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- 1 Pupil constriction/miosis
- 2 SSRI (Antidepressant) Withdrawl Syndrome
- 3 Synthesis
- 4 Heart rate
- 5 Benefits and detriments
- 6 Britannica rephrase/reference?
- 7 Make it easier
- 8 Neuromod effects
- 9 Poison
- 10 Memory
- 11 Nitrogen
- 12 Yu and Dayan paper links
- 13 Digestive muscles opposite adrenalin
- 14 Would Chantix (Varenicline) fit in?
- 15 THC an anticholinesterase?
- 16 Categories
- 17 Dose dependant inhibition vs stimulation
- 18 Assessment comment
- 19 Should "chlorine" read "choline"?
- 20 Choline bitartrate?
- 21 hornet venom
Acetylcholine is also used as a medication for intraocular injection under the trade name Miochol or Miochol-E. It's used during glaucoma or cataract surgery, I believe, to induce miosis (constriction of the pupils). Could someone add this to the page? —Preceding unsigned comment added by 220.127.116.11 (talk) 03:52, 10 December 2008 (UTC)
SSRI (Antidepressant) Withdrawl Syndrome
I have found a number of articles that discuss the side effects of withdrawl from antidepressants, such as Paxil. These articles refer to a disruption in the body's production of aetylcholine as a key instigator of the withdrawl symptoms. I am hoping that someone with the appropriate medical qualifications could include a discussion of such withdrawl symptoms and their relationship with aetylcholine in the article. (ie: http://bipolar.about.com/cs/antidep/a/0207_ssridisc1.htm)
The article states that acetylcholine is an ester of acetic acid and choline. I am not a chemist so I am unclear how the ruling is on this issue, but in order to state that acetylcholine is an ester of acetic acid and choline, does this presuppose that acetylcholine is synthesized from acetic acid and choline? Because, after reviewing the literature, the origin of the acetyl moiety is most likey from glucose or pyruviate. Niubrad (talk) 12:56, 23 June 2008 (UTC)
May someone please tell me how does the acetylcholine decrease the heart rate? It is obvious that is slows the heart down, but how? What caused that slowing down of the hear rate? -Unknown
- It does so via activation of muscarinic receptors (ACh is the main muscarinic receptor agonist), and by doing that is considered a big part of Parasympathetic nervous system Svizac 07:49, 1 June 2007 (UTC)
Muscarinic receptors mainly have an IPSP (inhibitory post-synaptic potential) meaning they slow down/inhibit the action of what they are on. Acetylcholine can bind to these or to nicotinic receptors (which can create an EPSP - excitatory potential) which has the reverse effect. - E.H. —Preceding unsigned comment added by 18.104.22.168 (talk) 04:12, 2 October 2007 (UTC)
Benefits and detriments
Acetylcholine -- beneficial or detrimental? I've read both that acetylcholine is beneficial for preventing conditions such as Alzheimer's, but also that acetylcholine may promote tumor growth. Is the choice between cancer and dementia? --Thoric 22:06, 3 Jun 2005 (UTC)
- It seems that an important part of neuromodulators like ACh is that they can be present at a range of levels.. having different amounts of a neuromodulator changes the way neuronal circuits perform by, e.g., enhancing or suppressing plasticity, altering adaptation of firing, activating or inactivating various metabolic processes and ion channels, etc.. thus you shouldn't only think about the level of a neuromodulator, but also about the available range: keeping the levels constant for a long period of time will tend to disrupt the system.. in alzheimer's, for instance, cholinergic cells die off and thus the brain is stuck in a low-ACh mode, which causes problems like memory impairment.. on the other hand, if ACh levels were kept artificially high, I would guess there might be problems with things like memory recall (or perhaps, as you say, tumor growth, though I'm not familiar with that particular effect) Digfarenough 22:54, 16 December 2005 (UTC)
It says that Acetylcholine binds to the Ach Receptors in muscle cells and causes release of Sodium ions causing the muscle to contract, but that's not what my anatomy textbook says about it (and it was released just last year!), it says that it causes release of Calcium ions. Should I change this or delete that statement or what? Miroku Sanna 22:14, 12 November 2005 (UTC)
- "ACh affects a number of body systems including the cardiovascular system by acting as a vasodilator, by decreasing cardiac rate, and by decreasing cardiac contraction; the gastrointestinal system by such activities as increasing peristalsis in the stomach and by increasing the amplitude of digestive contractions; and the urinary tract by such actions as decreasing the capacity of the bladder and increasing the voluntary voiding pressure. It also affects the respiratory system and stimulates secretion by all glands that receive parasympathetic nerve impulses."
