Author
Alan A. Boulton
Other affiliations: Saskatchewan Health
Bio: Alan A. Boulton is an academic researcher from University of Saskatchewan. The author has contributed to research in topics: Monoamine oxidase & Dopamine. The author has an hindex of 39, co-authored 183 publications receiving 5253 citations. Previous affiliations of Alan A. Boulton include Saskatchewan Health.
Papers published on a yearly basis
Papers
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TL;DR: The neurochemical, neuropharmacological, and neurophysiological findings that lead to propose that PE is a neuromodulator of catecholamine neurotransmission in the CNS are reviewed.
Abstract: Since the identification of 2-phenylethylamine (β-phenylethylamine; PE) as a biogenic amine, there has been much discussion about what role, if any, it may have in the CNS. Indeed, the low endogenous concentration of PE in the brain and its relatively low potency in behavioral and pharmacological experiments have led some researchers to conclude that perhaps PE possessed no physiological role at all but that it was merely a metabolic by-product. Our findings have caused us to conclude otherwise, and in this article we review the neurochemical, neuropharmacological, and neurophysiological findings that lead us to propose that PE is a neuromodulator of catecholamine neurotransmission in the CNS.
253 citations
TL;DR: The concentrations of β-phenylethylamine in some tissues of male Wistar rats were (ng/g) and the use of an isotopically labelled internal standard improves the precision and sensitivity of the analysis.
Abstract: A procedure for the quantitative evaluation of some amines present in mammalian tissues has been developed. It includes isolation of the amines by ion exchange chromatography followed by conversion to dansyl derivatives, chromatographic separation, and quantitation by the mass spectrometric integrated ion current technique. The use of an isotopically labelled internal standard improves the precision and sensitivity of the analysis.The concentrations of β-phenylethylamine in some tissues of male Wistar rats were (ng/g); brain 1.8 ± 0.4, heart 5.7 ± 3.1, kidney 20.5 ± 2.2, liver 2.0 ± 0.7, lung 4.0 ± 1.4, and spleen 4.7 ± 2.7. In the brain the hypothalamus contained 25.3 ± 5.0, the cerebellum 3.4 ± 0.5, the stem 2.2 ± 0.9, the caudate nucleus 8.0 ± 0.3, and the 'rest' 1.1 ± 0.2 ng/g, respectively.
190 citations
TL;DR: A procedure for the quantitative evaluation of m-tyramine in mammalian tissues is described, which involves isolation of the amine by ion-exchange chromatography, followed by conversion to the dansyl derivative, chromatographic separation, and quantitation by the mass spectrometric integrated ion current technique using an isotopically labelled internal standard.
Abstract: A procedure for the quantitative evaluation of p-tyramine in mammalian tissues is described It involves isolation of the amine by ion-exchange chromatography, followed by conversion to the dansyl
155 citations
TL;DR: The concentrations of tryptamine in some tissues of male Wistar rats were higher than expected, and in the brain, the hypothalamus contained 0.32 ± 0.05 ng/g (mean ± mean deviation).
Abstract: A procedure for the quantitative measurement of tryptamine in mammalian tissues is described. The amine is isolated by ion-exchange chromatography, converted to its dansyl derivative, further purif...
128 citations
TL;DR: The irreversible inhibition of MAO by cigarette smoke may well be related to the low platelet MAO associated with cigarette smokers as previously reported and the implication of such cigarette smoke-caused reduction ofMAO activity in relation to Parkinsonism is discussed.
118 citations
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TL;DR: This work evaluates claims and some counter-claims made about the physiological importance of these enzymes and the potential of their inhibitors in the light of what the authors know, and still have to learn, of the structure, function and genetics of the monoamine oxidases and the disparate actions of their inhibitor.
Abstract: Monoamine oxidase inhibitors were among the first antidepressants to be discovered and have long been used as such. It now seems that many of these agents might have therapeutic value in several common neurodegenerative conditions, independently of their inhibition of monoamine oxidase activity. However, many claims and some counter-claims have been made about the physiological importance of these enzymes and the potential of their inhibitors. We evaluate these arguments in the light of what we know, and still have to learn, of the structure, function and genetics of the monoamine oxidases and the disparate actions of their inhibitors.
1,173 citations
TL;DR: MAO A and B knock-out mice are valuable models for investigating the role of monoamines in psychoses and neurodegenerative and stress-related disorders and show increased reactivity to stress.
Abstract: Cloning of MAO (monoamine oxidase) A and B has demonstrated unequivocally that these enzymes are made up of different polypeptides, and our understanding of MAO structure, regulation, and function has been significantly advanced by studies using their cDNA. MAO A and B genes are located on the X-chromosome (Xp11.23) and comprise 15 exons with identical intron-exon organization, which suggests that they are derived from the same ancestral gene. MAO A and B knock-out mice exhibit distinct differences in neurotransmitter metabolism and behavior. MAO A knock-out mice have elevated brain levels of serotonin, norephinephrine, and dopamine and manifest aggressive behavior similar to human males with a deletion of MAO A. In contrast, MAO B knock-out mice do not exhibit aggression and only levels of phenylethylamine are increased. Mice lacking MAO B are resistant to the Parkinsongenic neurotoxin, 1-methyl-4-phenyl-1,2,3,6-tetra-hydropyridine. Both MAO A and B knock-out mice show increased reactivity to stress. These knock-out mice are valuable models for investigating the role of monoamines in psychoses and neurodegenerative and stress-related disorders.
1,119 citations
TL;DR: A signalling pathway in which nitric oxide generation that follows apoptotic stimulation elicits S-nitrosylation of GAPDH, which triggers binding to Siah1 (an E3 ubiquitin ligase), nuclear translocation and apoptosis, which is prevented by NO deletion is reported.
Abstract: S -nitrosylated GAPDH initiates apoptotic cell death by nuclear translocation following Siah1 binding
1,015 citations
TL;DR: Data support the feasibility of extrasynaptic or volume transmission in the extracellular space by measuring the volume fraction and tortuosity, a measure of hindrance of cellular obstructions.
880 citations
TL;DR: It is shown here that resveratrol is a substrate-specific activator of yeast Sir2 and human SirT1 and that in three different yeast strain backgrounds, resver atrol has no detectable effect on Sir2 activity in vivo, as measured by rDNA recombination, transcriptional silencing near telomeres, and life span.
747 citations