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)

The antidepressant characteristics of three indole alkylamines were investigated and compared with phenelzine and imipramine by utilising specific pharmacological tools like reserpine, amphetamine, tryptamine and tetrabenazine for determining their possible mechanism of action. Amongst the three indole compounds investigated, indole-3-(2-aminopropyl)-acetate (U-14 164E), indole-3(2-aminobutyl)-d-acetate (u-17 312E) and beta-phenethylhydrazine (phenelzine) produced complete antagonism to reserpine induced sedation, hypothermia as well as facilitation of convulsive seizures. Some of these features suggest that MAO inhibition might be a common mechanism of action of these indoles. The potentiation of CNS effects of tryptamine by these compounds is an outstanding feature of MAO inhibitors, while imipramine is ineffective. Qualitative differences between these indoles and imipramine are evident in the tetrabenazine test. The potentiation of amphetamine induced motor excitation and pentobarbitone narcosis has been explained.
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PMID:A study of antidepressant activity of some indole alkylamines. 2 69

The effect of chlormadinone acetate (24 mg/day) upon the plasma levels of pituitary gonadotropins and gonadal hormones on the number of generalized convulsions and spike EEG density was studied in a group of epileptic children with intractable seizures and with clinical signs suggestive of hyperandrogenism. In each case, the effect of chlormadino ne was evaluated in relation to hormone levels and seizures observed during a control period and under the effect of placebo, as follows: Control (PC); Chlormadinone acetate (PCL1); Placebo (PP); Chlormadinone acetate (PCL2). In a male child, the number of convulsive attacks observed in the control period (26/month) was reduced during PCL1 (2/month), increased during PP (12/month) and reduced again during PCL2 (0/month). Spike EEG density showed a parallel course to the clinical attacks. In this case, control testosterone levels were markedly high (40 ng/ml) and decreased during PCL1 to 4.0, increased again during PP to 34.0 and decreased again during PCL2 to 1.2 ng/ml. Plasma levels of pituitary gonadotropins were unchanged during the entire period of study. In other cases, neither the number of epileptic attacks nor spik e EEG density were apparently affected by this treatment and plasma levels of pituitary gonadotropins and gonadal hormones were also unchanged. These findings suggest that a latent state of hyperandrogenism may be detected in some epileptic patients with intractable seizures and that chlormadinone may reduce convulsive attacks in these patients, probably by decreasing plasma testosterone levels.
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PMID:[Effect of chlormandinone acetate upon seizures in epileptic children with latent signs of hyperandrogenism]. 5 36

A 10-year-old boy with idiopathic epilepsy refractory to treatment from age 4 and with clinical signs of hyperandrogenism was treated with chlormadinone acetate (24 mg/day) during two alternate periods of 3 months. The administration of chlormadinone was associated with a marked clinical and electroencephalographic improvement as well as a concomitant decrease in the levels of plasma testosterone and delta4 androstenedione. No changes in plasma gonadotropins were observed. Placebo had no effect neither in seizures nor in the concentration of hormones in the plasma. Since chlormadinone acetate is not a very potent gonadotropin inhibitor in males, it is suggested that the clinical and electroencephalographic improvement associated with the use of this compound, might be the consequence of a decrease in the plasma levels of androgens, mainly testosterone.
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PMID:Improvement of intractable idiopathic epilepsy with chlormadinone acetate. A case report. 6 43

Intracerebroventricular administration of 10--20 microgram of steroid-O-sulfates induced hypermotility, agitation, salivation, EEG abnormalities, stereotypies, wet dog shakes and seizures. Equivalent effects resulted from 30--200 microgram morphine sulfate (H2SO4 salt), 50 microgram EGTA or 300--400 microgram of sodium sulfate or phosphate, but not chloride, nitrate or acetate. Non-steroid sulfates, steroid glucuronides and steroid phosphates were inactive. Naloxone, previously found to antagonize the excitatory effects of androsterone sulfate, failed to antagonize those of cortisol sulfate, sodium sulfate or EGTA. These findings suggest a role for extracellular calcium ions and for sulfate derived from circulating steroids in central responses to opiates.
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PMID:Opiate-like excitatory effects of steroid sulfates and calcium-complexing agents given cerebroventricularly. 21 60

Sulthiame has been used by most investigators in psychomotor seizures, other focal seizures and grand-mal, usually in conjuction with other anticonvulsants. Reports on its use in myoclonic epilepsy and as a sole anti-convulsant are few and inconclusive. The present report presents the results of a study carried out on the use of sulthiame in 54 cases of myoclonic epilepsies originating in infancy, childhood and adolescence. The different types of myoclonic epilepsy are defined. An illustrative case report is included. Results indicated that sulthiame is the drug of choice, often as the sole anti-convulsive agent, in cases of "juvenile myoclonic epilepsy". In the myoclonic encephalopathies of childhood (the so-called "minor motor epilepsy" or Lennox-Gastaut syndrome), which are notoriously refractory to therapy, sulthiame appears to be an efficacious adjunct to currently-used agents, including benzodiazepines, succinimides, dipropyl acetate, steriods and a ketogenic diet.
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PMID:The use of sulthiame- in myoclonic epilepsy of childhood and adolescence. 24 84

