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beta phenylethylamine/seizures
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MAO-B inhibitor deprenyl and beta-phenylethylamine potentiate [D-ALA2]-Met-enkephalinamide-induced seizures.
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The relationship between deprenyl (MAO-B inhibitor), beta-phenylethylamine (PEA, MAO-B substrate) and [D-Ala2]-Met-enkephalinamide (DALA)-induced seizure was studied in the urethane-anaesthetized rats. A combined electromyographic (EMG) and electrocorticographic (ECoG) method was used. PEA (20-100
Beta-phenylethylamine inhibits K+ currents in neocortical neurons of the rat: a possible mechanism of beta-phenylethylamine-induced seizures.
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beta-Phenylethylamine (beta-PEA), an endogenous amine synthesized in the brain, serves as a neuromodulator and is involved in the pathophysiology of various neurological disorders such as depression, schizophrenia, and attention-deficit hyperactivity disorder. beta-PEA fully exerts the physiological
Pharmacology of beta-phenylethylamine-induced seizures in mice.
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The endogenous trace amine beta-phenylethylamine (PE) produced tonic-clonic seizures in male Swiss mice when administered in doses of 125-200 mg/kg. The number of mice exhibiting PE-induced seizures, the latency to onset of first seizure and the latency to loss of the righting reflex were dose
Beta-phenylethylamine (PEA): an endogenous anxiogen? Three series of experimental data.
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Like the anxiogenic drugs caffeine, pentylenetetrazole, and yohimbine, the endogenous neuroactive monoamine beta-phenylethylamine (PEA) is effective in three tests for anxiogens in mice. In a social interaction test it reduced both the number and duration of contacts. In a conflict situation test (a
Evidence that a preferred substrate for type B monoamine oxidase mediates stimulus properties of MAO inhibitors: a possible role for beta-phenylethylamine in the cocaine cue.
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In the experiment, rats were trained to discriminate 5 mg/kg cocaine HCl from saline in a two-bar drug discrimination procedure. Stimulus generalization experiments were carried out with six inhibitor drugs of monoamine oxidase. The rank order of absolute potency of these drugs in inducing stimulus
[3H]-Flunitrazepam binding in the presence of beta-phenylethylamine and its metabolites.
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It has recently been reported that the concentration of beta-phenylethylamine (PEA) was elevated in the plasma of an individual experiencing convulsions because of an overdose of tranylcypromine. Also, high concentrations of PEA, injected into mice, were reported to induce convulsions. This
Behavioral effects of β-phenylethylamine and various monomethylated and monohalogenated analogs in mice are mediated by catecholaminergic mechanisms.
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The effects of the administration [intraperitoneally, 15 and 75 mg/kg, except α-MePEA (amphetamine, AMPH) at 5 and 10 mg/kg] of β-phenylethylamine (PEA), its methylated (o-Me-, p-Me-, α-Me-, β-Me-, N-Me-, p-OMe-, N,N-di-Me-, and 3,4-diOH-N-Me-), para-halogenated (Br-, Cl-, F-, and I-), and other
[Differences and similarity in the interaction of fenibut, baclofen and diazepam with phenylethylamine].
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The derivatives of GABA and beta-phenylethylamine (PEA) the tranquilizer phenibut and muscle relaxant baclofen (p-chloro-beta-phenyl-GABA, lioresal) diminished all studied effect of PEA in mice, namely seizures, sedation, excitation, hyperthermia. Diazepam diminished only seizures whereas
Neurokynurenines (NEKY) as common neurochemical links of stress and anxiety.
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The following NEKY have been studied: 1-kynurenine (KYN), 3-hydroxyKYN (3HKYN), kynurenic (KYNA), anthranilic (ANT), 3-hydroxyANT (3HANT), quinolinic (QUIN), picolinic (PICA), xanthurenic (XAN), nicotinic (NIC) acids, 3-indole-pyruvate (IPA), nicotinamide (NAM). NEKY antagonize the central effects
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