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 intraperitoneally administered dihydropyridine calcium channel blocker-nifedipine (NIF) 5 mg/kg and diphenylhydantoin (DPH) 5 mg/kg were studied on hippocampal kindling and maximum electro shock thresholds (MEST). All the NIF injected rats showed complete suppression of behavioral seizure after the 3rd injection. Few of the DPH rats had increased epileptic activity for two days and others--absence of Grade--5 seizure after the 5th DPH injection. However, all showed partial seizure suppression subsequently. Neither NIF nor DPH could suppress the after discharge (AD). MEST were not affected by NIF although DPH showed a complete suppression of posterior limb extensor tone in all the rats.
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PMID:Dihydropyridine group of calcium channel antagonist in epilepsy. 813 43

The voltage-sensitive calcium channel probe 125I-omega-GVIA conotoxin has been shown to be a developmental marker in whole brain preparations of Swiss Webster mice. The present study looks more carefully at regional dissections of the mouse brain (cerebrum, cerebellum, and brain stem) at postnatal day 8 and postnatal day 16. 125I-omega-GVIA conotoxin binding, thought to be presynaptic, showed a dramatic increase between postnatal days 8 and 16 in the cerebral cortex, a decrease in the cerebellum, and no change in the brain stem. The dramatic cerebral cortex increases indicated by these binding data correspond to a critical period between postnatal day 11 and postnatal day 14 in Swiss Webster mice; during this critical period, dendrites exhibit rapid outgrowth, sensory modalities come on line, electroencephalographic patterns mature, and the cortex reaches adult proportions. This period parallels a similar initiation of electrical maturation in the 28- to 32-week neonatal human brain. We conclude from these data that the unusual clinical presentation of neonatal seizures is not just the result of immature myelin formation. It includes incomplete synapse formation linking the cortex to the brain stem.
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PMID:Regional differences in the critical period neurodevelopment in the mouse: implications for neonatal seizures. 815 Oct 90

The anticonvulsant effect of the dihydropyridine calcium channel blocker, nimodipine (NMD) was evaluated against electroshock-induced seizures in mice. At 1 h postdosing, NMD elicited a dose-dependent reduction in the occurrence of tonic hindlimb extension (THE) after maximal electroshock (MES). The calculated ED50 for NMD was 87 mg/kg. A single dose of NMD (75 mg/kg) produced a significant (p < 0.05) reduction in occurrence of THE for < or = 12 h postdosing. NMD was detectable for < or = 6 h, and plasma and brain drug concentrations correlated well (r = 0.677, p < 0.01) for that period. At 1 h postdose, a single dose of NMD (75 mg/kg) produced a 40% increase (p < 0.001) in the threshold for tonic seizures as determined by minimal electroshock (Min-ES). NMD is an effective anticonvulsant against experimental seizures induced by electroshock. The pharmacodynamic effect of NMD appears to extend beyond the time anticipated from the pharmacokinetic profile.
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PMID:Dose-response relationships with nimodipine against electroshock seizures in mice. 815 70

The calcium channel blockers verapamil (VPM) and nimodipine (NMD) were administered to adult or immature (16-day-old) rats to determine their effects on amygdala-kindled seizures. The afterdischarge threshold (ADT) kindling rate and degree of postictal refractoriness were determined for two doses of VPM (0.5 and 5.0 mg/kg in rat pups and 2 and 10 mg/kg in adult rats) or 30 mg/kg nimodipine (NMD). Neither VPM nor NMD affected the ADT of the amygdala in adult or immature rats. VPM retarded the rate of kindling in both adult and immature rats in a dose-dependent manner; the number of stimulations required to progress through seizure stages were increased. NMD 30 mg/kg reduced the kindling rate and AD duration in both adult and immature rats. Neither drug was able to suppress recurrent seizures elicited by repetitive stimulation. These results suggest that verapamil, and possibly NMD may be of clinical utility in treatment of epilepsy, especially complex partial seizures.
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PMID:Calcium channel blockers verapamil and nimodipine inhibit kindling in adult and immature rats. 815 71

Two dihydropyridine type calcium channel blockers (CCBs) were studied for any protective or therapeutic effect upon cocaine-induced toxicity and death in rats. To test for the protective effects, rats were pretreated with vehicle (control), nifedipine or nimodipine, intraperitoneally (IP) 30 minutes prior to an LD85 of cocaine, or intravenously (IV) 10 minutes prior to cocaine administration. Animals receiving IP control vehicle developed seizures in 5.6 +/- 1.0 minutes and respiratory arrest in 9.8 +/- 1.4 minutes. Animals pretreated IP with nifedipine or nimodipine developed seizures and respiratory arrest significantly sooner than the controls, although the overall incidences of seizures and respiratory arrest were not significantly different. Pretreatment with IV CCBs resulted in similar findings. To test the therapeutic effect of CCBs given following cocaine overdose, rats were administered cocaine IP and then treated with IV nifedipine or nimodipine once seizures occurred. In these animals, there was no significant difference in the incidence or time to respiratory arrest compared to vehicle controls. This study demonstrates that neither pretreatment nor posttreatment with the CCBs nifedipine or nimodipine reduces cocaine toxicity in this rodent model.
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PMID:Cocaine toxicity and the calcium channel blockers nifedipine and nimodipine in rats. 816 94

