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Related Concept Videos

Drugs Affecting Neurotransmitter Release or Uptake01:21

Drugs Affecting Neurotransmitter Release or Uptake

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...
Adrenergic Neurons: Neurotransmission01:27

Adrenergic Neurons: Neurotransmission

Postganglionic sympathetic fibers (except those supplying the sweat glands) releasing noradrenaline or norepinephrine are called noradrenergic or adrenergic neurons. Noradrenaline, dopamine, adrenaline, or epinephrine are collectively called "catecholamines" as they contain a catechol moiety and an amine side chain. The five stages of neurotransmitter release involve their synthesis, storage, release, reuptake and metabolism.
Synthesis: Catecholamine synthesis requires tyrosine, which is taken...
Drugs Affecting Neurotransmitter Synthesis01:29

Drugs Affecting Neurotransmitter Synthesis

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, which converts...
Adrenergic Agonists: Indirect-Acting Agents01:25

Adrenergic Agonists: Indirect-Acting Agents

Indirect-acting adrenergic agonists potentiate the effects of endogenous catecholamines through different mechanisms without directly binding to adrenoceptors.
One mechanism involves depleting stored catecholamines by displacing them from synaptic vesicles. These agents, known as "displacers," are transported into vesicles at the expense of noradrenaline. Examples include amphetamine and tyramine, which lack a catechol moiety, resulting in prolonged action, improved oral bioavailability, and...
Neurochemical Transmission: Sites of Drug Action01:26

Neurochemical Transmission: Sites of Drug Action

Neurochemical transmission, the conduction of electrical impulses between neurons mediated by neurotransmitters, plays a vital role in various physiological processes. Autonomic drugs exert their effects by modulating neurotransmission within the autonomic nervous system. For instance, drugs such as hemicholinium block the precursor uptake necessary for synthesizing acetylcholine, an essential autonomic neurotransmitter. Following synthesis, neurotransmitters are stored in vesicles. Metyrosine...
Desensitization and Tachyphylaxis01:20

Desensitization and Tachyphylaxis

Tachyphylaxis is described as a rapid decrease in response to a drug after repeated or continuous administration of the same drug dose. It is a phenomenon where the body becomes less responsive to a particular substance or intervention over time, requiring higher doses or stronger interventions to achieve the same effect. It results from adaptive changes in the body's receptors, signaling pathways, or physiological processes that occur in response to prolonged exposure to a stimulus.
Several...

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A Plate-Based Assay for the Measurement of Endogenous Monoamine Release in Acute Brain Slices
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Reserpine-induced reduction in norepinephrine transporter function requires catecholamine storage vesicles.

Prashant Mandela1, Michelle Chandley, Yao-Yu Xu

  • 1Department of Pharmacology & Toxicology, University of Mississippi Medical Center, Jackson, MS 39216, USA.

Neurochemistry International
|February 24, 2010
PubMed
Summary
This summary is machine-generated.

Reserpine inhibits norepinephrine transporter (NET) activity by reducing its maximum transport capacity, independent of cell surface trafficking or signaling pathways. This novel mechanism requires catecholamine storage vesicles for NET regulation.

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A Convenient Method for Extraction and Analysis with High-Pressure Liquid Chromatography of Catecholamine Neurotransmitters and Their Metabolites
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Published on: March 1, 2018

Area of Science:

  • Neuroscience
  • Pharmacology
  • Molecular Biology

Background:

  • Reserpine, a vesicular monoamine transporter (VMAT) inhibitor, depletes norepinephrine (NE) and influences NE transporter (NET) expression.
  • Understanding the molecular mechanisms of NET regulation by reserpine is crucial for developing novel therapeutic strategies.

Purpose of the Study:

  • To investigate the molecular mechanisms by which reserpine regulates the norepinephrine transporter (NET) in cultured cells.
  • To elucidate the role of catecholamine storage vesicles and intracellular signaling in reserpine-mediated NET regulation.

Main Methods:

  • Cultured rat PC12 cells, SK-N-SH cells, and HEK-293 cells transfected with rat NET (293-hNET) were used to study reserpine's effects on [(3)H]NE uptake.
  • Inhibition of intracellular signaling cascades and depletion of catecholamines were employed to dissect the mechanism of action.
  • Binding assays were performed to assess reserpine's interaction with NET.

Main Results:

  • Reserpine rapidly decreased [(3)H]NE uptake in PC12 cells, primarily by reducing the V(max) of transport.
  • This effect was dependent on catecholamine storage vesicles, as it was diminished in SK-N-SH cells and absent in 293-hNET cells.
  • Reserpine's action was independent of NET trafficking and known intracellular signaling pathways.
  • Pre-treatment with alpha-methyl-p-tyrosine abolished reserpine's inhibitory effect on [(3)H]NE uptake.

Conclusions:

  • Reserpine non-competitively inhibits NET activity through a Ca(2+)-independent process.
  • Catecholamine storage vesicles are essential for reserpine's regulation of NET function.
  • This study reveals a novel mechanism for modifying NET activity, potentially leading to new therapeutic approaches for NET-related disorders.