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Related Experiment Videos

Trace amines in hepatic encephalopathy

D D Mousseau1, R F Butterworth

  • 1Neuroscience Research Unit, St-Luc Hospital, University of Montreal, Québec, Canada.

Progress in Brain Research
|January 1, 1995
PubMed
Summary
This summary is machine-generated.

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Hepatic encephalopathy (HE) may involve trace amines like octopamine, but evidence suggests increased tryptophan metabolism and its metabolite tryptamine are more critical. This impacts brain function in liver dysfunction.

Area of Science:

  • Neuroscience
  • Biochemistry
  • Gastroenterology

Background:

  • Hepatic encephalopathy (HE) is a neuropsychiatric syndrome linked to liver dysfunction.
  • Early hypotheses suggested trace amines (tyramine, octopamine) act as false neurotransmitters in HE.
  • Previous treatments with L-Dopa showed some improvement, supporting the false neurotransmitter theory.

Purpose of the Study:

  • To evaluate the hypothesis that trace amines contribute to hepatic encephalopathy (HE).
  • To explore the role of tryptophan metabolism and its metabolite, tryptamine, in HE pathogenesis.
  • To analyze the correlation between HE severity and specific neurochemical changes.

Main Methods:

  • Review of existing hypotheses and clinical trial data regarding trace amines in HE.

Related Experiment Videos

  • Analysis of animal models (hepatic devascularization, portacaval shunt) with induced coma.
  • Measurement of serum/urine octopamine levels and brain octopamine concentrations.
  • Assessment of central nervous system (CNS) tryptophan concentrations and indoleacetic acid (IAA) levels.
  • Evaluation of [3H]tryptamine receptor densities in HE patient brain tissue.

    • Main Results:

    • The trace amine hypothesis faced challenges due to lack of adverse effects from octopamine and equivocal L-Dopa trial results.
    • Increased octopamine levels were observed in rat brains and correlated with HE grade in humans.
    • Hepatic dysfunction alters CNS tryptophan, correlating with indoleacetic acid (IAA) levels.
    • Significantly decreased [3H]tryptamine receptor densities were found in HE patient brains.

    Conclusions:

    • The direct role of catecholamine-like trace amines in HE is questionable.
    • Evidence supports a pathophysiological role for increased tryptophan metabolism in HE.
    • Tryptamine, a neuroactive metabolite of tryptophan, is implicated in the development of HE.