Dopamine Economics


This post proposes a model for the mechanics of D2sh in relation to flow states, and why this mechanism is useful and in what scenarios it would be naturally triggered. This topic is only one hypothesis for the functionality of these receptors, as there are possibly alternate interpretations as well.

WARNING: This post is a bit outdated and rambley, please check out newer content instead if this is your first time. I will be updating these posts in the future when I have time. Skip to the section about the D2sh for more relevant info. This is one of my first posts before I started citing everything too. 

This cacti looks so structurally interesting. It felt networked.



Let’s start with the concept of depression. Depression is complex. It could involve dopamine that’s sent to some section of a behavioral region that induces stationary behavior, such as laying in bed. Still, dopamine is a motivation chemical in this instance, despite the counter-intuitiveness, but also has other functions, or at least it appears, but we can redefine motivation, or ignore the concept and focus on dopamine, as a meaningful concept itself, and not see it as some arbitrary symbol. I think that other neurotransmitters, such as serotonin wouldn’t control motivation except via manipulating the dopamine system.

Lack of motivation does not exist in its most true form unless maybe catatonia is somehow this. Keep this in mind, as we will soon investigate my thoughts on the D2sh receptor, which inhibits dopamine release, presumably capable of halting motivation if D2sh activity in the brain is abnormally high.

People can have excessive motivation to do things that won’t build their future, especially if their future seems unpredictable to them. Motivation is driven by being able to predict. Because it is goal-oriented and the more the goal appears in reach, the more that you will be chasing it. It seems more worth the energy, in essence. The main problem is that our society presents many very easy goals, in the form of video games and junk food, they grant us satiation.

One form of depression could be the feeling that one’s future is unpredictable.

Increased dopamine via releasers or when under the effect of an agonist, would increase risk taking, which is why it may temporarily help depressed people reach for their unpredictable goals. They feel more manic and risky, which means less fear of failing unpredictable goals.

I extend this notion of motivation to dopamine’s functions within muscular control too. It’s a chain of motivation, from the brain, to the muscles, leading to action. And I think many regions are designed like dopamine filters to create a kind of cellular politics. Dopamine is the voting system of our mind, and money is the dopamine of our hive. Action is when a region’s votes win and make it to muscle movement. The first layers are very thought-based. And our thoughts are not very different from muscles being stimulated. They are just groups of cells being stimulated.

Motive is the center of all human thought and behavior. Without motive we are motionless, we are rocks. It could be argued that motive is the most important key to defining what is alive. The sensation of stimulatory dopamine is not one of pleasure, but the psychological itch, you seek to make it stop. We can tell that motivation is not pleasurable because we wish to leave the motivated state by reaching our goal. Otherwise, why not stay in a state of motivation, indefinitely, basking in its pleasure? The brain is a system of individual cells that compete for their dominance, for a need to activate a thought or an action that a cell has function over. These cells communicate their significance which is changed by environmental stimuli and various neurochemical activities.


Clearly, not every dopamine receptor is motivation-linked. D2sh would possibly a-motivational, especially towards habitual reward-seeking behavioral loops, and in essence, non-novel stimuli/rewards. This receptor could be more about becoming observant, reducing dopamine stimulation and focusing on observing the sources of dopamine to learn them. Especially in the case of novelty. One may shut off many stream of dopamine signals, and look for the largest perceptual signal causing the novelty effect. D2 long receptors, which are known to act stimulating, and not inhibit dopamine release, may cause focusing on the target of novelty once it has been discovered, or for every novel signal occurring within an environment where novelty is plentiful. Such is the state of psychedelia, and this explains why so many people anecdotally claim that psychedelics are like being a child again, and experiencing life anew.

This makes sense because D2 receptors also connect to the same receptors involved in sensation, the ones that produce anti anesthetic effects and cause psychedelia. It is an observational system. It detects novelty because normalized non-novel stimuli would give routine dopamine levels. Routine dopamine levels would be less likely to trigger rare effects, and receptors would be regulated in a way that causes repetitive binding activity. Novel stimuli might have more dopamine than is typical, resulting in higher probability that D2sh is activated.

Even without this mechanic, D2sh receptors stop dopamine flow and are inherently going to activate more likely if dopamine is higher. This means more stopping of dopamine flow.

The effects on normal linear dopamine signals would be disrupted more frequently if D2sh was more active. This means maybe the dopamine slips into neighboring neurons more likely than linear paths, that are typical. Even if it’s not literally linear, there are established common paths, perhaps what the default mode network represents, and D2 would logically derail dopamine signals to peripheral dopaminergic neuronal activity.

This would also be dose-dependent. Increasing D2sh activity would increasingly change consciousness to become less linearly-deep and more laterally-wide. The default mode network will likely dissolve as well, diffusing into what could appear as a more chaotic state.

The effect this would have on attention, would be diffusion. Diffusion of attention would mean not focusing on a singular thing. Eventually you’d become aware of many things. The purpose of this mechanic is to find things. This is so the source of novelty that causes a non-routine excessive dopamine release must be found, studied, and explained.

