Rereading The Hungry Brain, I notice my review missed one of my favorite parts: the description of the motivational system. It starts with studies of lampreys, horrible little primitive parasitic fish:

How does the lamprey decide what to do? Within the lamprey basal ganglia lies a key structure called the striatum, which is the portion of the basal ganglia that receives most of the incoming signals from other parts of the brain. The striatum receives “bids” from other brain regions, each of which represents a specific action. A little piece of the lamprey’s brain is whispering “mate” to the striatum, while another piece is shouting “flee the predator” and so on. It would be a very bad idea for these movements to occur simultaneously – because a lamprey can’t do all of them at the same time – so to prevent simultaneous activation of many different movements, all these regions are held in check by powerful inhibitory connections from the basal ganglia. This means that the basal ganglia keep all behaviors in “off” mode by default. Only once a specific action’s bid has been selected do the basal ganglia turn off this inhibitory control, allowing the behavior to occur. You can think of the basal ganglia as a bouncer that chooses which behavior gets access to the muscles and turns away the rest. This fulfills the first key property of a selector: it must be able to pick one option and allow it access to the muscles. Many of these action bids originate from a region of the lamprey brain called the pallium…

Spoiler: the pallium is the region that evolved into the cerebral cortex in higher animals.

Each little region of the pallium is responsible for a particular behavior, such as tracking prey, suctioning onto a rock, or fleeing predators. These regions are thought to have two basic functions. The first is to execute the behavior in which it specializes, once it has received permission from the basal ganglia. For example, the “track prey” region activates downstream pathways that contract the lamprey’s muscles in a pattern that causes the animal to track its prey. The second basic function of these regions is to collect relevant information about the lamprey’s surroundings and internal state, which determines how strong a bid it will put in to the striatum. For example, if there’s a predator nearby, the “flee predator” region will put in a very strong bid to the striatum, while the “build a nest” bid will be weak… Each little region of the pallium is attempting to execute its specific behavior and competing against all other regions that are incompatible with it. The strength of each bid represents how valuable that specific behavior appears to the organism at that particular moment, and the striatum’s job is simple: select the strongest bid. This fulfills the second key property of a selector – that it must be able to choose the best option for a given situation… With all this in mind, it’s helpful to think of each individual region of the lamprey pallium as an option generator that’s responsible for a specific behavior. Each option generator is constantly competing with all other incompatible option generators for access to the muscles, and the option generator with the strongest bid at any particular moment wins the competition.

The next subsection, which I’m skipping, quotes some scientists saying that the human motivation system works similarly to the lamprey motivation system, except that the human cerebrum has many more (and much more flexible/learnable) options than the lamprey pallium. Humans have to “make up our minds about things a lamprey cannot fathom, like what to cook for dinner, how to pay off the mortgage, and whether or not to believe in God”. It starts getting interesting again when it talks about basal ganglia-related disorders:

To illustrate the crucial importance of the basal ganglia in decision-making processes, let’s consider what happens when they don’t work. As it turns out, several disorders affect the basal ganglia. The most common is Parkinson’s disease, which results from the progressive loss of cells in a part of the basal ganglia called the substantia nigra. These cells send connections to the dorsal striatum, where they produce dopamine, a chemical messenger that plays a very important role in the function of the striatum. Dopamine is a fascinating and widely misunderstood molecule that we’ll discuss further in the next chapter, but for now, its most relevant function is to increase the likelihood of engaging in any behavior. When dopamine levels in the striatum are increased – for example, by cocaine or amphetamine – mice (and humans) tend to move around a lot. High levels of dopamine essentially make the basal ganglia more sensitive to incoming bids, lowering the threshold for activating movements…Conversely, when dopamine levels are low, the basal ganglia become less sensitive to incoming bids and the threshold for activating movements is high. In this scenario, animals tend to stay put. The most extreme example of this is the dopamine-deficient mice created by Richard Palmer, a neuroscience researcher at the University of Washington. These animals sit in their cages nearly motionless all day due to a complete absence of dopamine. “If you set a dopamine deficient mouse on a table,” explains Palmiter, “it will just sit there and look at you. It’s totally apathetic.” When Palmiter’s team chemically replaces the mice’s dopamine, they eat, drink, and run around like mad until the dopamine is gone.

