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

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

High-performance liquid chromatography with electrochemical detection was used to measure the regional concentrations of monoamines and metabolites in the brains of rats killed 2 or 4 weeks after kindling of generalized seizures with amygdaloid stimulation. Each kindled rat was compared to a yoked control that received brief trains of non-convulsive low-frequency stimulation of the amygdala. Two weeks after kindling we found a significant depletion of noradrenaline (NA) in the ipsilateral frontal cortex, a significant depletion of serotonin (5-HT) in the stimulated amygdala and contralateral hypothalamus, and no significant changes in concentration of dopamine (DA). Four weeks after kindling we found significant depletions of NA in the stimulated amygdala and ipsilateral hypothalamus, a significant depletion of 5-HT in the ipsilateral hippocampus, and no significant changes in DA. These findings generally fail to replicate previous reports of monoaminergic correlates of kindling. Furthermore, the alterations in monoamines produced by kindling do not fall into a simple and readily interpretable pattern.
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PMID:Monoaminergic correlates of kindling. 382 19

Several studies indicate that brain noradrenaline (NA) depletion facilitates the occurrence of epileptogenic syndromes in various animal models. In cobalt-induced epilepsy in the rat activity is associated with a cortical NA denervation. In order to search for cortical adrenoceptor modifications, inonophoretic studies and adrenoceptor binding assays were performed. At the period of maximal seizure activity, there was a significant supersensitivity of cortical neurons to the ionophoretic application of NA. An increase in the density of beta-adrenoceptor binding sites was observed. No modification in alpha 1- and alpha 2-adrenoceptor binding sites was found. This suggests that in cobalt-induced epilepsy there is a denervation supersensitivity which rests on a selective involvement of beta-adrenoceptors.
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PMID:Chronic cobalt-induced epilepsy: noradrenaline ionophoresis and adrenoceptor binding studies in the rat cerebral cortex. 390 Feb 90

Behavioural, neurochemical and histopathological changes induced by systemic injection of kainic acid were investigated at various doses of the neurotoxin (3, 6 and 10 mg/kg s.c.). There was a positive correlation between the dose of kainic acid and the extent of both the acute neurochemical changes 3 h after the injection (increases of 3,4-dihydroxyphenylacetic acid and 5-hydroxyindoleacetic acid levels and a decrease in noradrenaline levels in all brain regions investigated), the acute histopathological changes (shrinkage and condensation of nerve cells and brain oedema in the entire forebrain) and the extent of behavioural alterations (immobility, 'wet dog shakes' and limbic seizures). However, the slope of the dose-response curves was very steep. Late and irreversible alterations included losses of the enzyme markers glutamic acid decarboxylase and choline acetyltransferase and, histopathologically, incomplete parenchymal necrosis and haemorrhages. These changes, however, were restricted to a few brain regions, the most important being the hippocampus, amygdala, entorhinal and pyriform cortex, and olfactory bulb, and they were seen only in animals which had undergone severe convulsions. It is suggested that the irreversible brain lesions in this animal model of limbic (temporal lobe) epilepsy are not solely induced by a direct action of kainic acid, but may be caused--at least in part--by additional, secondary pathogenetic mechanisms.
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PMID:Kainic acid-induced seizures: dose-relationship of behavioural, neurochemical and histopathological changes. 402 98

alpha-Methyl-p-tyrosine, a catecholamine synthesis inhibitor, was studied to determine its effects against ethanol-induced withdrawal symptoms in mice. Signifilcant (P < 0.001) potentiation of the withdrawal convulsion score induced by ethanol vapour exposure for three days was observed in mice. The synergistic effect was not due to alteration of ethanol metabolism. These results indicate that reductions in catecholamines (dopamine and noradrenaline) augment seizure activity induced by subchronic exposure to ethanol.
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PMID:Effects of catecholamine synthesis inhibition on ethanol-induced withdrawal symptoms in mice. 447 4

1. Drugs have been applied micro-electrophoretically to units in the hippocampal cortex of the anaesthetized cat, and their effects on cell firing were recorded simultaneously.2. L-Glutamate rapidly and powerfully excited hippocampal units, an effect which was quickly reversed on stopping the expelling current. The local application of L-glutamate also excited a fast seizure discharge at 15-50/sec. Both these effects of L-glutamate were strongly depressed by fimbrial stimulation.3. gamma-Aminobutyric acid had a strong depressant action on all the units on which it was tested; the time course of this effect was rapid.4. ACh excited half the units to which it was applied. Characteristically this excitation developed slowly over many seconds and persisted after stopping the expelling current. Most cholinoceptive units were found to be concentrated in the superficial layer of the cortex corresponding to the hippocampal pyramidal cells and their main dendritic processes.5. Atropine selectively blocked the excitation of cholinoceptive units by ACh, but not the excitation by L-glutamate. No cholinoceptive units were blocked by dihydro-beta-erythroidine, though several were selectively blocked by dimethyl (+)-tubocurarine.6. The most usual effect seen with 5-HT was depression, though several units were found to be excited. Some of the units tested with 3-hydroxytyramine (dopamine) or noradrenaline were found to be depressed.
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PMID:Micro-electrophoretic studies of neurones in the cat hippocampus. 594 16