Make it easier
Is it possible to add a chapter that explains what acetylcholine is and does in easier words? Thanks, --Abdull 20:34, 20 April 2006 (UTC)
- Acetylcholine has not only an influence of your body, so it "navigate" the vagus and with it the digestion. Also it influence the blood pressure and the heartbeat and so on.
But this is not all. A. is also a very important neurotransmitter in the brain. In the quantity it is after glutamatic and gaba one of the higest concentrated neurotransmitter. It is necessary for memory and concentration. You need it for learning. Acetylcholine influences positive mood and drive. With deanol or centrophenoxin/meclophenoxat, you can enhance this. -Fackel 21:55, 30 May 2006 (UTC)
- Well you need glutamate, gaba, dopamine and serotonin for learning as well, and for attention, and for awareness, and for wellbeing. You should definitely NOT enhance Ach levels pharmacologically unless you are diagnosed with a specific deficit, otherwise you will (further) disrupt the balance in these systems. A common way of enhancing the awareness through Ach is by drinking coffee btw; cafeine inhibits adenosine in some way, which lifts Ach inhibition in the forebrain. However, this kind of awareness is very different from the awareness you get from a good night of sleep, a stress-free and positive disposition, professional motivation, a good social environment, physical exercise and what not ;) — Preceding unsigned comment added by 22.214.171.124 (talk) 08:43, 27 October 2011 (UTC)
I've added a section on neuromodulatory effects of ACh. The information came from the Hasselmo (1995) paper I added to the reference (including a link to a pdf online, I hope that's an acceptable thing to do). —The preceding unsigned comment was added by Digfarenough (talk • contribs).
- Same thing with a Yu/Dayan paper. —The preceding unsigned comment was added by 126.96.36.199 (talk • contribs).
The sentence in the introduction,
- Acetylcholine is an example of a totally untraceable poison
- Unlikely. That post appears to have been made on Sept 4 2006, which is much more recent than the claim in the article. Indeed, that post appears to quote other parts of this article as well. digfarenough (talk) 22:33, 7 September 2006 (UTC)
- Sorry, didn't see that. raptor 01:47, 10 September 2006 (UTC)
The article makes no mention of the relationship between ACh and memory. I don't know specifically what the relationship is, but only that it supposedly plays "a vital role in learning and memory" (p. 52, Psychology, 6th Edition, David G. Myers).
- Well, it's hinted at in the neuromodulatory effects section, but it's true that there's no section specifically on memory effects from a behavioral perspective. It seems to be the modulatory effects on plasticity (and perhaps on, e.g., changing the relative strength of inputs to hippocampal region CA1 from CA3 versus entorhinal cortex) that are most relevant. If subjects are given scopolamine (an ACh antagonist) before being given a list of words to remember, they will later be impaired in trying to recall the list. If, however, the subjects are given the scopolamine after reading the list but before trying to recall, they will be unimpaired. The most obvious suggestion then is that scopolamine prevents synaptic plasticity from occuring that allows the list of words to be encoded, but doesn't prevent subsequent retrieval from those synapses. If someone wants to prettify up that explanation and add it to the article, they should feel free. A good reference for that study is Rusted and Warburton (1989), PMID 2693994. The study was simulated based on the above interpretation of plasticity modulation in Hasselmo and Wyble (1997), PMID 9475612. digfarenough (talk) 18:13, 9 November 2006 (UTC)
I note that the Nitrogen end of the molecule has 3 methyl groups instead of 2 (and an electron pair, like most organo-nitrogen compounds do). How is this possible?—Preceding unsigned comment added by 188.8.131.52 (talk • contribs)
- Nope, there is no electron pair. The nitrogen has four substituents, the electron pair is shared with a substituent, rendering the nitrogen cationic. Hope this helps. --Dirk Beetstra T C 22:17, 30 November 2006 (UTC)
The link "Yu, AJ & Dayan, P (2005). Uncertainty, neuromodulation, and attention. Neuron 46 681-692. " points to a different paper. The quoted paper is in PubMed, not free online.184.108.40.206 02:13, 28 December 2006 (UTC)
- Thanks for pointing that out: I'm fixing the link now to the free copy on Peter Dayan's webpage. Also, I've moved this comment to the bottom of this talk page: it is preferred that new items be added to the bottm and given titles for easier reference. digfarenough (talk) 03:09, 28 December 2006 (UTC)