Consider my Out Of The Box thought experiment:

Imagine you are locked in a room by a group of mad scientists. You did not give consent, and you know nothing about what is going on.

The scientists come into the room to visit you periodically. They give you a stack of unlimited pieces of paper, and drawing utensils.

You begin to track every event and detail, hoping to find the meaning behind this situation.

Eventually, you begin to notice patterns in the events, due to order of events, and due to the time that each event occurs.

Imagine that you did this, and rationalized details about the physical appearance of each scientist. You begin to form a profile of each scientist, and begin to understand the outside world. You eventually realize the possible lifestyles each scientist lives. Some have dirtier hands. Some have muscles. Various details, combined with the data of their schedules forms a picture. You reach a point where you can reasonably assume the hobbies, family life, or other details about each scientist, all within your box prison.

This is what it means to think outside the box, and this is what it means to be psychotic. 

The oustide-of-the-box in this thought experiment represents a highly novel and unknown stimuli, in other words, a factor of the unknown, can trigger a more loose thinking, perhaps an effect that typically occurs until enough evidence forms around the stimuli, and crystallized knowledge forms. This could also be the effect of D2sh but with a different cognitive function. If stimuli is very novel, you will need to think outside the box, to a larger degree, because there are less known facts about the stimuli, and more intuitive measures must be taken. Just like I am doing in this very post! The core of this D2sh idea is that it diffuses attention, whether this diffusion is based in perception or our internal thoughts may not matter, but as the effect becomes more prominent within the realm of thoughts, we expect the thoughts to become disordered, tangential, while perception would tend to increase, promoting a state of mind that allows you form loose associations for faster derivation of meaning. Perhaps the narrative of perception can become more gestalt, and shift towards hallucinatory states.

Addiction is known to cause lower D2 receptor count. D1 receptors are associated with dynorphin, which is a model for addiction, expressed in depth in my post Waking Nightmares. D2 receptors would normally suppress D1 activity and therefore slow the effects of dynorphin as well. Psychedelics interact with D2 occasionally, but certainly interact with the 5HT2a-D2 heteromer system. They are thought to abolish addictions after a single dose.

The default mode network is another relevant aspect to this topic. The DMN is thought to be both repetitively and commonly used pathways in the brain. Psychedelics disrupt this network, and diffuse the paths in the brain. This could be due to D2sh mechanics of the 5HT2a-D2 heteromer system.

Another relevant concept is Low Latent Inhibition. LLI has been associated to creativity, psychosis, and perceptual differences.

This model even be able to explain why psychotic people would experience less illusions. I provided a model for this in my post Marijuana, Cognition, and Perception.

A case could be made, that all illusions are a form of memory, and they form for efficient processing. Using memory constructs to form perceptions of familiar and common images that we are exposed to, such as faces, the corners of rooms, and 3-dimensional data, would allow faster processing and less time spent deciphering data as if it were novel. The ‘motion aftereffect’ illusion occurs when staring at a source of consistent motion, where eventually when looking at a static image, the perception of motion continues after the stimuli has ceased (3). This would show that the illusion is developed via exposure to the stimuli, and this would make sense of cultural differences found with optical illusions (10). Being exposed to grid-roads vs being exposed to forests, reveal drastically different stimuli that each group is exposed to on a frequent basis. Illusions are in some sense, memory-based abstractions, created from familiarity and exposure to common stimuli. Illusions would allow for faster processing, reduction of details, assumption-recognition-based processing as opposed to sensory-observation-based processing and interpreting of observations.

There is correlation between illusions failing, and proneness to schizophrenia, such as the case of depth inversion illusions, or ‘hollow mask illusions’ (7). It may be that, increasing doses of NMDA antagonists, would decrease perception, and that illusions are the highest form of perception, relying on a combination of stimuli and memory, as opposed to stimuli alone. So, with increasing doses of NMDA antagonists, we could expect the highest forms of perception to vanish first, which would put pressure on visual processing, and eventually visual failure, where an excess of details are surpassing the ability to distinguish and process the details.

By increasing illusions, visual data may be increasingly abstract and simplified, resulting in faster processing of novel stimuli, or simply that there is less novel stimuli to process, as it has been turned into illusions/memories already.

The post this is quoted from, presents a glutamatergic model for the illusion axiom. It could be that both mechanisms are intertwined, and for a mechanistic utility that aides in pattern detection in novel situations. Illusions might exist to represent familiar data that is repetitious enough to be automated. In novel situations, there is less familiar data to be assumed into automations, and thus we should expect a reduction of illusions. It is known that D2 receptors reduce NMDA activity in the prefrontal cortical neurons. I couldn’t find much more about this topic yet, but if D2 inhibits NMDA receptor activity, then it might also make familiar environments appear less familiar, as the effects are increased. This might aide in boosting awareness of details of sensory data, instead of relying on habituated illusions. Another possibility is that mGlu2 receptors are involved in maintaining illusions and blocking them reduces the associated illusion, while promoting glutamate release that enhances general perception. This could explain the psychedelic effects that are linked to glutamatergic pathology.

Likely, serotonin would have the role of keeping track of the cycles of your routine via dopaminergic heteromers. But also highly likely NMDA or other glutamate signals could track dopamine activity through heteromers. So it can be habitual dopaminergic responses in the usual cases, then the novel object disrupts the expected level of dopamine, triggering the D2sh effect and diffusing attention, and also disrupting whatever you were focusing on, whatever habit or routine you have, and directing attention more chaotically. Narrow focus doesn’t help you find a source of novelty, but a wide lens very much expands the quantity of perceptual data we would be aware of. This allows for a higher degree of pattern recognition between observed stimuli and thoughts.

We have a lot of research pertaining to the behavioral correlates to these mechanics already. Such as mental disorders and behavioral effects of ligands.

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3 thoughts on “Dopamine Economics

  1. One question: if lets say someone with depression takes an ssri (escitalopram),which inhibits dopamine in mesolimbic areas to a great extend and then reduces the dose about 25%. Could this result in dopamine supersensitivity as a result of prolonged inhibition. Antipsychotics for example do this by blocking d2 receptors postsynaptically; dopamine receptors become supersensitive and so on. How could phasic vs tonic dopamine dysregulation contribute to people highly sensitive to even an extreme slowly taper. I can’t imagine that this phenomenon is induced by reduced sert inhibition.
    Another question I have regarding ADHD: As there is some evidence that phasic dopamine levels are increased in adhd individuals (creating novel seeking tendencies) and tonic levels are reduced possibly responsible for sustanined attention I was wondering what impact stimulants like amp or mph would have on these individuals (myself). Stimulants seem to shift the phasic/tonic dopaminergic acivity to a more normal state, decreasing burst and spike activity of phasic dopamine activity. In my case the problem is that the shift towards tonic enhancement is too much, resulting in boredom. I imagine that this could be due to enhanced tachyplaxia as I’m no unknown to depressive episodes, substance abuse etc. Could presynaptic d2 hypersensitivity play a factor in this due to prolonged stress and kappa oppiod receptor activation and the resulting dopaminergic prolonged inhibition ?

    ps: are you spanish ?


    1. sry if you have a hard time reading the mess I just wrote but I’m not really into correcting 😀


  2. Another question I have: my mother was a schizophrenic, a pretty bad case to be honest.
    When I abused drugs (cocaine and mdma) I suffered a great deal of panic attacks; the fear of becoming schizophrenic myself. I suffered derealization and to some extend depersonalization for about 6 month to a great extent. It slowly faded and I was left with anhedonia and all kind of atypical reactions to drugs as you can imagine. I encountered my fear and I’m now half way through it, that is emotional reactivity has returned to aprox 70% after 5 years of not touching MDMA or analogs. I continued taking cocaine abusively and alcohol ( was never a fan of alcohol in the first place) as well. I certainly have ADHD, since various shrinks diagnosed me after hearing me speaking about my symptoms. Needless to say that I still have anxiety to some extent and I take escitalopram 7 mg daily to deal with it. I felt a great deal of tiredness after quieting MDMA, what makes sense. I was never the type of individual that got paranoid from taking cocaine or other stimulants even if I abused it to extremes but after I began to take escitalopram I often had pseudohallucinations when I was sleep deprived or mixed to much vyvanse (100mg) with some benzos etc.
    Could it be that 5HT2A receptor activation due to sert inhibition from escitalopram and some form of d2 postsynaptic activation from stress and/or amp could lead to this kind of hallucinations where one is capable of telling that they are fake. My theory is that my low hedonic capacity and the from this estimated d2 postsynaptic understimulation lead me to being able of distinguishing the hallucinations. Maybe polymorphism of the 5HT2A receptor produces too much activation of this receptor and together with some d2 postsynapic activation I was able to distinguish between reality and what is not. 5HT2A overstimulation by SSRI coupled with some d2 postsynaptic activation ( but not enough to produce psychosis) could explain this or am I totally wrong ? A second Hypothesis of mine is the of d2 presynaptic hypersensitivity due to dynorfin etc. The hallucinations I saw ( things morphing into people etc.) where trying to produce an illusion of deception, I could have perfectly interpreted it as real but I did not.
    Could it also be that because my mother being schizophrenic I gained and studied psychosis to some extent and the mere awareness of mine of psychosis being by definition a state where the individual can not distinguish reality from what is real lead me into not believing it ?
    Imo the dynorphin and/ or the insufficient d2 postsynaptic receptor activation that produced the insight in me.

    Any thoughts on this ? Sry for bombarding you with all this comments but for me it is like a dream coming true to talk to somebody who is interested in this stuff and suffered from mental illness as well contrary to people who just read studies based on generic sample sizes…

    Saludos amigo 😀


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