The same can happen to humans with basal ganglia injuries:

Consider Jim, a former miner who was admitted to a psychiatric hospital at the age of fifty-seven with a cluster of unusual symptoms. As recorded in his case report, “during the preceding three years he had become increasingly withdrawn and unspontaneous. In the month before admission he had deteriorated to the point where he was doubly incontinent, answered only yes or no questions, and would sit or stand unmoving if not prompted. He only ate with prompting, and would sometimes continue putting spoon to mouth, sometimes for as long as two minutes after his plate was empty. Similarly, he would flush the toilet repeatedly until asked to stop.” Jim was suffering from a rare disorder called abulia, which is Greek for “an absence of will”. Patients who suffer from abulia can respond to questions and perform specific tasks if prompted, but they have difficulty spontaneously initiating motivations, emotions, and thoughts. A severely abulic patient seated in a bare room by himself will remain immobile until someone enters the room. If asked what he was thinking or feeling, he’ll reply, “Nothing”… Abulia is typically associated with damage to the basal ganglia and related circuits, and it often responds well to drugs that increase dopamine signaling. One of these is bromocriptine, the drug used to treat Jim…Researchers believe that the brain damage associated with abulia causes the basal ganglia to become insensitive to incoming bids, such that even the most appropriate feelings, thoughts, and motivations aren’t able to be expressed (or even to enter consciousness). Drugs that increase dopamine signaling make the striatum more sensitive to bids, allowing some abulic patients to recover the ability to feel, think, and move spontaneously.

All of this is standard neuroscience, but presented much better than the standard neuroscience books present it, so much so that it brings some important questions into sharper relief. Like: what does this have to do with willpower?

Guyenet describes high dopamine levels in the striatum as “increasing the likelihood of engaging in any behavior”. But that’s not really fair – outside a hospital, almost nobody just sits motionless in the middle of a room and does no behaviors. The relevant distinction isn’t between engaging in behavior vs. not doing so. It’s between low-effort behaviors like watching TV, and high-effort behaviors like writing a term paper. We know that this has to be related to the same dopamine system Guyenet’s talking about, because Adderall (which increases dopamine in the relevant areas) makes it much easier to do the high-effort behaviors. So a better description might be “high dopamine levels in the striatum increase the likelihood of engaging in high-willpower-requirement behaviors”.

But what is high willpower requirements? I’m always tempted to answer this with some sort of appeal to basic calorie expenditure, but taking a walk requires less willpower than writing a term paper even though the walk probably burns way more calories. My “watch TV” option generator, my “take a walk” option generator, and my “write a term paper” option generator are all putting in bids to my striatum – and for some reason, high dopamine levels privilege the “write a term paper” option and low dopamine levels privilege the others. Why?

I don’t know, and I think it’s the most interesting next question in the study of these kinds of systems.

But here’s a crazy idea (read: the first thing I thought of after thirty seconds). In the predictive processing model, dopamine represents confidence levels. Suppose there’s a high prior on taking a walk being a reasonable plan. Maybe this is for evo psych reasons (there was lots of walking in the ancestral environment), or for reinforcement related reasons (you enjoy walking, and your brain has learned to predict it will make you happy). And there’s a low prior on writing a term paper being a reasonable plan. Again, it’s not the sort of thing that happened much in the ancestral environment, and plausibly every previous time you’ve done it, you’ve hated it.

In this case, confidence in your new evidence (as opposed to your priors) is a pretty important variable. If your cortex makes its claims with high confidence (ie in a high-dopaminergic state), then its claim that it’s a good idea to write a term paper now may be so convincing that it’s able to overcome the high prior against this being true. If your cortex makes claims with low confidence, then it will tentatively suggest that maybe we should write a term paper now – but the striatum will remain unconvinced due to the inherent implausibility of the idea.

In this case, sitting in a dark room doing nothing is just an action plan with a very high prior; you need at least a tiny bit of confidence in your planning ability to shift to anything else.

I mentioned in Toward A Predictive Theory Of Depression that I didn’t understand the motivational system well enough to be able to explain why systematic underconfidence in neural predictions would make people less motivated. I think the idea of evolutionarily-primitive and heavily-reinforced actions as a prior – which logical judgments from the cortex have to “override” in order to produce more willpower-intensive actions – fills in this gap and provides another line of evidence for the theory.