Talk:Catecholamine

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This article was the subject of a Wiki Education Foundation-supported course assignment, between 3 September 2019 and 12 December 2019. Further details are available on the course page. Student editor(s): Hogyuchoi93. Peer reviewers: E razo0821.

Above undated message substituted from Template:Dashboard.wikiedu.org assignment by PrimeBOT (talk) 16:57, 16 January 2022 (UTC)

INN vs BAN

I think it makes sense to use the INN (i.e. epinephrine) over the BAN (i.e. adrenaline). AFAIK, this is convention at WP-- see paracetamol (acetaminophen) and pethidine (meperidine). Nephron  T|C 06:01, 14 December 2006 (UTC)

The above suggestion is a valid point. I would like to say that I remember writing on this article when it was a stub and am guilty of using the BAN over the INN. This is a result of my being taught in the UK and raises another point. Of the younger users within the UK, very few will be able to identify Epinephrine as opposed to Adrenaline due to level of eductaion. In this case, I would suggest the use of "Epinephrine", but a note at the beginning stating that they are exactly the same. (Mubinchoudhury 22:06, 22 December 2006 (UTC))

I'm a first year university student and most UK-written physiology books now make a point of adrenaline and epinephrine being two ways of saying the same thing. I'd imagine most UK students can deduce this now a days. --Iscariot 23:26, 11 February 2007 (UTC)

Yes, INN is the standard here on wikipedia. I just had to revert some edits that changed the names back to BAN (i.e. "epinephrine" was changed to "adrenalin", "norepinephrine" was changed to "noradrenalin"). Fuzzform 01:53, 4 May 2007 (UTC)

Structure of NE (norepinephrine)

I was checking out the page and i see that NE has an OH at the bottom position, shouldn't it be at the upper left (3') position? I'm not 100% sure on the nomenclature but i think it goes counter clockwise (because of the doublebond)

If my nomenclature is right and since you can't change the conformation of a benzene ring and since all catecholamines should have hydroxyl groups at the 3' and 4' positions then that image should be updated

Thanks!

Prz36 05:18, 29 March 2007 (UTC) : )

EDIT: well i guess technically it doesnt matter (they both are right), but i do think epinephrine and norepinephrine should match in the way the structures look. thanks again Prz36 05:24, 29 March 2007 (UTC)

Serotonin

Any reason as why this isnt mentioned? --90.184.165.134 (talk) 16:16, 7 March 2008 (UTC) That would be me --David Munch (talk) 16:16, 7 March 2008 (UTC)

Yes... Seratonin isnt a catecholamine. It is uptaken via NAT transporters with epinepherine and is broken down using MAO, but it is not a catecholeamine. If memory serves me right, 5-HT is derived from tryptophan- an essential amino acid, but is not derived from tyrosine directly (so cannot be a catecholamine). It is however a Monoamine. --User:Mubinchoudhury —Preceding comment was added at 10:44, 27 April 2008 (UTC)

MAOI action of amphetamines

While I am aware that Selegeline, which has an amphetamine backbone, is an MAO-B inhibitor, I'm pretty sure that unsubstituted amphetamine is only a very weak MAOI, a weak synapse flow reverser and primarily is a DAT inhibitor (like Ritalin and cocaine). Moreover, meth's MAOI action is non-existent, its DAT binding is lower, and it mainly acts to reverse flow at the synapse (which is why it's potentially neurodegenerative - dopamine free radical build up inside the vesicle).

Could somebody clarify this in the "Degradation" section?

Furthermore, I'm unaware of any action on adrenaline for MAOIs and amphetamines. I guess it's possible, since adrenaline is built from norepinephrine, but I've just never seen it mentioned in literature. I'm interested in this, because, having ADHD, I wonder if it's just my norepinephrine and dopamine levels that they (stimulants and ADHD) change, or is it adrenaline, too? People with ADHD DO show blood-sugar abnormalities, so there's some weight to the idea, and as I said, adrenaline is built from noradrenaline, so it'd make sense that a roadblock at noradrenaline also limits supply of adrenaline. Most likely scenario is that adrenaline is ignored because it's not psychoactive.

Cheers. 210.215.140.180 (talk) 11:15, 29 August 2008 (UTC)

Lower catecholamines?

Anyone know of anything that can lower catecholamines? —Preceding unsigned comment added by Interestedperson (talk • contribs) 06:20, 13 October 2008 (UTC)

Is this correct?

