I noticed that peeing is rewarding? What the hell?! How did enough of my (human) non-ancestors die because peeing wasn't rewarding enough? The answer is they weren't homo sapiens or hominids at all.
I would split it into two questions:
I do think there’s a generic answer to (2) in terms of learning algorithms etc., but no need to get into the details here.
As for (1), you’re wasting energy by carrying around extra weight of urine. Maybe there are other factors too. (Eventually of course you risk incontinence or injury or even death.) Yes I think it’s totally possible that our hominin ancestors had extra counterfactual children by wasting 0.1% less energy or whatever. Energy is important, and every little bit helps.
There are about ~100-200 different neurotransmitters our brains use. I was surprised to find out that I could not find a single neurotransmitter that is not shared between humans and mice (let me know if you can find one, though).
Like you said, truly new neurotransmitters are rare. For example, oxytocin and vasopressin split off from a common ancestor in a gene duplication event 500Mya, and the ancestral form has homologues in octopuses and insects etc. OTOH, even if mice and humans have homologous neurotransmitters, they presumably differ by at least a few mutations; they’re not exactly the same. (Separately, their functional effects are sometimes quite different! For example, eating induces oxytocin release in rodents but vasopressin release in humans.)
Anyway, looking into recent evolutionary changes to neurotransmitters (and especially neuropeptides) is an interesting idea (thanks!). I found this paper comparing endocrine systems of humans and chimps. It claims (among other things) that GNRH2 and UCN2 are protein-coding genes in humans but inactive (“pseudogenes”) in chimps. If true, what does that imply? Beats me. It does not seem to have any straightforward interpretation that I can see. Oh well.
Another factor for the evolutionary benefit of peeing promptly is it decreases the risk of Urinary Tract Infections. It also lets you drink more water.
I wonder if the carrots were implemented as a means of encouraging doing more of the thing than the organism would do otherwise. If there were no carrot aspect to hunger, the organism would only eat just enough to stop the pain of hunger but no more, missing the opportunity to build up fat stores for the future. If there were no carrot aspect to peeing, the organism would expel just enough to make the pain go away but wouldn't empty the tank, so to speak, making them carry around some tiny amount of extra weight than otherwise. This might be a just-so story, but it's the answer that comes to mind for me.
o The machinery for repair by homologous recombination is just insane
o Think about it before clicking the link: How would you make sure DNA doesn't get as tangled as cabled earphones?
The links for both of these go to the same place, a video on homologous recombination. Was the second link supposed to be to somewhere else?
Thanks for spotting! Fixed!
help of course, but I was thinking of
Topoisomerase, which untangles DNA. My understanding is if you pull separate strands, Topoisomerase finds the local the crossing points that are under pressure and unties them by cutting and gluing. After being cut and before being glued, the DNA stays attached to the Topoisomerase, so the double strand doesn't just fall apart.
I presume it would be an overview of histone molecule. DNA is often kept compacted by wrapping around one, like a rope coiled around a baseball.
When reasoning about why humans feel loneliness, don't only think about the human ancestral environment. Mice feel lonely too!
The mechanisms that mammals and birds use for emotions around loneliness probably evolved, 325-500 million years ago. However, there are plenty of mammals and birds that evolve to be solitary and are thus unlikely to feel loneliness.
If you look farther back in evolutionary history, it tells you about how the basic mechanisms work but different species turned those mechanisms quite differently.
If something is stable against mutations over the last million years it either needs to be deeply interlinked with other mechanisms or it needs to be produce a survival advantage that prevents mutations from deleting it.
I was surprised to find out that I could not find a single neurotransmitter that is not shared between humans and mice (let me know if you can find one, though). An example of interfaces as a scarce resource?
It's easier to have mutations that mean that a neurotransmitter is produced in a new context or that a receptor to a neutrotransmitter does something new than having both a newly produced neurotransmitter and new receptors at the same time.
Mice (and rodents in general) don't have β‑MSH.
Maybe this is just part of a larger machinery where your nervous system hands out a reward when you satisfy a strong urge (homeostatic feedback control circuit) back to homeostasis?
I would think that's part of the explanation. It's also worth noting that peeing is a bodily process that comes with the need to relax parts of the body that otherwise usually aren't relaxed. Relaxation can feel rewarding even if the rewarding feeling is not the purpose.
I think the reason peeing/pooping is rewarding is that they can also be painful. If pooping is more painful than not-pooping, an animal might delay pooping for an unhealthy amount of time. They are also activities that take time and require attention, so pooping/peeing when no more-rewarding activity is available is probably a good idea in general.
>I was surprised to find out that I could not find a single neurotransmitter that is not shared between humans and mice (let me know if you can find one, though).
As far as I can tell, this is true. The closest I could find is a single subtype of receptor that a frameshift mutation in a primate ancestor made nonfunctional.
https://www.sciencedirect.com/science/article/pii/S0021925818352189
I suspect you'd have to go even further back in terms of divergent ancestry to find actual differences in the neurotransmitter substances themselves. There are definitely differences in receptors and affinities, but the actual chemicals? From a quick search, you'd have to go all the way to ctenophores, which are so different that some have posited they evolved nervous systems independently.
Here are some things I learned over the last year that past me would have found somewhat non-obvious or that were surprising to me at the time: