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Certain drugs can affect how neurotransmitters called catecholamines, are released or taken back up in the adrenergic neuron. They can have different effects on the body's sympathetic transmission. Reserpine, a natural compound found in the Rauwolfia shrub, blocks a transporter called vesicular monoamine transporter (VMAT), which leads to a buildup of catecholamines in the cell and reduces sympathetic transmission. Another drug called guanethidine works in multiple ways, including blocking...
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Drugs affecting neurotransmitter synthesis can impact the adrenergic neuron and the synthesis of neurotransmitters. For example, α-methyltyrosine and carbidopa target specific enzymes involved in catecholamine synthesis. α-methyltyrosine inhibits the enzyme tyrosine hydroxylase, which converts tyrosine into dopamine. By blocking this enzyme, α-methyltyrosine reduces dopamine production and other catecholamines. Carbidopa, on the other hand, inhibits the enzyme dopa decarboxylase,...
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The elimination half-life and drug clearance of drugs following nonlinear kinetics can vary with dosage. The Michaelis-Menten parameters and drug concentration influence these factors. As the dose increases, the elimination half-life tends to lengthen, resulting in a reduction in clearance and a disproportionately larger area under the curve. The total clearance can be derived from the Michaelis-Menten equation for drugs following a one-compartment model.
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Related Experiment Videos

Fenfluramine and 5-hydroxytryptamine?. Part 1: Is fenfluramine or norfenfluramine involved in the decrease of brain

J Duhault, C Malen, M Boulanger

    Arzneimittel-Forschung
    |November 1, 1975
    PubMed
    Summary
    This summary is machine-generated.

    Fenfluramine and its metabolite, de-ethylated fenfluramine, reduce brain 5-hydroxytryptamine (5-HT) levels. The metabolite plays a key role in the sustained depletion of 5-HT after fenfluramine administration.

    Related Experiment Videos

    Area of Science:

    • Neuroscience
    • Pharmacology

    Background:

    • Fenfluramine is known to decrease brain 5-hydroxytryptamine (5-HT) levels.
    • De-ethylated fenfluramine is a known metabolite of fenfluramine.

    Purpose of the Study:

    • To investigate the role of de-ethylated fenfluramine in the 5-HT lowering effects of fenfluramine.
    • To determine if the fenfluramine metabolite mediates the depletion of brain 5-HT.

    Main Methods:

    • Comparative analysis of 5-HT lowering effects.
    • Measurement of drug brain levels in rats.
    • Assessment of the time course of fenfluramine and its metabolite in the brain.

    Main Results:

    • Both fenfluramine and de-ethylated fenfluramine were found to decrease brain 5-HT stores.
    • The metabolite, de-ethylated fenfluramine, was detected in the rat brain after fenfluramine injection.
    • Comparative studies indicated an initial effect of fenfluramine, followed by increasing involvement of its metabolite in sustained 5-HT depletion.

    Conclusions:

    • The depletion of brain 5-HT by fenfluramine may be mediated by its metabolite, de-ethylated fenfluramine.
    • De-ethylated fenfluramine contributes significantly to the sustained reduction of brain 5-HT levels following fenfluramine administration.