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Drugs Affecting GI Tract Motility: Serotonin Receptor Agonists01:23

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Serotonin, a crucial neurotransmitter synthesized by enterochromaffin cells, plays a cardinal role in regulating gastrointestinal (GI) motility. With over 90% of the body's total serotonin in the GI tract, its influence on digestive processes is profound. Serotonin is swiftly released upon various stimuli, such as food boluses or certain drugs, triggering intrinsic sensory neurons in the myenteric plexus and extrinsic vagal and spinal sensory neurons. This leads to the activation of the...
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Tricyclic Antidepressants (TCAs), including Desipramine (Norpramin), Imipramine (Tofranil), Clomipramine (Anafranil), and Amitriptyline (Elavil), inhibit serotonin and norepinephrine reuptake and also block other receptors. They are used for depression, pain conditions, and insomnia. Common adverse effects include anticholinergic effects, sedation, orthostatic hypotension, and weight gain. They have a narrow therapeutic window and so require plasma-level monitoring. Abrupt discontinuation can...
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Atypical antidepressants, including bupropion (Wellbutrin), mirtazapine (Remeron), nefazodone (Serzone), trazodone (Desyrel), and vilazodone (Viibryd), offer unique mechanisms of action. Bupropion weakly inhibits dopamine and norepinephrine reuptake, aiding depression treatment and smoking cessation, with a low risk of sexual dysfunction. Mirtazapine enhances serotonin and norepinephrine neurotransmission, leading to sedation, increased appetite, and weight gain. As a result, it helps treat...
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Nonlinear Pharmacokinetics: Dependence of Elimination Half-Life and Dose Clearance01:23

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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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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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Related Experiment Video

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The Forced Swim Test as a Model of Depressive-like Behavior
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Fenfluramine long-term administration and brain serotonin

J Duhault, M Boulanger

    European Journal of Pharmacology
    |May 15, 1977
    PubMed
    Summary

    Long-term fenfluramine use lowers brain serotonin (5-HT) levels similarly to acute doses. Serotonin levels recover after drug withdrawal, indicating fenfluramine does not cause 5-HT neuron degeneration.

    Area of Science:

    • Neuroscience
    • Pharmacology
    • Neurochemistry

    Background:

    • Fenfluramine is known to affect serotonin (5-HT) levels.
    • The long-term effects of fenfluramine on 5-HT neuron integrity are not fully understood.

    Purpose of the Study:

    • To investigate the impact of long-term fenfluramine administration on brain serotonin levels.
    • To determine if fenfluramine causes degenerative lesions in serotonin neurons.
    • To assess the reversibility of fenfluramine-induced changes in serotonin levels.

    Main Methods:

    • Administered fenfluramine chronically to a study model.
    • Measured brain serotonin (5-HT) levels after acute and long-term drug exposure.
    • Assessed serotonin levels at 48 hours post-drug withdrawal.

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    Main Results:

    • Both acute and long-term fenfluramine administration significantly decreased brain 5-HT levels.
    • Brain serotonin levels returned to baseline control values 48 hours after fenfluramine withdrawal.
    • No evidence of degenerative lesions in 5-HT neurons was observed.

    Conclusions:

    • Long-term fenfluramine administration causes a reversible decrease in brain serotonin.
    • The mechanism of fenfluramine's effect on serotonin levels does not involve the degeneration of 5-HT neurons.
    • Serotonin neuron function is preserved despite significant short-term depletion by fenfluramine.