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)

Effects of cocaine on the spread of epileptiform discharges within the limbic system were studied in cats prepared with bilateral arrays of indwelling electrodes. Low frequency focal electrical stimulation at threshold intensity was employed to initiate after-discharges in the hippocampus and amygdala. Latencies for the propagation of epileptiform activity to distant limbic sites were determined. Saline and drug tests were alternated, with 96-hr intervals between cocaine administrations. Three subconvulsant doses (1--10 mg/kg cocaine hydrochloride, injected intramuscularly) were tested in a counterbalanced order. Cocaine administration significantly increased the speed at which epileptiform discharges spread to the amygdala and to the hippocampus. This effect was dose-related, it followed both hippocampal and amygdalar stimulation and was evident in ipsilateral as well as contralateral projection sites. These changes were found when limbic seizure patterns were localized and also after fully developed motor convulsions were evoked. In addition, cocaine decreased the duration of the propagated discharges. These results suggest that subconvulsive doses of cocaine have an excitatory effect on the hippocampus and amygdala, increasing their sensitivity to repetitive discharges originating in distant sites. A concurrent inhibitory effect is suggested by the decreased duration of the propagated discharges.
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PMID:Effects of cocaine on propagation of limbic seizure activity. 53 57

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

1. The effects of chemically induced convulsions, clinically similar to those elicited by electroconvulsive treatment (ECT), on brain regional distribution of neuropeptide Y-, neurokinin A-, substance P- and neurotensin-like immunoreactivities were studied in the rat. 2. Pentylenetetrazole (PTZ) and bicuculline (BIC) were used to induce grand mal seizures. Rats were divided into three groups receiving one of the following treatments: Saline, PTZ (45 mg/kg) or BIC (1.5 mg/kg). 3. After sacrifice by focused microwave irradiation, brains were dissected, peptides extracted and measured by specific radioimmunoassays. 4. Repeated grand mal convulsions induced by PTZ, in similarity to ECT, markedly increased NPY-LI concentrations in frontal cortex and hippocampus. In contrast to ECT, no changes in NKA- or SP-LI levels were seen. NT-LI was lowered in striatum. 5. Bicuculline effects were more circumscribed: some animals developed grand mal and died while convulsing (peptides not measured), others did not develop generalized seizures and were sacrificed after the fourth treatment. 6. The results demonstrate a similar effect of PTZ and ECT on regional NPY-LI concentrations and raise the possibility that grand mal, regardless of etiology, is necessary for effects on peptides.
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PMID:Brain neuropeptides: changes by treatment with the convulsants pentylenetetrazole and bicuculline. 149 30

Infusions of an excitant amino acid, N-methyl-D-aspartate (NMDA) into the inferior colliculus (IC) render normal rats susceptible to audiogenic seizures (AGS) and/or spontaneous audiogenic-like seizures without tonic components. The excess excitant amino acid in the IC and the anticonvulsant effects of NMDA antagonists in genetically epilepsy-prone rats (GEPRs), along with innate norepinephrine (NE) deficits and anticonvulsant effects of NE agonists in these animals suggest a mutual role of excitant amino acids and NE in regulating AGS in GEPRs. Saline or 6-hydroxydopamine (6-OHDA, 4 micrograms/side in 2 microliters) was infused bilaterally into the locus coeruleus (LC) of normal male rats and guide cannulas were implanted into the IC. Two weeks later, NMDA was infused bilaterally into the IC (0.5 microliters; 10 nmol/side) and 10 min later the rats were subjected to an electric bell (110 db, 60 s) unless preceded by spontaneous tonic seizures. Tonic seizures were not observed in male rats following NMDA infusions in rats with LC infusions of saline. However, a marked increase in the incidence of tonic seizures was observed in the 6-OHDA-treated rats which were markedly depleted of brain NE as determined by HPLC. These findings indicate that a NE deficit greatly enhances the incidence of tonic convulsions and support the hypothesis that an excitant amino acid excess in the GEPR IC may act to initiate AGS, whereas the NE deficit may allow expression of the tonic components of AGS seen in some GEPRs.
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PMID:Effect of norepinephrine depletion on audiogenic-like seizures elicited by microinfusion of an excitant amino acid into the inferior colliculus of normal rats. 190 10

1. We studied the effects of a calcium antagonist diltiazem, as well as diazepam and phenytoin on hyperthermia induced seizures in unrestrained 15 day-old rats. 2. Saline injected animals exposed to an ambient temperature of 40 degrees C showed a gradual increase in body temperature reaching a maximum of 42 +/- 0.1 degree C at 50 min. 3. At this time all rats pups had generalized seizures. 4. Similar results were obtained when the animals were pretreated with phenytoin (100% showed seizures). 5. Animals receiving diltiazem had a temperature of 41.5 +/- 0.1 degree C at 90 min of exposure to 40 degrees C environment. 6. However, diltiazem completely prevented seizures. 7. The rats treated with diazepam showed lower temperature than in saline, diltiazem and phenytoin groups and no seizures were observed in this experimental group.
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PMID:Effects of diltiazem on hyperthermia induced seizures in the rat pup. 234 Oct 17

