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)

Infant rats, treated intracisternally with 6-hydroxydopamine or 5,7-dihydroxytryptamine, alone or in combination with desmethylimipramine or pargyline, at 5 to 7 days of age, had significant specific depletions of brain norepinephrine, dopamine, both of these amines, or serotonin at 2.5 months of age. Despite apparent long-term depletions of brain biogenic amines, susceptibility to audiogenically-induced seizures following chronic ethanol withdrawal in these animals was similar to that of controls. Amine-depleted rats also displayed spontaneous withdrawal-induced tremors, spastic motor activity and irritability. The interpretation of these preliminary findings with regard to the proposed role of the biogenic amines in the development of physical dependence on ethanol is discussed.
Drug Alcohol Depend
PMID:Effects of 6-hydroxydopamine or 5,7-dihydroxy-tryptamine on the development of physical dependence on ethanol. 56 50

Glutamate diethyl ester, a specific glutamate antagonist, attenuated the seizures and decreases in behavioral activity that were observed in mice during withdrawal. Prior to withdrawal, ethanol-dependent animals were supersensitive to kainic acid, a potent glutamate agonist, but they were not supersensitive to the convulsant drug pentylenetetrazol. These findings suggest that supersensitivity to glutamate develops during ethanol dependence, and that this phenomenon contributes to the signs of ethanol withdrawl.
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PMID:Glutamic acid and ethanol dependence. 56 32

Intravenous infusions were used to produce physical dependence upon ethanol in rats. The procedure proved to be safe, rapid, and reliable. Ethanol (30% v/v) was administered over a 7-day period. The mean daily dose ranged from 10--14 g/kg/day. Control rats were exposed to a comparable procedure except that saline, rather than ethanol, was infused. All ethanol treated rats that survived the intoxication period (n = 11) showed signs of physical dependence (moderate to severe, n = 8; mild, n = 3) following ethanol withdrawal. Saline treated rats (n = 8) did not show any of these symptoms. The most reliable ethanol withdrawal signs observed were: spontaneous seizure (n = 7), audiogenic seizure (n = 7), tremors (n = 6), tail stiffening (n = 10) and body rigidity (n = 9). These symptoms were analyzed in terms of their hour of onset and hour of maximum intensity following ethanol withdrawal. Application of the intravenous method for the study of ethanol self-administration is discussed.
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PMID:Induction of physical dependence upon ethanol in rats using intravenous infusion. 56 3

After 2 or 2.5 g of alcohol, rats previously subjected to low-intensity electrical stimulation of the amygdala showed first a suppression followed by a potentiation of motor seizures and afterdischarges.
J Stud Alcohol 1979 Mar
PMID:Increased susceptibility to kindled seizures in rats following a single injection of alcohol. 57 42

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

1-(2,6-Dimethylphenyl)-3-methylamidinourea hydrochloride (WHR-1142A, lidamidine hydrochloride) has been reported to be a potent antidiarrheal agent in laboratory animals. This study defines its effects on the cardiovascular and central nervous systems. At doses greater than 1 mg/kg i.v., WHR-1142A reduced cardiac output in the anesthetized dog primarily by depressing heart rate; the blood pressure was slightly elevated due to an increase in peripheral resistance. WHR-1142A was effective in reverting ouabain-induced ventricular arrhythmias to a sinus rhythm. Unlike diphenoxylate, WHR-1142A did not potentiate the CNS depressant effects of hexobarbital or ethanol. WHR-1142A did not block pentetrazole-induced convulsions, electroshock seizures or amphetamine aggregate toxicity. At high doses WHR-1142A caused a general CNS depressant effect was not related to a neuroleptic- or barbiturate-like action.
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PMID:Effects of lidamidine hydrochloride (WHR-1142A), a novel antidiarrheal agent on the cardiovascular and central nervous systems. 58 37

2-[Bicyclo(2,2,1)heptane-2-endo-3-endo-dicarboximido]-glutarimide (taglutimide, K-2004) proved to be a new sedative-hypnotic drug which did not produce any toxic effects when administered orally to mice even at a very high dosage. Central-nervous depression was demonstrated by a reduction in spontaneous motor activity, potentiation of the central-depressant effect of pentobarbital, antagonism of the central-stimulant effect of amphetamine after oral administration and by narcotic activity after i.v. administration of the drug. Furthermore, oral administration of taglutimide potentiated the analgesic action of morphine without being effective on its own. Only weak potentiation of chlorpromazine-induced catalepsy, but not of reserpine-induced catalepsy was observed after taglutimide pretreatment. The drug influenced neither motor co-ordination nor the toxicity of ethanol. Taglutimide exhibited no anticonvulsant activity with respect to maximum electroshock or strychnine-induced seizures. No effect on heart rate or blood pressure was demonstrable after taglutimide treatment in conscious dogs.
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PMID:Pharmacological properties of taglutimide, a new sedative-hypnotic drug. 58 13

Seizures were kindled in the amygdala and ventral hippocampus of rats until a stage 5 (clonic convulsion) was elicited. Stage 5 thresholds were than determined. Animals were then injected with either saline, or a 600 mg/kg, or 1600 mg/kg dose of 25% ethanol. The effect of each of these injections on seizure thresholds was assessed. The 1600 mg/kg dose caused a significant elevation in both AD and motor seizure thresholds, relative to the 600 mg/kg dose and saline, which did not differ. The elevation of seizure thresholds was significantly greater for animals with seizures kindled in the ventral hippocampus.
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PMID:Effects of alcohol on kindled seizure thresholds in rats. 69 47

Taurine was effective in reducing the hypnotic effect of ethanol but did not antagonize the effect of ethanol on seizure susceptibility, body temperature, or brain 5-HIAA concentration.
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PMID:Effect of taurine on some pharmacological properties of ethanol. 73 33

An ethanol withdrawal syndrome consisting of tremors and seizures can be induced in rats and mice. This syndrome closely resembles the physical signs observed in human patients during alcohol withdrawal. The criteria for an animal model of a human disease appear to be fulfilled regarding the etiological agent, course of illness, the similarity of physical and electrophysiological manifestations and response to therapeutic agents. Therefore these models should lend themselves for the elucidation of the pathogenesis at the molecular level of biological organization and for the development of new therapeutic approaches. Criteria for an optimal animal model of ethanol dependence are outlined. Withdrawal signs are classified into minor (startle threshold and exploratory behavior) and major types (tremors and seizures). Methods for quantification of tremors and seizures are described. The procedures for induction of the major withdrawal signs are classified according to the mode of ethanol administration designed to circumvent the animal's inherent aversion to the taste of ethanol: Oral (free feeding, behavioral modifications of free feeding and force feeding), parenteral and inhalation. Auxiliary procedures consist of pyrazole administration and weight reduction resulting in a decreased rate of ethanol metabolism. Exposure to low environmental temperatures increases consumption of ethanol containing diets without proportionately increasing the rate of ethanol metabolism. Auxiliary procedures for the induction of seizures during withdrawal consist of handling the animals and audiogenic stimuli. Advantages and limitations of various rodent models are evaluated in terms of the procedures (practicability, compounding variables) and their results (reproducibility, severity and yield of major withdrawal signs, objective quantification). It is concluded that none of the current methods fulfill all requisites for all types of experiments. The selection of methods best suited for a particular experiment depend upon its objectives.
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PMID:Induction of physical dependence on alcohol in rodents. 80 86


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