General Information of MET (ID: META00797)
Name Acetylcholine
Synonyms   Click to Show/Hide Synonyms of This Metabolite
2-(Acetyloxy)-N,N,N-trimethylethanaminium; ACh; Acetilcolina cusi; Acetyl choline ion; Acetylcholine; Acetylcholine L tartrate; Acetylcholine L-tartrate; Acetylcholine bromide; Acetylcholine cation; Acetylcholine chloride; Acetylcholine fluoride; Acetylcholine hydroxide; Acetylcholine iodide; Acetylcholine perchlorate; Acetylcholine picrate; Acetylcholine picrate (1:1); Acetylcholine sulfate (1:1); Acetylcholinium: acetyl-choline; Alcon brand OF acetylcholine chloride; Azetylcholin; Bournonville brand OF acetylcholine chloride; Bromide, acetylcholine; Bromoacetylcholine; Chloroacetylcholine; Choline acetate; Choline acetate (ester); Choline acetic acid; Ciba vision brand OF acetylcholine chloride; Cusi, acetilcolina; Fluoride, acetylcholine; Hydroxide, acetylcholine; Iodide, acetylcholine; Iolab brand OF acetylcholine chloride; L-Tartrate, acetylcholine; Miochol; O-Acetylcholine; Perchlorate, acetylcholine
Source Endogenous;Food;Drug;Cosmetic
Structure Type   Quaternary ammonium salts  (Click to Show/Hide the Complete Structure Type Hierarchy)
Organic nitrogen compounds
Organonitrogen compounds
Quaternary ammonium salts
PubChem CID
187
HMDB ID
HMDB0000895
Formula
C7H16NO2
Structure
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3D MOL 2D MOL
  Click to Show/Hide the Molecular/Functional Data (External Links/Property/Function) of This Metabolite
KEGG ID
C01996
DrugBank ID
DB03128
ChEBI ID
15355
FooDB ID
FDB012191
ChemSpider ID
182
METLIN ID
57
Physicochemical Properties Molecular Weight 146.21 Topological Polar Surface Area 26.3
XlogP 0.2 Complexity 115
Heavy Atom Count 10 Rotatable Bond Count 4
Hydrogen Bond Donor Count N.A. Hydrogen Bond Acceptor Count 2
Function
Acetylcholine (ACh) is a neurotransmitter. Acetylcholine in vertebrates is the major transmitter at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system. Its physiological and pharmacological effects, metabolism, release, and receptors have been well documented in several species. ACh has been considered an important excitatory neurotransmitter in the carotid body (CB). Various nicotinic and muscarinic ACh receptors are present in both afferent nerve endings and glomus cells. Therefore, ACh can depolarize or hyperpolarize the cell membrane depending on the available receptor type in the vicinity. Binding of ACh to its receptor can create a wide variety of cellular responses including opening cation channels (nicotinic ACh receptor activation), releasing Ca2+ from intracellular storage sites (via muscarinic ACh receptors), and modulating activities of K+ and Ca2+ channels. Interactions between ACh and other neurotransmitters (dopamine, adenosine, nitric oxide) have been known, and they may induce complicated responses. Cholinergic biology in the CB differs among species and even within the same species due to different genetic composition. Development and environment influence cholinergic biology. Pharmacological data clearly indicate that both muscarinic and nicotinic acetylcholine receptors have a role in the encoding of new memories. Localized lesions and antagonist infusions demonstrate the anatomical locus of these cholinergic effects, and computational modeling links the function of cholinergic modulation to specific cellular effects within these regions. Acetylcholine has been shown to increase the strength of afferent input relative to feedback, to contribute to theta rhythm oscillations, activate intrinsic mechanisms for persistent spiking, and increase the modification of synapses. These effects might enhance different types of encoding in different cortical structures. In particular, the effects in entorhinal and perirhinal cortex and hippocampus might be important for encoding new episodic memories. The role of ACh in attention has been repeatedly demonstrated in several tasks. Acetylcholine is linked to response accuracy in voluntary and reflexive attention and also to response speed in reflexive attention. It is well known that those with Attention-deficit/hyperactivity disorders tend to be inaccurate and slow to respond. Acetylcholine has been found to be a microbial product, urinary acetylcholine is produced by Lactobacillus.
Regulatory Network
Full List of Protein(s) Regulating This Metabolite
      Pore-forming PNC peptide (PNC)
            Cellular tumor antigen p53 (TP53) Click to Show/Hide the Full List of Regulating Pair(s):   1 Pair(s)
               Detailed Information Protein   Info click to show the details of this protein
               Regulating Pair Experim Info click to show the details of experiment for validating this pair [1]
                      Introduced Variation Knockout of TP53
                      Induced Change Acetylcholine concentration: decrease (Log2 FC=0.8)
                      Summary Introduced Variation         Induced Change 
                      Disease Status Colon cancer [ICD-11: 2B90]
                      Details It is reported that knockout of TP53 leads to the decrease of acetylcholine levels compared with control group.
References
1 Integrative omics analysis of p53-dependent regulation of metabolism. FEBS Lett. 2018 Feb;592(3):380-393.

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