Unanesthetized rats with chronic indwelling cannulas, engaged in food reinforced operant behavior, were infused intracerebroventricularly with a solution containing a trace concentration of 3H-dopamine (3H-DA) with or without prostaglandins (PGs). Approximately 45 minutes after the infusion was started, the procedure was changed to a push-pull perfusion. Perfusate from the ventricles contained significant quantities of the 3H-DA metabolites 3H-3,4-dihydroxyphenylacetic acid (3H-DOPAC), 3H-3-methoxy-4-hydroxyphenylacetic acid (3H-homovanillic acid, 3H-HVA), 3H-3-methoxytyramine (3H-3-MT), and the 3H-noradrenaline (3H-NA) metabolite 3H-3-methoxy-4-hydroxy-phenylethyleneglycol (3H-MHPG). The presence of PGF2 alpha decreased the amount of 3H-DOPAC, 3H-HVA, and 3H-3-MT in perfusate, while PGE1 had the opposite effects. d-Amphetamine (0.5 mg/kg, 1P) affected the recovery of these metabolites from perfusate in a manner similar to PGF2 alpha and opposite to PGE1. PGF2 alpha and the highest (seizure-inducing) dose of PGE1 significantly decreased, while d-amphetamine significantly increased, the quantity of 3H-MHPG in perfusate. Therefore, PGs affect central dopaminergic and noradrenergic activity in vivo, as reflected by changes in their metabolic profiles, and may play a role in the response of the central nervous system to drugs which act through catecholaminergic mechanisms.
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PMID:A comparative study of the effects of prostaglandins and d-amphetamine on the metabolism of 3H-dopamine continuously presented to rat brain in vivo. 609 23

Behavioural, histopathological and neurochemical changes induced by systemic injection of kainic acid (10 mg/kg, s.c.) were investigated in rats. The most pronounced behavioural changes were strong immobility ("catatonia"), increased incidence of "wet dog shakes", and long-lasting generalized tonic-clonic convulsions. The behavioural symptoms were fast in their onset and lasted for several hours. Two distinct phases of histopathological and neurochemical changes were observed. (1) Early partially reversible changes were seen up to 3 h after kainic acid injection. They consisted of shrinkage and pyknosis of neuronal perikarya together with swelling of dendrites and axon terminals. These changes were accompanied by generalized signs of edema throughout the whole brain. Neurochemically, there was a marked decrease in noradrenaline levels (up to 70%) and an increase in levels of 5-hydroxyindoleacetic acid, 3,4-dihydroxyphenylacetic acid and homovanillic acid (up to 200%) in all analysed brain regions, suggesting a strongly increased firing rate of aminergic neurones during the period of generalized seizures. These histological and neurochemical changes were found in all the brain regions examined; they were greatly reduced or only sporadically seen after 1-3 days, when the animals had recovered from the seizures. (2) Late irreversible changes developed 24 h and later following kainic acid injection. They consisted of incomplete tissue necrosis with loss of nerve cells and oligodendrocytes, demyelination, astroglial scar formation, small perivenous hemorrhages and extensive vascular sprouting. The changes were restricted to the pyriform cortex, amygdala, hippocampus (most pronounced in the CA1 sector), gyrus olfactorius lateralis, bulbus olfactorius and tuberculum olfactorium. Neurochemically, a selective decrease was seen in choline acetyltransferase activity (40%) of the amygdala/pyriform cortex area, and of glutamate decarboxylase activity in the dorsal hippocampus (45%) and amygdala/pyriform cortex (55%). No such changes were found in the frontal cortex and the striatum/pallidum. Since at these later time periods the widespread early changes in monoamine metabolism were mostly normalized, loss of acetylcholine and gamma-aminobutyric acid neurons in the affected brain regions represented a selective neurochemical change typical for this stage of kainic acid action. The observed neurochemical and histopathological changes may be directly related to the excitotoxic and convulsive properties of kainic acid. However, brain edema resulting in herniation damage of the basal portions of the brain in addition to disturbances of microcirculation and +
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PMID:Kainic acid induced seizures: neurochemical and histopathological changes. 614 39

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

The preferential alpha 2-noradrenergic agonist clonidine dose-relatedly increased the onset of seizures and mortality times, and decreased severity in rats treated with D,L-allylglycine. These effects were reduced by a dose (2.5 mg/kg) of the preferential alpha 2-antagonist yohimbine, which was itself inactive on the allylglycine seizures. Yohimbine 10 mg/kg alone decreased onset and mortality times. The preferential alpha 1-antagonist prazosin had a slight anticonvulsant effect. These results suggest that the reduction of NA release at alpha 2-noradrenergic receptors or antagonism of noradrenaline effects at alpha 1-receptors exerts seizure suppressant effects.
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PMID:Alpha-noradrenaline modulation of D,L-allylgycine seizures. 627 58


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