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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...
Sympathetic Signaling01:31

Sympathetic Signaling

Sympathetic signaling, a vital part of the autonomic nervous system, plays a crucial role in mobilizing the body's resources in response to stress or emergencies. It involves the transmission of nerve impulses from sympathetic preganglionic fibers to postganglionic fibers. This results in the release of specific neurotransmitters and activation of adrenergic receptors.
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Drugs Affecting Neurotransmitter Synthesis01:29

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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, which converts...
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Adrenergic Agonists: Therapeutic Uses

Adrenergic agonists have diverse therapeutic uses across various medical conditions and emergencies.
Emergency and Intensive Care Unit (ICU) applications: Pressor agents increase blood pressure, heart rate, and contractility in shock and organ failure situations. Dopamine can induce vasodilation and stimulate adrenoceptors. Endogenous catecholamines are effective in treating cardiogenic shock. α2-agonists like clonidine can reverse anesthesia-induced hypertension.
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Vagus Nerve Stimulation As an Adjunctive Neurostimulation Tool in Treatment-resistant Depression
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Published on: January 7, 2019

Noradrenergic function in suicide.

Ghanshyam N Pandey1, Yogesh Dwivedi

  • 1The Psychiatric Institute, Department of Psychiatry, University of Illinois at Chicago 60612, USA. Gnpandey@psych.uic.edu

Archives of Suicide Research : Official Journal of the International Academy for Suicide Research
|June 15, 2007
PubMed
Summary

Noradrenergic function, specifically tyrosine hydroxylase (TH) and certain adrenergic receptors, may play a role in suicidal behavior. Studies show increased protein expression of TH, alpha2-, and beta2-adrenergic receptors in the brains of suicide victims.

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08:32

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Published on: December 18, 2014

Area of Science:

  • Neuroscience
  • Psychiatry
  • Molecular Biology

Background:

  • Suicidal behavior research has primarily focused on serotonin.
  • Emerging evidence suggests noradrenergic system dysfunction may also contribute to suicide pathophysiology.

Purpose of the Study:

  • To review existing noradrenergic studies related to suicide.
  • To explore the role of norepinephrine-related molecules in suicidal behavior.

Main Methods:

  • Review of studies on tyrosine hydroxylase (TH), the norepinephrine biosynthetic enzyme.
  • Analysis of research on alpha- and beta-adrenergic receptors.
  • Examination of signaling cascades linked to beta-adrenergic receptors.

Main Results:

  • Increased protein expression of TH was observed in postmortem brains of suicide victims.
  • Elevated levels of alpha2- and beta2-adrenergic receptors were found in suicide victims.
  • Consistent alterations in noradrenergic system components suggest a potential link to suicidal behavior.

Conclusions:

  • Noradrenergic system abnormalities, including TH and adrenergic receptor changes, are implicated in the pathophysiology of suicide.
  • Further extensive research is required to fully elucidate the role of noradrenergic function in suicidal behavior.