paradoxical sleep (PS). There was no PS rebound during the DDC withdrawal days. These results suggest that the reduction of PS produced by DDC and the absence of PS rebound may be due to a lowering in norepinephrine in the brain. In other experiments rats were injected with DDC (500 mg/kg i.p.) daily for 3 days and whole brains were analysed chemically. Norepinephrine was significantly decreased, while 5-hydroxytryptamine, 5-hydroxyindolacetic acid, dopamine and homovanilic acid were unchanged. Seizure activity appeared during relaxed wakefulness in all rats treated with DDC. Taken together it seems that lowering of brain NE is responsible for the appearance of seizure activity and also, for PS reduction. PS reduction might, per se, produce seizure activity.
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PMID:Sleep-waking cycle and behaviour after diethyldithiocarbamate in the rat. 615 81

Norepinephrine (NE) depletion of the cerebral cortex after lesion of the ipsilateral locus ceruleus (LC) causes abnormalities of cerebral oxidative metabolism when the cortex is stimulated to increased energy demand (Harik, S. I., J. C. LaManna, A. I. Light, and M. Rosenthal (1979) Science 206: 69-71; LaManna, J. C., S. I. Harik, A. I. Light, and M. Rosenthal (1981) Brain Res. 204: 87-101). These abnormalities were exhibited as decreased mitochondrial reducing equivalent flow. One possible cause of this would be the decreased availability of oxidative metabolic substrates in the NE-depleted cortex. We therefore investigated the effect of unilateral LC lesion and the resultant depletion of ipsilateral endogenous NE on glycogen and other energy metabolites in the cerebral cortex of rats under three conditions: (1) at "rest," (2) when energy demand is inncreased markedly by seizures, and (3) during total cerebral ischemia. We report no differences in cerebral metabolites between NE-depleted and control hemispheres at "rest." In seizures and ischemia, however, the increase in the level of adenosine 3':5'-monophosphate (cyclic AMP) and the breakdown of glycogen were impaired considerably in the NE-depleted cortex. The data suggest that depletion of central NE impairs cerebral glycogenolysis in response to increased energy demands and ischemia. Such impairment may be mediated via a cyclic AMP-related mechanism.
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PMID:Norepinephrine regulation of cerebral glycogen utilization during seizures and ischemia. 627 95

Norepinephrine, dopamine, and 5-hydroxytryptamine concentrations were determined in the central nervous systems of genetically epilepsy-prone rats (GEPR) and in control rats. Norepinephrine concentrations were abnormal in all major areas of the central nervous system of the GEPR, with decrements existing in the telencephalon, hypothalamus-thalamus, midbrain, pons-medulla and spinal cord. An increment in the concentration of this neurotransmitter existed in the cerebellum. Dopamine concentrations were normal in all areas of the GEPR brain. Abnormalities in 5-hydroxytryptamine concentrations were also present in the GEPR. They were exclusively decrements and occurred in the telencephalon, hypothalamus-thalamus, midbrain, and pons medulla. Concentrations of this neurotransmitter were normal in the cerebellum and spinal cord. Coupled with our earlier pharmacologic data, these observations support our concept that noradrenergic and/or 5-hydroxytryptaminergic decrements are etiologically important in seizure susceptibility in the GEPR. The lack of abnormalities in brain dopamine concentrations strengthens our hypothesis that dopaminergic transmission does not regulate seizure susceptibility in this model.
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PMID:Abnormalities in monoamine levels in the central nervous system of the genetically epilepsy-prone rat. 628 98

The influence of dopamine, levodopa and apomorphine on maximal electroconvulsive seizure was studied in young chicks, adult cocks and rats. The susceptibility of chicks to maximal electroshock seizure increased with age between 1 to 7 days. Low to moderate doses of dopamine (12.5-150 mg/kg, i.p.), levodopa (6.25-25 mg/kg, s.c.) and apomorphine (0.25-2.0 mg/kg, s.c.) significantly (P less than 0.005) protected chicks against electroshock seizure, while high doses (200-400 mg/kg, i.p. of dopamine, 50-200 mg/kg, s.c. of levodopa and 2.5-5 mg/kg, s.c. of apomorphine) enhanced electroshock seizure in 1 to 7 day old chicks. However, when 14 day old chicks were used, these dopaminoceptor agonists protected the chicks against maximal electroshock seizure. Noradrenaline (1-40 mg/kg, i.p.) had no significant effect on electroshock seizure in chicks. Both pimozide (4 mg/kg, i.p.) and haloperidol (0.4 mg/kg, i.p.) antagonized the effects of levodopa (12.5 and 50.0 mg/kg, i.p.) and apomorphine (0.5-5 mg/kg, s.c.) on maximal electroshock seizure. The seizure susceptibility of both adult rats and fowls to electroshock was not altered by dopamine (12.5-400 mg/kg, i.p.). Central dopamine neurotransmission might be involved in the biphasic dose-dependent effects of dopamine, levodopa and apomorphine on maximal electroshock seizure in young chicks.
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PMID:Influence of dopamine, levodopa and apomorphine on maximal electroconvulsive seizure in the domestic fowl (Gallus domesticus). 650 36


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