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

In mice chronically treated with ethanol (in a liquid diet containing 6% ethanol ad libitum for 2 weeks), brain tryptophan hydroxylase (TPH) activity was increased (by 30-45% in whole brain), while brain tyrosine hydroxylase activity remained unchanged. Such chronic ethanol treatment also induced susceptibility to audiogenic seizures during withdrawal (60% incidence). When ethanol treatment was given to adrenalectomized (Adx) mice, the increase of brain TPH activity and the development of withdrawal audiogenic seizures were both prevented. In Adx mice receiving daily injections of corticosterone (0.5 mg/mouse), the ethanol-induced increase of brain TPH activity and the occurrence of withdrawal audiogenic seizures were both restored. Similarly, the ethanol-induced increase of liver alcohol dehydrogenase activity (by 60%) was prevented in Adx mice and restored by corticosterone replacement. It was noted that in all three cases replacement with such large doses of the corticoid did not enhance the ethanol effects, but merely restored the effects to the levels observed in intact mice. Apparently, glucocorticoids are required in a permissive role in order for the ethanol effects to occur.
Drug Alcohol Depend
PMID:The permissive role of glucocorticoids in the development of ethanol dependence and tolerance. 2 Oct 65

Chronic bipolar electrodes were implanted in cortical, limbic, diencephalic and mesencephalic regions of the rat. Following recovery from surgery the rats were maintained for 14--26 days on a liquid diet in which 35--42% of total calories were provided by ethanol. Following ethanol withdrawal, electrographic and behavioral monitoring was continued for 8--10 h. The withdrawal of ethanol resulted in the time-dependent appearance of a variety of withdrawal signs including tail arching, ataxia, rigidity, tremor and spontaneous and audiogenic convulsions. These behavioral signs were accompanied by the development of epileptiform abnormalities across wide-spread brain regions. Analysis of preconvulsive spike activity revealed a greater spike frequency in limbic, mesencephalic and non-specific diencephalic regions, as compared to those in cortex and specific diencephalon. Seizure discharge during the tonic-clonic phase of the primary audiogenic convulsion was initiated in the mesencephalon or amygdala, but spread rather extensively to the remainder of the brain. In those instances, however, where multiple convulsions occurred following the audiogenic convulsions, there was a marked decline in spread of seizure discharge to the cortex. These results were interpreted to support the notion that some degree of neuroanatomical specificity exists in the genesis of epileptiform abnormalities during ethanol withdrawal. A comparison of these results with those studying the neural mechanisms underlying other forms of generalized epilepsy was made. It is hypothesized that central pacemaking regions such as medial thalamus or reticular formation may serve to organize isolated epileptiform activity into coherent patterns of paroxysmal activity throughout the brain during the ethanol withdrawal syndrome.
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PMID:Ethanol dependence in the rat: role of non-specific and limbic regions in the withdrawal reaction. 8 50

Several antiepileptic drugs, such as carbamazepine and clonazepam, have low bioavailability in solid form and are insoluble in an aqueous solution. Alcohol solvents are often employed as vehicles when these drugs are studied in animal models. Secondary and particularly tertiary alcohols are suspected of some anticonvulsant activity. The present research evaluated the possibility that polyethylene glycol 400 (PEG 400) might be efficacious, toxic, or both. Monkeys (N = 11) rendered epileptic by aluminum-hydroxide were administered PEG 400 by constant rate (1 ml/hr) intravenous infusion for 3--4 weeks, preceded and followed by several weeks of baseline. At a concentration of 60%, PEG 400 significantly reduced seizure frequency, but also exhibited severe side effects. These findings suggest that experimental testing of anticonvulsants may be compromised when this or similar solvents are used chronically.
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PMID:Efficacy and toxicity of the solvent polyethylene glycol 400 in monkey model. 10 3

Thirty rats were randomly assigned to three groups. Group 1 was given a 21-day exposure to an ethanol (EtOH) liquid diet, while Groups 2 and 3 were given equivalent amounts of an isocaloric non-EtOH liquid diet. Group 1 rats had withdrawal syndromes following EtOH removal. After a two-week recovery period, Groups 1 and 2 were both exposed to an EtOH diet, while Group 3 again received an isocaloric non-EtOH liquid diet. Groups 1 and 2 were withdrawn after 12 days of EtOH exposure and were rated with a behavioral withdrawal rating scale, for which interobserver reliability estimates were determined. Previously dependent (Group 1) rats showed more severe withdrawal syndromes, including a higher incidence of seizures, than rats undergoing their initial withdrawal (Group 2). Studies that do not agree with this finding are discussed.
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PMID:Potentiation of ethanol withdrawal by prior dependence. 10 20

