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  • Kinetics  (1)
  • Sexual reflexes  (1)
  • humans  (1)
  • moclobemide  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Biochimica et Biophysica Acta (BBA)/Biomembranes 815 (1985), S. 128-134 
    ISSN: 0005-2736
    Keywords: (Erythrocyte membrane) ; Kinetics ; Membrane permeability ; Membrane resealing
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Medicine , Physics
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Experimental brain research 88 (1992), S. 313-320 
    ISSN: 1432-1106
    Keywords: Serotonin ; Ventral medulla ; Sexual reflexes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Neurons in the region of the rostral nucleus paragigantocellularis (nPGi) mediate the inhibition of spinal sexual reflexes. Anatomical and pharmacological evidence is presented supporting a role for 5-hydroxytryptamine (5-HT) in this inhibition. Neurons in the rostral nPGi project to the ventral horn in the vicinity of the pudendal motoneurons. A significant number (78% ipsilateral) of these neurons contain 5-HT. Anterograde tracing with Phaseolus leucoagglutinin (PHA-L) confirmed the nPGi projection to pudendal motoneuron and interneuronal areas of the lumbar cord. 5-HT immunoreactive fibers and presumptive terminals surround the pudendal motoneurons. Urethral stimulation, in the anesthetized male rat, elicited penile erections, ejaculation and rhythmic contractions of the perineal muscles, we have used the term coitus reflex to describe this response. Intrathecal injection of 5-HT (4–50 µg) abolished the coitus reflex. Methysergide (1–10 mg/kg i.v.) prevented the 5-HT induced blockade of the coitus reflex. These data support the hypothesis that 5-HT is involved in the descending inhibition of spinal sexual reflexes.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Neurochemical research 18 (1993), S. 1023-1027 
    ISSN: 1573-6903
    Keywords: Phenelzine ; monoamine oxidase ; bioactive amines ; humans ; urinary excretion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Phenelzine [2-phenylethylhydrazine] (PLZ), a potent inhibitor of monoamine oxidase (MAO)-A and-B, is used widely in psychiatry. We have studied the effects of PLZ administration on urinary excretion of several bioactive amines and their metabolites in psychiatric patients. Urine samples (24-hour) were collected prior to treatment and again at 2 and 4 weeks of treatment with PLZ (30–90 mg daily in divided doses). Amines and metabolites analyzed included 2-phenylethylamine (PEA), m-and p-tyramine (m-and p-TA), phenylacetic acid (PAA), m-and p-hydroxyphenylacetic acid (m-and p-OH-PAA), tryptamine (T), 5-hydroxytryptamine (5-HT), 5-hydroxyindoleacetic acid (5-HIAA), normetanephrine (NME), 3-methoxy-4-hydroxyphenylglycol (MHPG), 3-methoxytyramine (3-MT), and homovanillic acid (HVA). Levels of PEA, p-TA, 5-HT, and T were elevated during treatment with PLZ, but no significant changes in urinary excretion of the acid metabolites PAA, p-OH-PAA, and 5-HIAA were observed. Urinary levels of the noradrenaline metabolites NME and MHPG were increased and decreased, respectively; a similar pattern was observed with the dopamine metabolites 3-MT and HVA. There was an elevation in levels of m-TA and a decrease in its acid metabolite m-OH-PAA during the treatment with PLZ.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Cellular and molecular neurobiology 19 (1999), S. 411-426 
    ISSN: 1573-6830
    Keywords: monoamine oxidase (MAO) ; MAO inhibitors ; metabolism ; phenelzine ; tranylcypromine ; deprenyl ; moclobemide ; brofaromine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract 1. The principal routes of metabolism of the following monoamine oxidase inhibitors (MAOIs) are described: phenelzine, tranylcypromine, pargyline, deprenyl, moclobemide, and brofaromine. 2. Acetylation of phenelzine appears to be a minor metabolic pathway. Phenelzine is a substrate as well as an inhibitor of MAO, and major identified metabolites of phenelzine include phenylacetic acid and p-hydroxyphenylacetic acid. Phenelzine also elevates brain GABA levels, and as yet unidentified metabolites of phenelzine may be responsible for this effect. β-Phenylethylamine is a metabolite of phenelzine, and there is indirect evidence that phenelzine may also be ring-hydroxylated and N-methylated. 3. Tranylcypromine is ring-hydroxylated and N-acetylated. There is considerable debate about whether or not it is metabolized to amphetamine, with most of studies in the literature indicating that this does not occur. 4. Pargyline and R(−)-deprenyl, both propargylamines, are N-demethylated and N-depropargylated to yield arylalkylamines (benzylamine, N-methylbenzylamine, and N-propargylbenzylamine in the case of pargyline and amphetamine, N-methylamphetamine and N-propargylamphetamine in the case of deprenyl). These metabolites may then undergo further metabolism, e.g., hydroxylation. 5. Moclobemide is biotransformed by C- and N-oxidation on the morpholine ring and by aromatic hydroxylation. An active metabolite of brofaromine is formed by O-demethylation. It has been proposed that another as yet unidentified active metabolite may also be formed in vivo. 6. Preliminary results indicate that several of the MAOIs mentioned above are substrates and/or inhibitors of various cytochrome P450 (CYP) enzymes, which may result in pharmacokinetic interactions with some coadministered drugs.
    Type of Medium: Electronic Resource
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