Astral Codex Ten

dopamine

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dopamine

Article

dopamine is a recurring concept in the Astral Codex Ten archive, appearing 6 times across 6 issues between March 26, 2021 and August 13, 2024. The archive places it in contexts such as “Guyenet describes various brain regions making “bids” to the basal ganglia, using dopamine as the “currency""; “the popular conception of dopamine isn’t that far off. It does seem to play some kind of role in drive/reinforcement/craving”; “dopamine is computing RPE on a moment-by-moment basis”. It most often appears alongside nucleus accumbens, VTA, Andres.

Metadata

  • Category: Concepts
  • Mention count: 6
  • Issue count: 6
  • First seen: March 26, 2021
  • Last seen: August 13, 2024

Appears In

Source Context

Recovered passages from the original issue text. When the raw archive preserved outbound links inside the source passage, they are listed directly under the quote.

Toward A Bayesian Theory Of Willpower
March 26, 2021 · Original source
I've previously quoted Stephan Guyenet on the motivational system of lampreys (a simple fish used as a model organism). Guyenet describes various brain regions making "bids" to the basal ganglia, using dopamine as the "currency" - whichever brain region makes the highest bid gets to determine the lamprey's next action. "If there's a predator nearby", he writes "the flee-predator region will put in a very strong bid to the striatum".
Inline links: motivational system of lampreys
This ties the decision-making process into the rest of the brain. At the deepest level, the brain isn't really an auction or an economy. But it is an inference engine, a machine for weighing evidence and coming to conclusions. Your perceptual systems are like this - they weigh different kinds of evidence to determine what you're seeing or hearing. Your cognitive systems are like this, they weigh different kinds of evidence to discover what beliefs are true or false. Dopamine affects all these systems in predictable ways. My theory of willpower asserts that it affects decision-making in the same way - it's representing the amount of evidence for a hypothesis.
In fact, we can look at some of the effects of dopaminergic drugs to flesh this picture out further.
Unpredictable Reward, Predictable Happiness
September 13, 2022 · Original source
Seen on the subreddit: You Seek Serotonin, But Dopamine Can’t Deliver. Commenters correctly ripped apart its neuroscience; for one thing, there’s no evidence people actually “seek serotonin”, or that serotonin is involved in good mood at all. Sure, it seems to have some antidepressant effects, but these are weak and probably far downstream; even though SSRIs increase serotonin within hours, they take weeks to improve mood. Maxing out serotonin levels mostly seems to cause a blunted state where patients can’t feel anything at all.
Inline links: You Seek Serotonin, But Dopamine Can’t Deliver
In contrast, the popular conception of dopamine isn’t that far off. It does seem to play some kind of role in drive/reinforcement/craving, although it also does many, many other things. And something like the article’s point - going after dopamine is easy but ultimately unsatisfying - is something I’ve been thinking about a lot.
(is this just the Sinclair Method? Then how come drinking on the Sinclair Method is usually neutral rather than aversive, given that the drinker must be getting less reward than predicted? Is it because we’re blocking opioids rather than dopamine? Why are we doing that?)
Inline links: Sinclair Method
Highlights From The Comments On Unpredictable Reward
September 30, 2022 · Original source
I think really digging into the neural nitty gritty may prove illuminative here. Dopamine release in nucleus accumbens (which is what drives reward learning and thus the updating of our predictions) is influenced by at least three independent factors:
1. A "state prediction error" or general surprise signal from PFC (either directly or via pedunculopontine nucleus and related structures). This provokes phasic bursting of dopamine neurons in the Ventral Tegmental Area.
2. The amount and pattern of GABAergic inhibition of VTA dopamine neurons from NAc, ventral pallidum, and local GABA interneurons. At rest, only a small % of VTA DA neurons will be firing at a given time, and the aforementioned surprise signal alone can't do much to increase this. What CAN change this is the hedonic value of the surprising stimulus. An unexpected reward causes not just a surprise signal, but a release of endorphins from "hedonic hotspots" in NAc and VP, and these endorphins inhibit the inhibitory GABA neurons, thereby releasing the "brake" on VTA DA neurons and allowing more of them to phasically fire.
Highlights From The Comments On Jhanas
October 31, 2022 · Original source
> H5: Jhanas should show increased activation compared to the rest state in the dopamine reward system of the brain (NAc in the ventral striatum and medial OFC). A broad range of external rewards stimulate this system (food, sex, beautiful music, and monetary awards), so extreme joy in jhana may be triggered by the same system (the VTA is also part of this system, but is too small to image with standard fMRI methods, but see [35] for successful imaging methods).
Now, what does the released dopamine do? In PFC (via the mesocortical pathway), it draws attentional resources to the surprising stimulus and its plausible causes, gating out the processing of other, less relevant stimuli. Simultaneously, in NAc, it strengthens connections between PFC inputs and the endorphin-releasing cells, thereby wiring together the hedonic features of the reward and the sensory features of any cues predictive of it. This imbues the cue with the ability to release the GABAergic brake on VTA DA neurons all by itself. Phenomenologically, it results in us "liking" the cue as much (or nearly as much) as we like the reward (this is what allows, e.g., animal trainers to reinforce behavior with only the sound of a clicker that has previously been paired with food).
So, speculatively, if Jhana is somehow short-circuiting NAc to trigger without specific signals from PFC, are we weakening the existing connections from PFC that previously triggered NAc? Something like normalizing the weights over a bunch of input signals, but with the new input signal being "non-causal / Jhanic stimulation"? Thus reducing the weight of other causal hedonic pleasures (like casual sex in this example)? So these signals from PFC would not elicit as much dopamine response through NAc activation as they did pre-Jhana.
The Psychopharmacology Of The FTX Crash
November 16, 2022 · Original source
Emsam is a brand of selegiline, a medication used since the 1960s to treat Parkinson’s disease. Selegiline is a MAOB inhibitor2. MAOB is an enzyme that breaks down dopamine3. If you inhibit it, you get more dopamine. So in a very broad sense, selegiline gives you more dopamine.4
Inline links: selegiline, 2, 3, 4
Dopamine does many things in many brain systems. Here’s an oversimplified chart:
Everyone wants “magic bullets” - drugs that can increase dopamine in one of these ways, but not any of the others. Treat attention problems without causing hallucinations. Cure tremors without causing hypersexuality. But it’s tough. There are dozens of dopamine-based drugs, and all of them succeed in some ways and fail in others. Adderall mostly helps attention but sometimes causes a little paranoia on the side. Antipsychotics mostly prevent hallucinations and delusions, but also cause anhedonia. If a good doctor carefully chooses the right drug and dose, you’ll mostly get what you want. Otherwise, choose 2d4 random side effects from the appropriate side of the table.
Why Does Ozempic Cure All Diseases?
August 13, 2024 · Original source
The nucleus tractus solitarii uses neurotransmitter-GLP-1 to inhibit the ventral tegmental area, which then releases less dopamine into the nucleus accumbens. Dopamine levels in the nucleus accumbens act as a multiplier for reward (that is, a given reward feels more rewarding when there’s high dopamine in those areas).
Why? Isn’t addiction just the extreme version of normal wanting? Apparently not. None of these anti-addictive drugs affect wholesome rewards like the feeling of a job well done or a child’s smile. Just drug addictions, and a few compulsive behaviors like porn and gambling. Maybe the job well-done and the child’s smile get implemented partly through some system other than dopamine (oxytocin?), or maybe these medications lop off some extreme part of the reward distribution that only addictive drugs ever reach in real life. But why? Why did God give your brain a special lever that only porn and cocaine can pull?