Growing, mongrel dogs were fed high fat (22%), low calcium (.1%) semipurified and purified diets with and without 77 ppm lead as lead acetate to experimentally induce the seizures and lead encephalopathy historically associated with accidental canine lead toxicity. Seizures were observed in 44% of the lead toxic dogs and microscopic encephalopathy was observed in 89% of the lead toxic dogs. The encephalopathy was characterized by bilaterally symmetrical areas of vacuole formation involving the neuropile especially in a laminar pattern at the tips of the gyri of the cerebral cortex. The spongy state was accompanied by capillary activation and gliosis. These lesions are similar to those reported in accidental lead toxicoses in other species but previous efforts to experimentally induce these lesions in young dogs fed low-calcium, normal-fat (16%) purified diets have been unsuccessful.
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PMID:Lead-induced encephalopathy in dogs fed high fat, low calcium diets. 46 67

In order to determine the effects of acetate on signs and symptoms of hypoglycemic seizures, Swiss Webster albino mice were injected intraperitoneally with solutions of NaCl, NaHCO3, NH4Cl, Na-acetate, or NH4-acetate, followed by subcutaneous injection of 7 U of insulin/kg body wt. Administration of Na- or NH4-acetate delayed and reduced the incidence of hypoglycemic reactions. Reinjection with Na-acetate or repeated injections with NH4-acetate caused a return to normal behavior patterns for 60 and 75%, respectively, of the affected hypoglycemic experimental animals. Injections of control animals with NaHCO3 or NH4Cl showed that the results were not due to alkalosis or acidosis. Acetate administration significantly increased plasma acetate and citrate, but not glucose, lactate, beta-hydroxybutyrate, or acetoacetate concentrations. The results indicate that intraperitoneal administration of acetate directly acted to prevent signs of hypoglycemia from occurring and reversed its manifestations when they were present. The protective effect of acetate suggests that it may serve as a fuel for the brain.
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PMID:Effect of acetate on hypoglycemic seizures in mice. 48 41

A 63-year-old white female who was being treated for hypertension with lisinopril presented with seizures, altered mental status, and a serum sodium of 101 mEq/L. Serum sodium prior to initiation of lisinopril therapy was 137 mEq/L. The hyponatremia was corrected and did not recur after lisinopril was stopped. The hyponatremia may have been a result of polydipsia and inappropriate antidiuresis secondary to ACE-inhibitor therapy.
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PMID:Case report: severe symptomatic hyponatremia associated with lisinopril therapy. 131 75

Nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) are structurally related survival and differentiation factors for distinct sets of peripheral and central neurons. The regulation of NGF gene expression has been extensively studied in L929 mouse fibroblasts. L929 cells also express the BDNF gene. Northern blot hybridization analysis revealed 4 discrete BDNF mRNA species in L929 cells and rat hippocampus after induction of seizures with kainic acid. Serum as well as 12-O-tetradecanoyl phorbol-13-acetate (TPA) stimulated NGF and all 4 BDNF mRNAs in L929 cells. Treatment with both agents induced NGF mRNA to a much larger extent than the BDNF mRNAs. The induction of the BDNF mRNAs was rapid, with nearly maximal levels by 1 hr. In contrast, NGF mRNA induction occurred later and peaked at 4-6 hr. Both NGF and BDNF mRNA induction were inhibited by actinomycin D. Cycloheximide, on the other hand, inhibited only NGF but not BDNF mRNA induction. Corticosterone rapidly decreased NGF mRNA but not the BDNF mRNAs, and had no effect on seizure-induced NGF or BDNF mRNAs. Forskolin did not stimulate NGF or BDNF mRNAs. In contrast to NGF mRNA, forskolin did not interfere with the serum induction of BDNF mRNAs. These results demonstrate that 2 genes which encode closely related neurotrophic factors are differentially regulated in L929 cells. The molecular mechanisms which bring about this differential regulation remain to be elucidated.
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PMID:Differential regulation of the nerve growth factor and brain-derived neurotrophic factor genes in L929 mouse fibroblasts. 133 58

Pergolide (LY127809, CAS 66104-23-2), a non-selective dopamine agonist, was evaluated for broad behavioral properties in a wide range of pharmacological tests. The selective dopamine2(D2) agonist, bromocriptine, served as a reference standard for those tests where behavioral activity was noted with pergolide. Pergolide and bromocriptine were administered orally to mice at doses of 0.3-30 and 3-300 mg/kg, respectively. Both compounds produced biphasic effects on spontaneous activity, increased hexobarbital-induced sleep time, and lowered mouse body temperature. Qualitative changes with pergolide were observed with some mice showing hyporeactiveness, ptosis, slowed respiration and placing loss. Reserpine-induced hypothermia was reversed by pergolide with significant increases in the body temperature of reserpine-treated mice. However, a further reduction in the body temperature of reserpinized hypothermic mice was seen following bromocriptine administration. Acetic acid-induced writhing and performance on the rotarod were both impaired by higher doses of pergolide. Bromocriptine administration also reduced writhing at higher doses but did not alter performance on the rotarod. Pergolide had no effect on seizure activity as evaluated by electroshock, pentylenetetrazol (pentetrazol) or strychnine. Oxotremorine-induced tremors and salivation, grip strength, and tail-flick were not affected by pergolide. Neither pergolide nor bromocriptine altered established shuttle-avoidance behavior in rats at oral doses of 0.1 to 30 mg/kg. Behavioral assessment of pergolide in dogs was complicated by severe emetic responses at clinically relevant doses greater than 0.003 mg/kg. In summary, these data suggest that pergolide produces a behavioral profile which is characteristic of dopaminergics.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Behavioral characterization of the new potent nonselective dopamine agonist pergolide. 141 51


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