We have shown previously that the dihydropyridine calcium channel antagonist nitrendipine, given chronically, prevents the development of ethanol tolerance and physical dependence. The present study examines the effects on barbiturate tolerance and physical dependence. Nitrendipine, given acutely during withdrawal, provided little protection against barbiturate withdrawal, as measured by convulsive behaviour on handling. When nitrendipine was given chronically concurrently with the barbiturate, a prolonged protection against the withdrawal syndrome was seen. Acute nitrendipine significantly increased the latency of seizures in response to the partial benzodiazepine inverse agonist FG7142 during barbiturate withdrawal, but there was no effect on the seizure incidence in response to bicuculline. Chronic treatment with nitrendipine did not alter the development of tolerance to the ataxic or general anaesthetic actions of barbiturates, but evidence was found of a possible interaction between nitrendipine and pentobarbitone, which may have been pharmacokinetic. The results suggest that neuronal calcium channels may be involved to some degree in the development of the changes responsible for barbiturate withdrawal, but to a less extent than found previously for ethanol dependence.
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PMID:Dihydropyridine-sensitive calcium channels and barbiturate tolerance and withdrawal. 820 88

Treatment of rats with the central thiamine antagonist, pyrithiamine, results in severe neurological symptoms such as ataxia and convulsions. Induction of proto-oncogene c-fos expression, often related to seizure activity, has been detected in the brains of thiamine-deficient rats by means of Northern blot analysis and in situ hybridization. Region-selective increases of lactate observed following thiamine deficiency development are largely coincident with histologically vulnerable regions. When thiamine-deficient rats were treated with the calcium channel blocker, nicardipine, lesions associated with thiamine deficiency did not appear and there was no induction of c-fos mRNA expression. This suggests a neurocytoprotective role of nicardipine to neuronal cell damage in thiamine-deficient encephalopathy.
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PMID:Proto-oncogene c-fos induction in thiamine-deficient encephalopathy. Protective effects of nicardipine on pyrithiamine-induced lesions. 822 66

This overview summarizes the major and minor side effects and drug interactions of fluoxetine. The adverse reactions include the "serotonin syndrome", cardiovascular complications, extrapyramidal side effects such as akathisia, dyskinesias, and parkinsonian-like syndromes and an apparently increased risk of suicidality. Fluoxetine-induced mania and hypomania, seizures and sexual disorders are evaluated along with minor symptoms of allergic reactions, stuttering, hematological changes, psoriasis, and inappropriate secretion of the antidiuretic hormone. The major fluoxetine-drug interactions involve the amino acids L-dopa and L-tryptophan, anorexiants, anticonvulsants, antidepressants, anxiolytics, calcium channel blockers, cyproheptadine, lithium salts, and drugs of abuse. The underlying mechanism and the paradoxical effects of fluoxetine are addressed.
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PMID:Fluoxetine: adverse effects and drug-drug interactions. 825 2

The effects of calcium channel entry blockers on cocaine and amphetamine-induced behavioral responses were investigated. Cocaine and amphetamine produced dose-dependent increases in locomotor activity and stereotyped behavior with a maximum response at 40 and 1.2 mg/kg, respectively. The 1,4-dihydropyridine nimodipine and the benzothiazepine diltiazem were more effective in inhibiting cocaine (20 mg/kg)-induced responses than amphetamine (0.6 mg/kg)-induced responses. At doses of cocaine and amphetamine that caused seizures and death, nimodipine, nitrendipine and diltiazem did not offer any protection; rather, they potentiated the toxicities produced by these psychomotor stimulants.
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PMID:Effects of calcium channel entry blockers on cocaine and amphetamine-induced motor activities and toxicities. 825 57

Chlordiazepoxide is a benzodiazepine that is widely used as a minor tranquilizer. It is also effective in the treatment of acute alcohol withdrawal. In this setting, chlordiazepoxide acts as a sedative and prevents the development of epileptiform activity. Although benzodiazepines are known to augment gamma-aminobutyric acid-activated chloride channels, an action which at least partially accounts for their anticonvulsant properties, there is some evidence to suggest that voltage-activated calcium channels may also be the target of these agents. We therefore studied the effect of chlordiazepoxide in blocking two distinct types of voltage-activated calcium channels in N1E-115 neuroblastoma cells. Chlordiazepoxide reversibly blocked calcium channels in both closed and open configurations. It was slightly more potent in blocking the transient (T-type or type I) than the long-lasting (L-type or type II) type of calcium channels with apparent Ki values of 311 and 398 microM, respectively. In the presence of chlordiazepoxide, the currents of both types of calcium channel currents decayed more quickly than control, an observation that suggests open channel block. Chlordiazepoxide-induced block of T-type calcium channels was use dependent, increasing with an increase in stimulus frequency. This was due primarily to the acceleration of current decay and slowing of recovery from inactivation by chlordiazepoxide. These calcium channel blocking actions could contribute some to the sedative and anticonvulsant properties of chlordiazepoxide in patients suffering from acute alcohol withdrawal and in electric shock-induced seizures in animal models.
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PMID:Chlordiazepoxide block of two types of calcium channels in neuroblastoma cells. 838 Aug 61


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