Open main menu
Home
Random
Recent changes
Special pages
Community portal
Preferences
About Wikipedia
Disclaimers
Incubator escapee wiki
Search
User menu
Talk
Dark mode
Contributions
Create account
Log in
Editing
Tryptamine
(section)
Warning:
You are not logged in. Your IP address will be publicly visible if you make any edits. If you
log in
or
create an account
, your edits will be attributed to your username, along with other benefits.
Anti-spam check. Do
not
fill this in!
==== Gastrointestinal motility ==== Tryptamine produced by mutualistic bacteria in the human gut activates serotonin GPCRs ubiquitously expressed along the colonic epithelium.<ref name=":103"/> Upon tryptamine binding, the activated 5-HT<sub>4</sub> receptor undergoes a conformational change which allows its [[Gs alpha subunit|G<sub>s</sub> alpha subunit]] to exchange [[Guanosine diphosphate|GDP]] for [[Guanosine triphosphate|GTP]], and its liberation from the 5-HT<sub>4</sub> receptor and Ξ²Ξ³ subunit.<ref name=":103" /> GTP-bound G<sub>s</sub> activates [[adenylyl cyclase]], which catalyzes the conversion of [[Adenosine triphosphate|ATP]] into [[cyclic adenosine monophosphate]] (cAMP).<ref name=":103" /> cAMP opens chloride and potassium ion channels to drive colonic electrolyte secretion and promote intestinal motility.<ref name=":152"/><ref>{{Cite web|date=2018-06-15|title=Microbiome-Lax May Relieve Constipation|url=https://www.genengnews.com/topics/omics/microbiome-lax-may-relieve-constipation/|access-date=2020-12-11|website=GEN - Genetic Engineering and Biotechnology News|language=en-US}}</ref> [[File:Tryptamine_mechanism_of_action_in_the_human_gut.png|thumb|none|550px|Tryptamine promotes intestinal motility by activating serotonin receptors in the gut to increase colonic secretions.]]
Edit summary
(Briefly describe your changes)
By publishing changes, you agree to the
Terms of Use
, and you irrevocably agree to release your contribution under the
CC BY-SA 4.0 License
and the
GFDL
. You agree that a hyperlink or URL is sufficient attribution under the Creative Commons license.
Cancel
Editing help
(opens in new window)