Acetylcholine is a neurotransmitter with a wide range of applications within the central and peripheral nervous systems. This neurotransmitter acts on both muscarinic and nicotinic receptors. For the purposes of this thread, I'm going to focus on its applications within the brain, and specifically, its application on muscarinic receptors.
Many of us seek to boost our natural acetylcholine levels because acetylcholine is linked to attention, focus and memory. For example, Alzheimer’s patients have decreased levels of acetylcholine in their brains. This is why many Alzheimer’s treatments seek to increase acetylcholine levels, usually through acetylcholinesterase inhibition.
Many of us who experiment with nootropics also seek to boost our acetylcholine levels. We can do this through a variety of mechanisms, usually with acetylcholinesterase inhibitors, acetylcholine precursors, and substances that mimic acetylcholine (nicotine, acetylcarnetine). Evidence supports the theory that increasing acetylcholine levels can subsequently boost ones' learning capacity.
However, there are other implications that come with increased levels of acetylcholine. Primarily, I'm going to focus on mood-related implications. Some evidence supports the idea that depression is related to higher levels of acetylcholine!
Here are the links to the 2 sources I'm referencing: I apologize, I would find more sources for this info if I had more time. Interesting information nonetheless.
1) http://www.acnp.org/...1000095/CH.html
2) http://www.psychosom.../3/248.full.pdf
In regards to behavioral inhibition (source 1)
Significantly, increasing central cholinergic tone with such centrally active cholinomimetic agents as physostigmine, arecoline, and oxotremorine usually induces or enhances the behavioral analogs of depression in such models of depression. Thus, centrally acting cholinomimetic drugs consistently produce behavioral inhibitory effects including lethargy and hypoactivity, activation of the HPA axis, decreases in self-stimulation (43, 54, 55), increases in behavioral despair in the forced swim test, and decreases in saccharin preference (88).
It appears that cholinesterase inhibitors can decrease manic symptoms in manic-depressive humans, which supports the theory that increasing acetylcholine can decrease positive mood. (source 1)
However, there appears to be a link only between centrally acting cholinesterase inhibitors on reducing episodes of mania. Non-centrally acting cholinesterase did not exert the same effect.Several studies have shown that centrally active cholinergic agonists and cholinesterase inhibitors possess ant-manic properties. In a seminal study by Rowntree et al. (100), the centrally active cholinesterase inhibitor DFP was given to manic–depressive patients and normals. The normal subjects and remitted manic–depressives developed irritability, lassitude, depression, apathy, and slowness and/or poverty of thoughts.
In regards to depression: (source 1)
In addition to observations of depression-induction caused by DFP (100) and cholinomimetic insecticides (34), Janowsky et al. found induction and/or intensification of depressive symptoms in actively ill bipolar manic patients given physostigmine, as well as a worsening of depression in groups of unipolar depressed and schizoaffective depressed patients (45).
Also: (source 1)
Depressed moods have also been observed in subjects receiving acetylcholine precursors, including deanol, choline, and lecithin. Davis et al. (18) and Tamminga et al. (117) found that depressive symptoms occurred in some schizophrenic patients who were treated with choline, a phenomenon that was atropine-reversible. In a subgroup of cases, it was noted that depressed mood was a side effect of choline and lecithin treatments employed to try to reverse the memory deficits of Alzheimer's Disease (117). Also, Casey (9) observed that a depressed mood and, in some cases, a paradoxical hypomania occurred in some deanol-treated tardive dyskinesia and other movement-disorder patients. Thus, precursors of acetylcholine may induce a depressed mood, a finding that is consistent with the adrenergic-cholinergic imbalance hypothesis.
Source 2
The results indicate that virtually all
patients receiving physostigmine exhibit
symptoms consistent with a state of psychomotor
retardation. In addition, most
patients with an affective component to
their symptoms exhibit increased depressed
mood following physostigmine
administration.
The second document I read describes a link between a number of cholinesterase inhibitors and depressed mood. DFP (an insecticide) is cited in both documents, as well as physostigmine, among several others. I doubt if any of us will be taking these, but the point is that all of these compounds increase levels of acetylcholine. It has also been reported that acetylcholine precursors can induce depressed mood. In addition to this, compounds that decrease acetylcholine are associated with increased mood (buproprion, diproxymine). I’m not suggesting this is proof, or that this is a scientifically substantial post I’ve made here, but its interesting information to consider (especially if you're an avid self-medicator like myself!). I’m by no means saying that acetylcholine causes depression, but it could play a role.
Also, see the “Evidence that Acetylcholine May Cause Depression” chart on page 255 of source 2.
That being said, we all need acetylcholine, and being happy aint’ everything! But being smart isn’t either.
Edited by Orajel, 09 March 2012 - 11:47 PM.
