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olafurp@lemmy.world ⁨3⁩ ⁨days⁩ ago

• peopleproblems@lemmy.world ⁨2⁩ ⁨days⁩ ago

  Most of the neurotransmitters can’t. That’s like one of the things the blood brain barrier does - keeps the chemicals IN the brain as well.

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  • olafurp@lemmy.world ⁨2⁩ ⁨days⁩ ago

    Fun exception is endocannabinoids, giving you a runners high when running.

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• fizzle@quokk.au ⁨2⁩ ⁨days⁩ ago

  Im not a neuroscientist nor endocrinologist but i dont think it’s as simple as, your gut producing serotonin which travels to your brain and makes you happy.

  I just googled this and found a pretty direct rebuttal:

  The gut-brain axis is a bidirectional communication network that links the enteric and central nervous systems. This network is not only anatomical, but it extends to include endocrine, humoral, metabolic, and immune routes of communication as well. The autonomic nervous system, hypothalamic-pituitary-adrenal (HPA) axis, and nerves within the gastrointestinal tract, all link the gut and the brain, allowing the brain to influence intestinal activities, including activity of functional immune effector cells; and the gut to influence mood, cognition, and mental health.

  pmc.ncbi.nlm.nih.gov/articles/PMC6469458/

  As i said, I dont really know anything about this. However, there seems to be a large body of research supporting this hypothesis.

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  • olafurp@lemmy.world ⁨2⁩ ⁨days⁩ ago

    That’s true, the gut and the brain are tightly linked and are in constant communication with each other, an obvious example is hunger for example.

    I felt the need to comment this because serotonin and dopamine produced in the gut have completely different functions from the dopamine and serotonin in the brain. On top of that the body keeps those completely separate with the blood brain barrier so it can regulate those different functions individually.

    The gut does play a part in tryptophan production and extraction which passes the blood brain barrier and the brain uses to make serotonin so the gut does affect serotonin levels. But that’s just “eat healthy, feel good” type of stuff.

    I’m just not a fan of oversimplified version of this where people say “90-95% of serotonin is made in the gut, serotonin is the feel good hormone so gut affects happiness”. I mean, most people are aware that what you eat affects your mood but saying the gut is responsible for producing the hormones for the brain is just wrong when talking about dopamine and serotonin.

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    • fizzle@quokk.au ⁨2⁩ ⁨days⁩ ago

      That’s a fair clarification and I’ll happily admit I was in the “most of your serotonin is made in your gut” camp.

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  • macaw_dean_settle@lemmy.world ⁨2⁩ ⁨days⁩ ago

    You should use a better search like Bing or duckduckgo. googol sucks and was never any good.

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    • fizzle@quokk.au ⁨2⁩ ⁨days⁩ ago

      Actually I use a self hosted instance of searxng which pulls results from a bunch of different engines.

      You should… avoid starting sentences with “you should” because it’s irritating. Universally.

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      • prole@lemmy.blahaj.zone ⁨2⁩ ⁨days⁩ ago

        You’re not wrong, but your original commend did say that you googled it

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• scarabic@lemmy.world ⁨2⁩ ⁨days⁩ ago

  Is serotonin only effective within the brain?

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  • olafurp@lemmy.world ⁨2⁩ ⁨days⁩ ago

    It works both inside and outside, it just does something completely different when not in the brain.

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    • scarabic@lemmy.world ⁨2⁩ ⁨days⁩ ago

      Oh - what does it do outside the brain?

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      • olafurp@lemmy.world ⁨2⁩ ⁨days⁩ ago

        I feel like Wikipedia will be way better than explaining. I’ll put it here inside a spoiler tag. I don’t know a lot about this besides the basics so I won’t be able to do it justice. en.wikipedia.org/wiki/Serotonin

        Biological role > Outside the nervous system.

