Pharmacological studies with endogenous enhancer substances: β-phenylethylamine, tryptamine, and their synthetic derivatives
Abstract
The discovery of enhancer regulation in the mesencephalon and the concept that it plays a key role in the operation of innate and acquired drives [Neurochem. Res. 28 (2003) 1187] sets the trace amines (TAs) in their true physiological perspective. The regulation is defined as the existence of enhancer-sensitive neurons in the brain capable of working in a split-second on a high activity level due to endogenous enhancer substances. For the time being, only beta-phenylethylamine (PEA) and tryptamine are the experimentally analyzed examples. (-)-Deprenyl (selegiline), widely used in Parkinson's disease and Alzheimer's disease today, and known as the first selective monoamine oxidase (MAO) type-B inhibitor for decades, was identified as a PEA-derived synthetic mesencephalic enhancer substance. An important and convincing confirmation of the enhancer concept was the recent development of a highly specific and potent tryptamine-derived synthetic mesencephalic enhancer substance, (-)-1-(benzofuran-2-yl)-2-propylaminopentane [(-)-BPAP]. This substance, which is specific and hundreds of times more potent than selegiline, is now the best experimental tool to study the enhancer regulation in the mesencephalon and a promising candidate to significantly surpass the therapeutic efficiency of selegiline in depression, Parkinson's disease, and Alzheimer's disease.
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Beta-phenylethylamine derived from phenylalanine or tryptamine originated from tryptophan can exert beneficial actions such as mood control and appetite/satiety balance regulation when administered to humans.
“beta-phenylethylamine derived from phenylalanine or tryptamine originated from tryptophan can exert beneficial actions (such as mood control and appetite/satiety balance regulation) when administered to humans (Shimazu and Miklya, 2004).”
From Bioactive Molecules Released in Food by Lactic Acid Bacteria: Encrypted Peptides and Biogenic Amines (2016) · cites this paper as Shimazu and Miklya, 2004
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- Authors
- Shimazu, S., & Miklya, I.
- Affiliations
- Fujimoto Pharmaceutical Corporation (Japan) (JP)
- Semmelweis University (HU)
- Corresponding author
- Shimazu, Seiichiro
- Venue
- Progress in Neuro-Psychopharmacology and Biological Psychiatry
- Publisher
- Elsevier BV
- Published
- 2004-05
- Volume
- 28
- Issue
- 3
- Pages
- 421-427
- ISSN
- 0278-5846 (ISSN-L)
- OpenAlex
- W2070245731
- Cited by
- 57
- References
- 60
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 7 · 2023: 1 · 2022: 4 · 2021: 4 · 2019: 4 · 2018: 4 · 2017: 1 · 2016: 3 · 2015: 1 · 2014: 4 · 2013: 1 · 2012: 2
- FWCI
- 0.20
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Progress in Neuro-Psychopharmacology and Biological Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Keywords
- trace amines, enhancer regulation, phenylethylamine, tryptamine, selegiline, bilevel positive airway pressure, midbrain, monoamine oxidase B inhibition, depression, Parkinson's disease, Alzheimer's disease
- MeSH terms
- Animals, Antidepressive Agents, Benzofurans, Humans, Mesencephalon, Nervous System Diseases, Phenethylamines, Psychotropic Drugs, Selegiline, Tryptamines, Neuroprotective Agents
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