The enzymes of the cholinergic system have been investigated in discrete brain areas in alcohol-dependent rats, which were still intoxicated or were undergoing withdrawal. The ethanol intoxication resulted in a slight, but significant increase in choline acetyltransferase (CAT) activity in the caudate nucleus both 1 and 7 h after the last dose of ethanol. We also found a significant decrease in CAT activity in the temporal limbic cortex while rats were highly intoxicated. All other brain regions investigated, e.g., cerebellum, pons-medulla, frontoparietal cortex, hypothalamus and septum showed unchanged CAT activity. Rats were also analysed immediately following the onset of a withdrawal-induced audiogenic convulsive seizure where, in addition to the striatum, depressed CAT activity was observed in the hippocampus. In all the analysed situations acetylcholinesterase activity remained unchanged. These results show that ethanol intoxication leads to a perturbation in the synthetic capacity of acetylcholine in certain defined brain structures and that this may have some correlation to the observed behavioural impairments.
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PMID:Cholinergic involvement in ethanol intoxication and withdrawal-induced seizure susceptibility. 10 88

Adult C57BL/10Bg mice, normally resistant to audiogenic seizures, became susceptible when the mothers drank 10 per cent ethanol in water during pregnancy and for 14 days postpartem. Reserpine enhanced the incidence of seizures, and the effect was reversed by 5-hydroxytryptophan but not by dihydroxyphenylalanine. p-Chlorophenylalanine also enhanced the incidence of seizures, whereas alpha-methyl equals p equals tyrosine did not effect. Monsodium glutamate almost completely prevented seizures. These results are consistent with the interpretation that the serotonergic systems may be among those involved in the seizure mechanism induced by fetal and early exposure to ethanol.
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PMID:Effects of aminergic drugs and glutamic acid on audiogenic seizures induced by early exposure to ethanol. 12 3

Programmed-feeding polydipsia results in a reliable model of chronic alcoholism in the rat. High oral ethanol comsumption and a predictable withdrawal reaction associated with audiogenic seizures are produced. The maintenance of high blood ethanol levels for three weeks in 18 male Charles River rats was associated with audiogenic seizures after 6 or 8 hours of withdrawal. These chronic alcoholic rats had enhanced blood clearance of ethanol. The cerebral cortical crude mitochondrial fraction showed a decrease in total and magnesium-dependent adenosine triphosphatase activity in alcoholic and control (water-fed) rats compared with normal rats.
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PMID:Programmed feeding as a model of chronic alcoholism in the rat. 15 1

An outbreak of acute methyl alcohol intoxication occurred in Port Moresby, Papua New Guinea, in March 1977. Twenty-eight young men attended a drinking party and drank methyl alcohol. The amount consumed by each individual ranged from an equivalent of 60--600 ml of pure methanol. Three had prior ethanol ingestion. All 28 became ill 8--36 hours after drinking and were hospitalized. The most commonly observed clinical syndromes were: acute metabolic acidosis, severe visual impairment and acute pancreatitis. Four died within 72 hours after admission to the hospital. All had severe metabolic acidosis and visual impairment and three pancreatitis. Of 24 who recovered, 16 showed no residual complications, six had bi-lateral visual impairment and two had difficulty in speech as well as visual impairment. A three month follow-up examination showed no change in the findings. Coma, seizures and prolonged acidosis were poor prognostic signs. The estimated amount of consumed methanol and the rapidity of the appearance of signs of toxicity following methanol ingestion did not seem to influence the outcome of poisoning. The treatment of acute methyl alcohol intoxication in centres where dialysis is not available is discussed.
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PMID:An outbreak of acute methyl alcohol intoxication. 28 45

Parent C57BL/10Bg and DBA/1Bg inbred mice were fed 10% ethanol in their drinking solution during mating and pregnancy and/or early post parturition period. The susceptibility to audiogenic seizures and the open field behavior of their offspring were tested at age 29--33 days. Our previous experiments have indicated that continuous exposure to ethanol during pre- and neonatal periods enhanced the susceptibility to audiogenic seizures in both strains and decreased open field activity only in the strain C57. The present study, while confirming previous findings, assessed the relative contribution of the prenatal and the neonatal administration of ethanol to the behavioral changes. Among C57 mice, the neonatal period was most important for the induction of changes in seizures, but prenatal exposure which alone had no effect, enhanced the outcome of neonatal administration. Among DBA mice either period induced seizures, but the contribution of the neonatal period was the most significant. Early ethanol administration affected open field behavior only in C57 mice. There was an additive interaction between the two periods (latency), no effect by any period alone but together they produced a full effect (ambulation), or that either period alone was sufficent to produce a full effect (defecation).
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PMID:The relative contribution of pre- and neonatal ethanol administration to changes in mice behavior. 52 78

Mice were made physically dependent on ethanol by a 3-day period of alcohol inhalation with small daily injections of pyrazole. During this treatment the concentrations of norepinephrine, dopamine and 5-hydroxytryptamine were increased in brain with concomitant decrease in gamma-aminobutyric acid, RNA and DNA. However, the monoamine concentrations showed complete regression to normal levels at the time of maximal withdrawal seizure when GABA level was still elevated above the control values. Brain RNA and DNA concentrations remained low at this period. During the recovery phase, the pattern of neuronal components was almost the same as was observed at maximal withdrawal seizures. Pyrazole by itself did not produce significant changes in concentrations of the neuronal components of brain.
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PMID:Neurochemical aspects of ethanol dependence and withdrawal reactions in mice. 55 9


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