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Adrenergic Neurons: Neurotransmission01:27

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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.
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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...
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Drugs Affecting Neurotransmitter Release or Uptake01:21

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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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Cystic fibrosis (CF), an autosomal recessive disorder, significantly affects the function of exocrine glands. This genetically inherited disease is characterized by the production of thick and sticky mucus, which can severely affect various organs and systems in the body.
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Adrenergic Agonists: Chemistry and Structure-Activity Relationship01:16

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Adrenergic agonists' structure-activity relationship (SAR) determines their selectivity and efficacy. These agonists comprise a phenylethylamine moiety with an aromatic ring and an ethylamine side chain.
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Size Matters: Measurement of Capsule Diameter in Cryptococcus neoformans
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Catecholamines and virulence of Cryptococcus neoformans.

I Polacheck1, Y Platt, J Aronovitch

  • 1Department of Clinical Microbiology, Hebrew University-Hadassah Medical Center, Jerusalem, Israel.

Infection and Immunity
|September 1, 1990
PubMed
Summary

Cryptococcus neoformans uses catecholamines for melanin production, aiding survival in the brain. This process, mediated by phenoloxidase, protects the fungus from harmful oxidative stress in the brain environment.

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Area of Science:

  • Mycology
  • Pathogenic Fungi
  • Neuroscience

Background:

  • Cryptococcus neoformans is an opportunistic fungal pathogen that can cause life-threatening meningoencephalitis.
  • The brain is a primary site for C. neoformans infection, but the fungal survival mechanisms within this niche are not fully understood.
  • Catecholamines are abundant in the brain, but their role in C. neoformans pathogenesis and survival remains unclear.

Purpose of the Study:

  • To investigate whether catecholamines serve as essential nutrients for C. neoformans.
  • To determine if the brain is a preferred nutritional niche for C. neoformans concerning catecholamines.
  • To elucidate the role of phenoloxidase as a virulence factor in C. neoformans survival within the brain, particularly in response to oxidative stress.

Main Methods:

  • Comparison of wild-type C. neoformans (with phenoloxidase activity) and phenoloxidase-deficient mutants.
  • Exposure of both strains to an in vitro epinephrine oxidative system (epinephrine, Fe3+, H2O2).
  • Assessment of fungal survival rates and analysis of DNA damage in response to oxidative stress.

Main Results:

  • C. neoformans cannot utilize catecholamines as sole carbon or nitrogen sources, indicating they are not essential growth factors.
  • Wild-type C. neoformans demonstrated resistance to the epinephrine oxidative system, while mutants showed susceptibility with a 4-log decrease in survival per hour.
  • Mutant susceptibility correlated with damage to high-molecular-weight DNA, suggesting DNA damage as a cause of cell death.

Conclusions:

  • C. neoformans may survive in the brain by utilizing catecholamines for melanogenesis, a process that neutralizes harmful oxidative effects.
  • Phenoloxidase activity is crucial for C. neoformans resistance to the epinephrine oxidative system, highlighting its role as a virulence factor in the context of brain infection.
  • The ability to detoxify catecholamines contributes to C. neoformans' capacity to thrive in the catecholamine-rich environment of the brain.