amide/seizures

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Equipotent inhibition of fatty acid amide hydrolase and monoacylglycerol lipase - dual targets of the endocannabinoid system to protect against seizure pathology.

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Advances in the understanding of the endogenous cannabinoid system have led to several therapeutic indications for new classes of compounds that enhance cannabinergic responses. Endocannabinoid levels are elevated during pathogenic conditions, and inhibitors of endocannabinoid inactivation promote

Selective effect of oleamide, an endogenous sleep-inducing lipid amide, on pentylenetetrazole-induced seizures in mice.

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The anti-seizure effect of oleamide, an endogenous sleep-inducing fatty acid amide, was studied in mice. Oleamide, in the dose range 43.7-700.0 mg kg(-1), significantly and dose-dependently inhibited the seizures induced by pentylenetetrazole. However, oleamide showed no inhibitory action on the

Increased seizure susceptibility and proconvulsant activity of anandamide in mice lacking fatty acid amide hydrolase.

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A number of recent in vitro studies have described a role for endogenous cannabinoids ("endocannabinoids") as transsynaptic modulators of neuronal activity in the hippocampus and other brain regions. However, the impact that endocannabinoid signals may have on activity-dependent neural events in

Alterations in the pharmacokinetic properties of amide local anaesthetics following local anaesthetic induced convulsions.

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The comparative pharmacokinetic properties of lidocaine, bupivacaine, etidocaine and mepivacaine were investigated in convulsing and non-convulsing dogs. The same dose of a given local anaesthetic was administered as either a 30-s intravenous (IV) bolus to produce convulsions or as a 15-min IV

Anticonvulsant effects of N-arachidonoyl-serotonin, a dual fatty acid amide hydrolase enzyme and transient receptor potential vanilloid type-1 (TRPV1) channel blocker, on experimental seizures: the roles of cannabinoid CB1 receptors and TRPV1 channels.

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Selective blockade of anandamide hydrolysis, through the inhibition of the FAAH enzyme, has anticonvulsant effects, which are mediated by CB1 receptors. Anandamide, however, also activates TRPV1 channels, generally with an opposite outcome on neuronal modulation. Thus, we suggested that the dual

Central action of a catechol-amide seizure-inducing agent: opposing effect on tyrosine and tryptophan hydroxylase activity in vivo.

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The audiogenic seizure-inducing drug H13/04 was found to elicit opposing effects on the in vivo accumulation of 5-HTP (5-hydroxytryptophan) and DOPA (3,4-dihydroxyphenylalanine) in the brain following inhibition of L-amino acid decarboxylase. In strains of mice that normally do not exhibit

Influence of new gamma-hydroxybutyric acid amide analogues on the central nervous system activity in mice.

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The present study investigates the activity of four gamma-hydroxybutyric acid amide analogues (BM-68, BM-74, BM-75 and BM-76) in two models of chemically induced seizures, i.e. picrotoxin- and pentetrazole-induced seizures and in the thiopental-induced sleep test. The results of pharmacological in

Replacement of the peptide-backbone amides connecting Tyr-Gly and Gly-Gly in leucine-enkephalin with ketomethylene groups: synthesis and biological activity.

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A peptide analogue of Leu-enkephalin was synthesized in which the amide linkages between Tyr-Gly and Gly-Gly were replaced by ketomethylene groups. The resulting analogue, 12, had 1/4000th and 1/2400th the opiate receptor binding activity of Leu-enkephalin when (3H) [D-Ala2,D-Leu5]enkephalin and

Tachycardia and convulsions induced by accidental intravascular ropivacaine injection during sciatic block.

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Ropivacaine, a recently introduced local anesthetic of the amide family (1), seems to show less toxicity than bupivacaine (2-4). Nevertheless, both neurologic and cardiovascular toxicities are possible. Six cases of ropivacaine-induced convulsions have previously been reported (5-10), of which three

The glycine-prodrug, milacemide, increases the seizure threshold due to hyperbaric oxygen; prevention by 1-deprenyl.

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The novel glycine-prodrug anticonvulsant, milacemide (2-N-pentylaminoacetamide) (500 mg/kg), significantly increased (greater than 400% the seizure threshold induced by hyperbaric oxygen (4.5 atmosphere). This effect was significantly reduced by the selective inhibition of monoamine oxidase B by

Manipulation of fatty acid amide hydrolase functional activity alters sensitivity and dependence to ethanol.

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The aim of this study was to examine the role of fatty acid amide hydrolase (FAAH) on ethanol sensitivity, preference, and dependence. The deletion of FAAH gene or the inhibition of FAAH by carbamoyl-biphenyl-3-yl-cyclohexylcarbamate (URB597) (0.1 mg/kg) markedly increased the preference for

Evaluation of interactions between cannabinoid compounds and diazepam in electroshock-induced seizure model in mice.

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Several studies have shown that cannabinoids have anticonvulsant properties that are mediated through activation of the cannabinoid CB1 receptors. In addition, endogenous cannabinoid compounds (endocannabinoids) regulate synaptic transmission and dampen seizure activity via activation of the same

Effect of arachidonyl-2'-chloroethylamide, a selective cannabinoid CB1 receptor agonist, on the protective action of the various antiepileptic drugs in the mouse maximal electroshock-induced seizure model.

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The aim of this study was to determine the influence of arachidonyl-2'-chloroethylamide (ACEA - a highly selective cannabinoid type 1 [CB1] receptor agonist) on the protective action and acute adverse effects of carbamazepine, lamotrigine, oxcarbazepine, phenobarbital, phenytoin, and topiramate in

[Simple derivatives of amino acid neurotransmitters. Anticonvulsant evaluation of derived amides, carbamates and esters of glycine and beta-alanine].

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With GABA, glycine and beta-alanine are inhibitory amino acids. They act mainly in the spinal cord and in the brain stem via the strychnine sensitive glycine receptor. Glycine exhibits also a key rule in the excitatory neurotransmission in the N-methyl-D-aspartate receptor complex. These two

N-(benzyloxycarbonyl)glycine esters and amides as new anticonvulsants.

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Glycine is a small neutral amino acid exhibiting weak anticonvulsant activities in vivo. Recently, studies have demonstrated that N-(benzyloxycarbonyl)glycine (1) antagonized seizures superior to glycine in addition to activity in the maximal electroshock (MES) test, a convulsive model where glycine

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