The effects of the non-specific opiate antagonist L-naloxone and the inactive isomer D-naloxone, as well as the specific mu receptor antagonist beta-funaltrexamine, have been examined on hyperthermia-induced seizures in unrestrained 15 days old rats. Saline-injected animals exposed to an ambient temperature of 40 degrees C showed a gradual increase in body temperature reaching a maximum of 42 +/- 0.1 degrees C at 50 min exposure. At this time all the pups had seizures and died. Similar results were obtained when the animals were pretreated with different doses of D-naloxone and beta-funaltrexamine. Rats pretreated with L-naloxone also showed an increase in rectal temperature; but the temperature was lower than in saline-injected animals. Only high doses of L-naloxone prevented seizures and deaths. These data indicate that endogenous opioid peptides may play a role in seizures induced by hyperthermia and that receptors other than mu receptors could be involved in hyperthermia-induced seizures.
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PMID:High doses of L-naloxone but neither D-naloxone nor beta-funaltrexamine prevent hyperthermia-induced seizures in rat pups. 289 60

There is increasing evidence suggesting that endogenous opioid peptides play a role both in temperature regulation and in the etiopathology of seizures. We have studied the effects of the opioid antagonist naloxone on hyperthermia-induced seizures in unrestrained 15 day old rat pups. Saline injected control animals exposed to an ambient temperature of 40 degrees C for one hr showed a gradual increase in body temperature reaching a maximum of 42 degrees C at 50 min of exposure; at this time, all animals had convulsions and 86% died. Animals pre-treated with 10 mg/kg naloxone reached a maximum core temperature of 41 degrees C after 60 min at 40 degrees C and no convulsions or deaths were observed. When animals were exposed for 60 min to a 27 degrees C environment, saline controls maintained their normal body temperature throughout the experiment, while 5 mg/kg naloxone produced a marked hyperthermic effect. These experiments suggest that endogenous opioids may play a role in both temperature adaptation and hyperthermia-induced seizures in the rat pup.
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PMID:Naloxone prevents hyperthermia induced convulsions in the immature rat. 380 66

Strychnine toxicosis is characterized by inducible tetanic seizures and metaldehyde poisoning by fine fasciculations progressing to generalized tremors and seizures. Intoxication with 1080 causes seizures, random running movements, vomiting, defecation, urination, acidosis and hyperglycemia. Intoxication with rodenticides causing coagulopathy is characterized by hemorrhage into body cavities but not necessarily external hemorrhage. Anticholinesterase insecticides cause salivation, urination and defecation, while chlorinated hydrocarbon insecticides cause CNS disturbances. Ethylene glycol intoxication results in ataxia, depression, coma, vomiting and tachypnea, followed by acute renal failure. Urea poisoning causes bloat and CNS signs in cattle. Monensin intoxication in horses lasts several days and causes stiffness, colic, uneasiness and recumbency. Salt poisoning results in depression, seizures and hypernatremia. Lead poisoning is associated with central and peripheral nervous system signs, as well as increased numbers of nucleated RBC and basophilic stippling of RBC. Arsenic poisoning results in GI pain, diarrhea, weakness and death. Copper toxicosis in sheep is manifested by hemolytic anemia, hemoglobinemia and hemoglobinuria. Plants that may intoxicate domestic animals include sorghum, greasewood, halogeton, water hemlock, Japanese yew, larkspur, lupine, milk-weed, philodendron, oleander, castor bean and precatory bean.
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PMID:Practical toxicologic diagnosis. 649 3

Male Long-Evans rats were stereotaxically implanted bilaterally with bipolar electrodes in the central amygdala. Rats were then kindled once daily for 1 sec until 3 consecutive Stage V [25] kindled seizures were elicited. On the following day, animals were injected (IP) with either saline, naloxone (10 mg/kg), naltrexone (10mg/kg) or morphine sulfate (10 mg/kg) and again stimulated at the kindling stimulation parameters. Saline injected animals continued to show long bilateral AD's and behaviors (i.e., forelimb clonus, rearing, falling) typical of Stage V kindled animals. In contrast, rats injected with naloxone or naltrexone showed reduced behavioral seizures. Potentiation of post-ictal spiking by morphine in amygdaloid-kindled rats was also observed supporting previous reports [7,21]. In a second experiment, the reduction of kindled seizure serverity by naloxone was systematically replicated. It is concluded that opiates can significantly modify amygdaloid-kindled seizures, and that brain endorphins may play a role in the development or maintenance of an amygdaloid-kindled seizure focus.
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PMID:Opiate modification of amygdaloid-kindled seizures in rats. 708 32

Adenosine is an endogenous neuromodulator that suppresses excitatory neurotransmission. We postulated that adenosine-mediated mechanisms resist status epilepticus (SE) entry and limit SE severity. In the first experiment rats were given an adenosine agonist (2-chloroadenosine), an adenosine antagonist (aminophylline), or saline vehicle, prior to SE induction with pulsed-train current delivered to amygdala in successive 5-min current-on sessions. Saline-treated animals entered limbic SE, with predominantly exploratory behavior, after 6.0 +/- 0.9 current-on sessions. Aminophylline increased major convulsive activity during stimulation and resulted in entry into convulsive SE after only 2.1 +/- 0.1 sessions. 2-Chloroadenosine, in contrast, suppressed major convulsive activity during stimulation, and blocked (in 3/7) or delayed (4/7) SE entry, with successes requiring 12.8 +/- 0.9 stimulation sessions. In a second experiment, animals already in exploratory SE were administered a single injection of saline vehicle, aminophylline, or 2-chloroadenosine. Aminophylline converted exploratory SE into lethally severe convulsive SE. 2-Chloroadenosine suppressed SE behaviorally and electrographically, and protected recipients from the seizure-associated cerebral damage seen in saline-administered SE controls. These results support the hypothesis that endogenous adenosine mechanisms resist SE entry, modulate the severity of ongoing SE, and limit the anatomic spread of seizure activity.
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PMID:Effect of an adenosine antagonist and an adenosine agonist on status entry and severity in a model of limbic status epilepticus. 808 55


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