        Digestive tract (emetic) edit Serotonin regulates gastrointestinal (GI) function. The gut is surrounded by enterochromaffin cells, which release serotonin in response to food in the lumen. This makes the gut contract around the food. Platelets in the veins draining the gut collect excess serotonin. There are often serotonin abnormalities in gastrointestinal disorders such as constipation and irritable bowel syndrome.[75] If irritants are present in the food, the enterochromaffin cells release more serotonin to make the gut move faster, i.e., to cause diarrhea, so the gut is emptied of the noxious substance. If serotonin is released in the blood faster than the platelets can absorb it, the level of free serotonin in the blood is increased. This activates 5-HT3 receptors in the chemoreceptor trigger zone that stimulate vomiting.[76] Thus, drugs and toxins stimulate serotonin release from enterochromaffin cells in the gut wall which can induce emesis. The enterochromaffin cells not only react to bad food but are also very sensitive to irradiation and cancer chemotherapy. Drugs that block 5HT3 are very effective in controlling the nausea and vomiting produced by cancer treatment, and are considered the gold standard for this purpose.[77] Lungs edit The lung,[78] including that of reptiles,[79] contains specialized epithelial cells that occur as solitary cells or as clusters called neuroepithelial bodies or bronchial Kulchitsky cells or alternatively K cells.[80] These are enterochromaffin cells that like those in the gut release serotonin.[80] Their function is probably vasoconstriction during hypoxia.[78] Skin edit Serotonin is also produced by Merkel cells which are part of the somatosensory system.[81] Bone metabolism edit In mice and humans, alterations in serotonin levels and signalling have been shown to regulate bone mass.[82][83][84][85] Mice that lack brain serotonin have osteopenia, while mice that lack gut serotonin have high bone density. In humans, increased blood serotonin levels have been shown to be a significant negative predictor of low bone density. Serotonin can also be synthesized, albeit at very low levels, in the bone cells. It mediates its actions on bone cells using three different receptors. Through 5-HT1B receptors, it negatively regulates bone mass, while it does so positively through 5-HT2B receptors and 5-HT2C receptors. There is very delicate balance between physiological role of gut serotonin and its pathology. Increase in the extracellular content of serotonin results in a complex relay of signals in the osteoblasts culminating in FoxO1/ Creb and ATF4 dependent transcriptional events.[86] Following the 2008 findings that gut serotonin regulates bone mass, the mechanistic investigations into what regulates serotonin synthesis from the gut in the regulation of bone mass have started. Piezo1 has been shown to sense RNA in the gut and relay this information through serotonin synthesis to the bone by acting as a sensor of single-stranded RNA (ssRNA) governing 5-HT production. Intestinal epithelium-specific deletion of mouse Piezo1 profoundly disturbed gut peristalsis, impeded experimental colitis, and suppressed serum 5-HT levels. Because of systemic 5-HT deficiency, conditional knockout of Piezo1 increased bone formation. Notably, fecal ssRNA was identified as a natural Piezo1 ligand, and ssRNA-stimulated 5-HT synthesis from the gut was evoked in a MyD88/TRIF-independent manner. Colonic infusion of RNase A suppressed gut motility and increased bone mass. These findings suggest gut ssRNA as a master determinant of systemic 5-HT levels, indicating the ssRNA-Piezo1 axis as a potential prophylactic target for treatment of bone and gut disorders. Studies in 2008, 2010 and 2019 have opened the potential for serotonin research to treat bone mass disorders.[87][88] Organ development edit Since serotonin signals resource availability it is not surprising that it affects organ development. Many human and animal studies have shown that nutrition in early life can influence, in adulthood, such things as body fatness, blood lipids, blood pressure, atherosclerosis, behavior, learning, and longevity.[89][90][91] Rodent experiment shows that neonatal exposure to SSRIs makes persistent changes in the serotonergic transmission of the brain resulting in behavioral changes,[92][93] which are reversed by treatment with antidepressants.[94] By treating normal and knockout mice lacking the serotonin transporter with fluoxetine scientists showed that normal emotional reactions in adulthood, like a short latency to escape foot shocks and inclination to explore new environments were dependent on active serotonin transporters during the neonatal period.[95][96] Human serotonin can also act as a growth factor directly. Liver damage increases cellular expression of 5-HT2A and 5-HT2B receptors, mediating liver compensatory regrowth (see Liver § Regeneration and transplantation)[97] Serotonin present in the blood then stimulates cellular growth to repair liver damage.[98] 5-HT2B receptors also activate osteocytes, which build up bone[99] However, serotonin also inhibits osteoblasts, through 5-HT1B receptors.[100] Cardiovascular growth factor edit Main article: Cardiac fibrosis Serotonin, in addition, evokes endothelial nitric oxide synthase activation and stimulates, through a 5-HT1B receptor-mediated mechanism, the phosphorylation of p44/p42 mitogen-activated protein kinase activation in bovine aortic endothelial cell cultures.[clarification needed][101] In blood, serotonin is collected from plasma by platelets, which store it. It is thus active wherever platelets bind in damaged tissue, as a vasoconstrictor to stop bleeding, and also as a fibrocyte mitotic (growth factor), to aid healing.[102] Adipose tissue edit Serotonin also regulates white and brown adipose tissue function, and adipocytes are capable of producing 5-HT separately from the gut. Serotonin increases lipogenesis through HTR2A in white adipose tissue, and suppressed thermogenesis in brown adipose tissue via Htr3.[103]

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