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)

Norepinephrine turnover rates were estimated in the hypothalamus-thalamus, midbrain, pons-medulla and telencephalon of genetically epilepsy-prone rats (GEPR). In each of these 4 brain areas the endogenous norepinephrine levels were significantly lower in the GEPR than in control animals. In the hypothalamus-thalamus, midbrain and telencephalon the calculated norepinephrine turnover rates were also significantly lower in GEPRs than in control. These studies confirm and extend earlier observations relating seizures in the GEPR to decrements in central nervous system noradrenergic function.
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PMID:Abnormalities in norepinephrine turnover rate in the central nervous system of the genetically epilepsy-prone rat. 669 49

The authors investigated the value of high-dose thiopental (TH) therapy after 16-min complete global brain ischemia (GBI) in three groups of pigtailed monkeys, using a neck cuff model of GBI with 96 h intensive care postischemia (PI). Control group (n18): Normotension was restored within 2 min PI; paralysis/controlled ventilation was maintained for 48 h PI with 50% N2O/O2. Thiopental loading group (n13): Control treatment plus TH-loading with 90 mg/kg iv given from 5 to 65 min PI (mean peak TH plasma level 130 micrograms/ml). Thiopental anesthesia group (n14): Control treatment plus TH anesthesia with 90 mg/kg iv given over 12 h PI (sustained TH plasma levels of 25-35 micrograms/ml and EEG burst suppression). Norepinephrine requirement for blood pressure control PI was greater in the TH groups than in the control group (P less than 0.05). Lidocaine was needed for control of arrhythmias in the TH loading group. There was no significant difference in mortality or neurologic outcome between the groups. At 96 h PI seven of 11 animals were awake in the control group, compared with seven of 12 and six of 12 in the two TH groups. Neurologic deficit scores (NDS) for the survivors at 96 h PI were 23 +/- 6% (mean +/- SD) (n10) in the control group, compared with 25 +/- 9% (n11) and 26 +/- 12% (n10) in the two TH groups (NDS 100% = brain death, 0% = normal). Seizures PI (in 1-2 of each group) were associated with worse neurologic deficits.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Thiopental treatment after global brain ischemia in pigtailed monkeys. 669 50

Delta-aminolaevulinic acid (ALA) is suspected of being responsible for the neuropsychiatric symptoms of acute porphyria. The object of this study was to examine the effects of ALA in vivo on a range of behavioural and physiological functions which are known to be affected in the acute porphyric attack. Aminolaevulinic acid was administered by intraperitoneal or subcutaneous injection to mice in doses up to 1000 mg/kg and effects on nociception (hot-plate and abdominal constriction tests), CNS excitability (pentobarbitone sleep-time and pentylenetetrazole-induced seizures), motor co-ordination and grip (rotating rod test) were studied. Rats were given intravenous injections or infusions of ALA of up to 24 mg and changes in blood pressure, heart rate and ED50 for noradrenaline, acetylcholine and isoprenaline examined. No statistically significant effects were noted, using buffered solutions of ALA (pH 7.0-7.4). However, unbuffered solutions of ALA caused significant bradycardia and hypotension. These results do not support the hypothesis that ALA has significant acute neuropharmacological activity in vivo when the blood-brain barrier is intact.
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PMID:Neuropharmacology of delta-aminolaevulinic acid--I. Effect of acute administration in rodents. 672 34

The functions of the putative noradrenergic innervation of cerebral microvessels from the nucleus locus ceruleus remain ambiguous. Although most evidence indicates that such innervation does not have a major role in the control of cerebral blood flow, there are increasing indications that it modulates transport and permeability functions of the blood-brain barrier. In this study we investigated the effect of unilateral chemical lesioning of the locus ceruleus on the leakage of radioiodinated human serum albumin across the blood-brain barrier. Experiments were performed in awake and restrained rats under steady-state conditions and during drug-induced systemic arterial hypertension, and in anesthetized and paralyzed rats during bicuculline-induced seizures. Both hypertension and seizures are known to be associated with increased leakage of macromolecules across the blood-brain barrier. Albumin leakage into norepinephrine-depleted forebrain structures ipsilateral to the locus ceruleus lesion was compared with that of the contralateral side. There were no side-to-side differences in blood-brain barrier permeability to albumin under steady-state conditions, the stress of restraint, or angiotensin-induced hypertension, or after isoproterenol administration. Norepinephrine-induced hypertension and seizures, however, caused significant increases in albumin leakage into forebrain structures ipsilateral to the lesion. These results suggest that noradrenergic innervation of cerebral microvessels from the locus ceruleus helps preserve the integrity of the blood-brain barrier during pathophysiological states associated with hypertension and increased circulating catecholamines.
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PMID:The protective influence of the locus ceruleus on the blood-brain barrier. 674 91