"by decreasing the conductange of voltage-dependent M currents and Ca2+-dependent K+ currents." Conductange or conductance? What is M currents? There is no category in wikipedia with this name.Jlpdca 02:24, 30 December 2006 (UTC)
- Oops, conductance is what that should have been: it's fixed now. The M current is a depolarization-activated non-inactivating potassium current (as best I know). So as a neuron is depolarized toward firing threshold, the M current becomes active and asserts a hyperpolarizing influence, temporarily reducing the excitability of the neuron (thus also causing adaptation). Activation of muscarinic receptors suppresses the M current, so it reduces adaptation and increases excitability. digfarenough (talk) 20:10, 30 December 2006 (UTC)
The Yu and Dayan citation appears in Decision Making. This whole section is vague and unreferenced (except for the broken Yu and Dayan). I would like to replace this with a section on Memory, which is under reported, if no-one objects.Mountain9 (talk) 19:54, 22 December 2016 (UTC)
Digestive muscles opposite adrenalin
I was reading about this chemical and this article doesn't reflect what I read, could it be added or is it wrong?  It seems that Acetylcholine plays a role in contracting the muscles of the digestive system, whereas adrenalin relaxes them. It's pretty strange how it is also used to contract the skeletal muscles, but not the cardiac muscles. If anything you'd think the smooth muscle tissue of the heart would be more similar to one of them. As adrenaline is used in fight or flight to stop digestion (recuperation) and turn into a catabolic state, I'm guessing adrenalin does not similarly relax the skeletal muscles, and that Ach must have some sort of local effect so that when either digestion or skeletal muscle exertion occur the other does not simultaneously also do so. Tyciol 17:04, 23 March 2007 (UTC)
Would Chantix (Varenicline) fit in?
The smoking cessation aid
THC an anticholinesterase?
Is THC really an anticholinesterase. I couldn't find evidence to support this, and the claim is not referenced. It is under Alzheimer's on this page. perhaps someone could remove or reference it. —Preceding unsigned comment added by Aleph Mercure (talk • contribs) 11:13, 8 January 2008 (UTC)
- It's already included there, in some bizarre way. If you look at the category you will see it. I'm not well educated on the logic of categories so I won't express an opinion about whether that's the right way to do it. Looie496 (talk) 02:27, 5 August 2012 (UTC)
I think the emphasis on acetylcholine in the CNS as being a neuromodulator is unbalanced. It is both a neurotransmitter and a neuromodulator but the emphasis is strange. I'm not sure how best to fix this. Mountain9 (talk) 20:48, 21 December 2016 (UTC)
Dose dependant inhibition vs stimulation
The text indicates that various substances can either stimulate or inhibit ACh receptors in a dose dependant fashion, however it neither offers a citation, nor indicates the does. With substances such as Acetl-L-Carnitine where people may self medicate, this information is vital. — Preceding unsigned comment added by Leopardtail (talk • contribs) 15:20, 16 May 2014 (UTC)
The comment(s) below were originally left at several discussions in past years, these subpages are now deprecated. The comments may be irrelevant or outdated; if so, please feel free to remove this section., and are posted here for posterity. Following
|I came to this page to look for effects of Acetylcholine related to "flight or fight" responses. I found the page to be pretty jargony and didn't find the answer I was looking for.220.127.116.11 (talk) 22:14, 30 July 2009 (UTC)|
Last edited at 22:14, 30 July 2009 (UTC). Substituted at 06:36, 29 April 2016 (UTC)
Should "chlorine" read "choline"?
Central nervous system
In the central nervous system, ACh has a variety of effects as a neuromodulator upon plasticity, arousal and reward. ACh has an important role in the enhancement of alertness when we wake up, in sustaining attentionand in learning and memory. Damage to the chlorine(acetylcholine-producing) system in the brain has been shown to be associated with the Jonhorridge (talk) 20:21, 21 December 2016 (UTC)
I was just reading in the Wikipedia article on hornets that certain species' venom is spiked with acetylcholine which greatly enhances the potency of their venom. Perhaps this could be worked into this article somewhere. Ealtram (talk) 17:59, 29 March 2017 (UTC)