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yohimbine/crise épileptique
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Yohimbine-induced seizures involve NMDA and GABAergic transmission.
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The alpha 2-antagonist, yohimbine has been shown to dose-dependently induce clonic seizures in mice. The convulsant effects of yohimbine are not due to alpha 2-antagonism, as other alpha 2-antagonists, such as rauwolscine and idazoxan, did not produce seizures at doses up to 100 mg/kg. Since
Potentiation by yohimbine of pentylenetetrazol-induced seizures in rats: role of alpha 2 adrenergic receptors.
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10 mg/kg yohimbine significantly reduced the latency to the first convulsion of rats treated with 90 mg/kg pentylenetetrazol (PTZ) and markedly increased the number of animals showing generalized strong clonic seizures and dying within 1 h. All the animals treated with 20 mg/kg yohimbine and PTZ
The effect of clonidine and yohimbine on audiogenic seizures (AGS) in rats.
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Clonidine in high doses (0.5,1.0 mg/kg) significantly increased the latency for audiogenic seizures (AGS) in rats and reduced seizure severity. At a dose (0.05 mg/kg) which acts more specifically on presynaptic alpha 2-receptors, clonidine did not affect seizure latency, but showed a slight
[Effects of clonidine and yohimbine on semicarbazide-induced convulsion and electroconvulsive shock].
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Yohimbine can not exert its anticonvulsant action in genetically audiogenic seizure-prone mice.
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Enhancement of a diazepam withdrawal symptom by bicuculline and yohimbine.
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The role of the GABA system in producing a pentylenetetrazol-like interoceptive discriminative stimulus during withdrawal from diazepam was investigated in rats by determining the sensitivity of this system to GABAergic drugs before and after chronic treatment with diazepam. Food-restricted rats
Ang II and Ang III modulate PTZ seizure threshold in non-stressed and stressed mice: possible involvement of noradrenergic mechanism.
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The present study evaluated the effects of Angiotensin (Ang) Ang II and Ang III on pentylenetrazol (PTZ) seizure threshold in non-stressed and stressed mice as well as the possible participation of noradrenergic (NA) mechanism in their effects. While intracerebroventricular (i.c.v.) administered Ang
Hippocampal transcriptional and neurogenic changes evoked by combination yohimbine and imipramine treatment.
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Adjunct α2-adrenoceptor antagonism is a potential strategy to accelerate the behavioral effects of antidepressants. Co-administration of the α2-adrenoceptor antagonist yohimbine hastens the behavioral and neurogenic effects of the antidepressant imipramine. We examined the transcriptional targets of
Evidence that serotonin receptors are involved in the anticonvulsant effect of yohimbine in mice.
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The threshold of seizures induced by electroconvulsive shock (ECS) was determined in mice and the effects of alpha 2-adrenoceptor antagonists (yohimbine, rauwolscine, idazoxan), alpha 2-adrenoceptor agonists (clonidine, B-HT 920), serotonin antagonists (methysergide, metergoline) and a serotonin
Effect of catecholaminergic drugs on quinolinate- and kynurenine-induced seizures in mice.
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Administration of reserpine, trifluperidol, chlorpromazine, haloperidol, spiroperidol, and thioproperazine to adult mice shortened the latency and increased the number of animals with clonic seizures induced by 1-kynurenine sulfate or its metabolite quinolinic acid. Haloperidol dose-dependently
Involvement of the noradrenergic system in the seizures of epileptic El mice.
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We studied the role of the noradrenergic system in the seizures of epileptic El mice. To this end, the anticonvulsant activity of adrenergic drugs was tested with a scoring method, and the binding of [3H]dihydroalprenolol, [3H]prazosin and [3H]yohimbine was evaluated in whole brains and various
The role of α₂-adrenoceptors in the anti-convulsant effects of cannabinoids on pentylenetetrazole-induced seizure threshold in mice.
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Cannabinoid system plays a pivotal role in the seizure threshold modulation which is mainly mediated through activation of the cannabinoid CB₁ receptor. There is also several evidence of interaction between cannabinoid system and α₂-adrenoceptors in different paradigms. Using model of clonic seizure
Alpha-noradrenaline modulation of D,L-allylgycine seizures.
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The preferential alpha 2-noradrenergic agonist clonidine dose-relatedly increased the onset of seizures and mortality times, and decreased severity in rats treated with D,L-allylglycine. These effects were reduced by a dose (2.5 mg/kg) of the preferential alpha 2-antagonist yohimbine, which was
Pharmacological modulation of central monoaminergic systems and influence on the anticonvulsant effectiveness of standard antiepileptics in maximal electroshock seizure.
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The influence of various substances modulating the activity of central noradrenergic, serotonergic or dopaminergic neurotransmission systems on the anticonvulsant effectiveness of phenobarbital (phenytoin, carbamazepine) was investigated in mice using the maximal electroshock seizure test (MES). The
Inhibition of post-decapitation convulsions in the rat by dibenzothiepin neuroleptics via alpha 1-adrenoceptor blockade.
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The mechanisms involved in inhibitory effects of isofloxythepin, a newly synthesized dibenzothiepin neuroleptic, on post-decapitation convulsions were studied in rats. Isofloxythepin (0.05-2.0 mg/kg s.c.) inhibited post-decapitation convulsions in a dose-dependent manner as shown by the decrease in
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