The concentrations of dopamine, noradrenaline, and dihydroxyphenylacetic acid were determined in the amygdala, neostriatum, neocortex, hippocampus, brain stem, and hypothalamus of cats, which had had 9 to 14 tonic-clonic kindled seizures. No significant biochemical changes were observed compared to control cats. Pharmacological manipulations of dopamine receptors (haloperidol, apomorphine) did not modify the kindling procedure. According to the data it seems unlikely that dopamine plays a major role in amygdaloid kindling.
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PMID:Involvement of dopamine in amygdaloid kindling. 684 Feb 49

The role of the noradrenergic and the serotonergic systems in the development of hippocampal and amygdaloid kindling was studied. Dorsal noradrenaline bundle lesions markedly facilitated the formation of hippocampal and amygdaloid kindling. The most significant facilitation was observed in the earliest phase of kindling. Cortical noradrenaline content decreased by about 70% after dorsal noradrenaline bundle lesions. Midbrain raphe nuclei (both dorsal and medial raphe nuclei) lesions did not have any effect on the formation of both hippocampal and amygdaloid kindling. These results indicate that the dorsal noradrenaline bundle system plays an inhibitory role in the development of the seizure discharges and the behavioral convulsions in hippocampal and amygdaloid kindling.
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PMID:The role of noradrenergic and serotonergic systems in the hippocampal kindling effect. 687 24

The effects of tricyclic antidepressants; imipramine and doxepin, and of new antidepressants; mianserin, danitracen, trazodone, viloxazine and zimelidine, on seizures kindled from the rabbit amygdala were examined. Behavioral and bioelectrical seizures were kindled by a repeated daily stimulation of unilateral amygdala with a low intensity electric current (120 microamperemeter, 1 msec, 50Hz). The following parameters of kindled seizures were analyzed: 1-intensity of behavioral seizures according to a 6-point scale, 2-duration of behavioral seizures, 3-duration of bioelectrical (EEG) seizure activity. Only imipramine inhibited all parameters of kindled seizures. Doxepin, mianserin, danitracen and trazodone affected only two parameters. Zimelidine did not induce any changes of kindled seizure, and viloxazine prolonged duration of the bioelectrical seizure activity. It is likely that inhibition of seizures kindled from the rabbit amygdala is due to noradrenaline stimulating or serotonin inhibiting properties of the drugs, but independent of the antidepressive activity.
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PMID:The effects of antidepressant drugs on the seizures kindled from the rabbit amygdala. 725 68

Dihydroergotoxine administration shortened the latency of allylglycine-and picrotoxin-induced convulsions in rats and increased the incidence of convulsions elicited by picrotoxin, i.e., it lowered ED50 for picrotoxin. The same drug (0.1-10.0 mg/kg) decreased the levels of gamma-aminobutyric acid (GABA) in the caudate nucleus and cingulate cortex, but enhanced the aminooxyacetic acid induced accumulation of GABA indicating an increased synthesis of GABA in these brain regions. The concentrations of 5-hydroxytryptamine, 5-hydroxyindoleacetic acid, noradrenaline, and dopamine in the whole rate brain were not affected with doses of dihydroergotoxine up to 10.0 mg/kg, but this dose of the drug slowed down the turnover of dopamine, as evidenced by a diminished disappearance of dopamine induced by alpha-methyl-p-tyrosine administration. The results suggest that dihydroergotoxine decreases GABA-ergic transmission and, therefore, presumably lowers the seizure threshold.
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PMID:Dihydroergotoxine and the Seizure Threshold. 729 68

The rate and pattern of seizure development provoked by repeated electrical stimulation of the amygdala (kindling) was assessed in rats that had been pretreated with intracerebral injections of the selective catecholaminergic neurotoxin 6-hydroxy-dopamine. Rats with selective depletion of forebrain noradrenaline displayed a highly significant facilitation of both primary-site and secondary-site kindling, whereas no such effect occurred in rats with selective depletion of forebrain dopamine. The facilitative effects of noradrenaline depletion were apparently related to disinhibition of the spread of seizure discharge from the stimulated site rather than to increased epileptogenicity in the stimulated site itself. These results are consistent with previous evidence that noradrenaline reduces the susceptibility of the central nervous system to epileptiform activity, and they suggest that a lessening of seizure-suppressant noradrenergic function in the forebrain might be part of the mechanism underlying kindling.
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PMID:Role of forebrain catecholamines in amygdaloid kindling. 737 Aug

The state of seizures readiness in epileptic rats of Krushinsky--Molodkina line is characterised by interhemispheric synchroneity, revealed with electrophysiological methods parallely with the study of the catecholamine content in the brain tissue. On the contrary in animals insensitive to epileptogenic stimulus, considerable manifestations of the functional interhemispheric asymmetry were recorded. The monoaminoxidase inhibitor iprazide increasing the adrenaline and noradrenaline content in the brain and causing their uneven distribution between the hemispheres, leads to a sharp decline in the level of seizures readiness, which is accompanied by the appearance of bioelectrical and catecholamine asymmetry comparable with that in the animals resistent to the epileptogenic stimulus.
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PMID:[Effect of a monoamine oxidase inhibitor on the level of seizure readiness and functional asymmetry of the brain]. 738


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