"For example, MDMA (Ecstasy) is a reduced product of a double condensation of dopamine with formaldehyde, in which the two dihydroxyphenyl groups are bridged by a methyl." Dopamine does not have a N-methyl however, shouldn't it be MDA instead? —Preceding unsigned comment added by 75.3.244.124 (talk) 05:57, 15 July 2010 (UTC)

"Derived" in second paragraph

The second paragraph states "Catecholamines derive from the amino acid tyrosine" and the word "derive" is tagged as . Would "metabolized" be a better word? I'm not entirely familiar with the jargon so I'm not sure if that word is accurate. --76.92.71.27 (talk) 17:21, 27 June 2012 (UTC)

---

I think derive is not at all ambiguous. Catecholamines are synthetised (not metabolized) from tyrosine, so they derive from it, just like steroid hormones derive from cholesterol. I removed the ambiguous tag, it is clear as it is, especially with the gigantic picture of catecholamine synthesis below. Gould80 (talk) 07:36, 15 November 2012 (UTC)

Why does Methyltyrosine redirect here?

This word is not mentioned in the page. This is often a problem with Wikipedia redirects. 86.174.188.81 (talk) 22:23, 26 January 2013 (UTC)

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Receptors

I do not have time to address it now, but discussion of receptors is notably absent (despite this page redirecting from catecholamine receptor). 173.91.8.59 (talk) 16:06, 20 December 2023 (UTC)

Relevant content

Tauopathy

A recent meta-analytic study found that a dysfunction in the locus coeruleus (LC)-catecholamine system may play a critical role in the pathogenesis of Alzheimer’s disease (AD). During a physiological state of stress, the locus coeruleus stimulates the release of a catecholamine known as norepinephrine (NE). As locus coeruleus neurons produce norepinephrine, norepinephrine's toxic metabolite DOPEGAL (3,4-dihydroxyphenylglycolaldehyde) may cause neurotoxicity at higher levels. Consequentially, DOPEGAL stimulates asparagine endopeptidase (AEP). Asparagine endopeptidase cleaves residue N368 into aggregation-prone forms which propagate tau pathology, thus leading to braak staging. Since the locus coeruleus is one of the earliest brain regions to accumulate hyperphosphorylated tau, abnormal tau spreads to connected regions like the entorhinal cortex, hippocampus, and frontal cortex. Daniel 020125 (talk) 23:44, 9 August 2025 (UTC)

This concept remains speculative for how it may have a role in Alzheimer's pathology. The sources you used in Special:Diff/1303738406 are premature, conjectural, and WP:PRIMARY (the NeuroImage report is primary research - just 47 subjects).

This is a better review discussing neuroinflammation and a possible effect of locus coeruleus and norepinephrine degeneration, but the evidence presented remains clearly based on preliminary lab studies, i.e., too premature for the encyclopedia, with no WP:MEDRS review covering this idea. Zefr (talk) 00:43, 10 August 2025 (UTC)

However, the content is not only based on one study... Cause and effect --> Noradrenaline has to be metabolized right? If DOPEGAL is the chemical noradrenaline metabolizes into, how can that fact be speculative? If the LC activates faster because of past trauma [development of disorder 101], does the level of neurotransmitter release change? These are questions that have already been answered before. Here is my point: FACT --> DOPEGAL stimulates asparagine endopeptidase (AEP). What does AEP do? FACT --> It cleaves residue N368. How do you define this issue: speculation or observation and discovery? Daniel 020125 (talk) 00:55, 10 August 2025 (UTC)

hey I added it back but i tried to make the changes based on the your feedback A recent meta-analytic study found that a dysfunction in the locus coeruleus (LC)-catecholamine system may play a critical role in the pathogenesis of Alzheimer’s disease (AD). During a physiological state of stress, the locus coeruleus stimulates the release of a catecholamine known as norepinephrine (NE). As locus coeruleus neurons produce norepinephrine, norepinephrine's toxic metabolite DOPEGAL (3,4-dihydroxyphenylglycolaldehyde) may cause neurotoxicity at higher levels. Laboratory studies indicate that DOPEGAL can activate asparagine endopeptidase (AEP). Asparagine endopeptidase cleaves residue N368 into aggregation-prone forms which propagate tau pathology, thus leading to braak staging. Since the locus coeruleus is one of the earliest brain regions to accumulate hyperphosphorylated tau, abnormal tau spreads to connected regions like the entorhinal cortex, hippocampus, and frontal cortex. While several biochemical steps have been demonstrated in experimental models, their integrated role in human AD still remain under investigation. Daniel 020125 (talk) 01:10, 10 August 2025 (UTC)

Wikipedia is not a research report or graduate student thesis discussing conjecture from the lab, but rather should be based on established facts that reflect mainstream scientific agreement. Please do not speculate from in vitro or animal research, WP:MEDANIMAL.

See WP:MEDASSESS, bottom of left pyramid (where your sources are), whereas the article should be using sources of high evidence quality at the top of the pyramid. Zefr (talk) 03:00, 10 August 2025 (UTC)

As a new editor, please understand WP:MEDRS and use high-quality review sources. Studies in rats, in vitro, or preliminary human studies are insufficient for making firm conclusions about brain mechanisms in the encyclopedia. Zefr (talk) 02:48, 10 August 2025 (UTC)

References