Do It Like You Dopamine It

By Neuroskeptic | May 15, 2010 9:40 pm

Neuroskeptic readers will know that I’m a big fan of theories. Rather than just poking around (or scanning) the brain under different conditions and seeing what happens, it’s always better to have a testable hypothesis.

I just found a 2007 paper by Israeli computational neuroscientists Niv et al that puts forward a very interesting theory about dopamine. Dopamine is a neurotransmitter, and dopamine cells are known to fire in phasic bursts - short volleys of spikes over millisecond timescales – in response to something which is either pleasurable in itself, or something that you’ve learned is associated with pleasure. Dopamine is therefore thought to be involved in learning what to do in order to get pleasurable rewards.

But baseline, tonic dopamine levels vary over longer periods as well. The function of this tonic dopamine firing, and its relationship, if any, to phasic dopamine signalling, is less clear. Niv et al’s idea is that the tonic dopamine level represents the brain’s estimate of the average availability of rewards in the environment, and that it therefore controls how “vigorously” we should do stuff.

A high reward availability means that, in general, there’s lots of stuff going on, lots of potential gains to be made. So if you’re not out there getting some reward, you’re missing out. In economic terms, the opportunity cost of not acting, or acting slowly, is high – so you need to hurry up. On the other hand, if there’s only minor rewards available, you might as well take things nice and slow, to conserve your energy. Niv et al present a simple mathematical model in which a hypothetical rat must decide how often to press a lever in order to get food, and show that it accounts for the data from animal learning experiments.

The distinction between phasic dopamine (a specific reward) vs. tonic dopamine (overall reward availability) is a bit like the distinction between fear vs. anxiety. Fear is what you feel when something scary, i.e. harmful, is right there in front of you. Anxiety is the sense that something harmful could be round the next corner.

This theory accounts for the fact that if you give someone a drug that increases dopamine levels, such as amphetamine, they become hyperactive – they do more stuff, faster, or at least try to. That’s why they call it speed. This happens to animals too. Yet this hyperactivity starts almost immediately, which means that it can’t be a product of learning.

It also rings true in human terms. The feeling that everything’s incredibly important, and that everyday tasks are really exciting, is one of the main effects of amphetamine. Every speed addict will have a story about the time they stayed up all night cleaning every inch of their house or organizing their wardrobe. This can easily develop into the compulsive, pointless repetition of the same task over and over. People with bipolar disorder often report the same kind of thing during (hypo)mania.

What controls tonic dopamine levels? A really brilliantly elegant answer would be: phasic dopamine. Maybe every time phasic dopamine levels spike in response to a reward (or something which you’ve learned to associate with a reward), some of the dopamine gets left over. If there’s lots of phasic dopamine firing, which suggests that the availability of rewards is high, the tonic dopamine levels rise.

Unfortunately, it’s probably not that simple, as signals from different parts of the brain seem to alter tonic and phasic dopamine firing largely independently, and this would mean that tonic dopamine would only increase after a good few rewards, not pre-emptively, which seems unlikely. The truth is, we don’t know what sets the dopamine tone, and we don’t really know what it does; but Niv et al’s account is the most convincing I’ve come across…

ResearchBlogging.orgNiv Y, Daw ND, Joel D, & Dayan P (2007). Tonic dopamine: opportunity costs and the control of response vigor. Psychopharmacology, 191 (3), 507-20 PMID: 17031711

CATEGORIZED UNDER: animals, drugs, mental health, papers
  • http://www.blogger.com/profile/06286666448883809089 Pietr Hitzig

    What a great review! Thank you so very much.

    Serotonin (5-HT), almost ubiquitously, is the antipodal regulator to dopamine (DA). In other words, they are reciprocal modulators. Dopamine promotes incentive salience (motivation), 5-HT decreases it.

    DA: THIS IS VERY IMPORTANT. GET OFF YOUR ASS!
    5-HT
    : Who the f**k cares. Chill, baby.

    DA and 5-HT precursors or agonists, used together, appear to block addictive craving although definitive studies are clearly needed.

    I would highly recommend this Richard Rothman 2008 review. Richard, a senior NIDA researcher, has been working on dual deficit replacement for nearly 20 years.

  • Anonymous

    @Pietr Hitzig

    Your “PURSOR Protocol” sound plausible but there a few weird things:
    Why is it that the precursors have to be mixed with oil and sweeteners and tasted instead of just being in pills?
    Isn't there some “psychological” effect?
    Also, how did you came up with this idea?

  • http://www.blogger.com/profile/06286666448883809089 Pietr Hitzig

    1. Absorption thru the buccal mucosa permits immediat epassage of each preursor thru the blood brain barriet. When you swallow, first pass is hepatic and they are there metabolized.
    2. With flavoring I serendipitously found that one can titrate by taste. Both monoamine precursor starts off pleasant to taste and then IMO when a sufficiency is met, they both taste sour.

    Weintraub effectively used fenfluramine and phentermine for weight control. The former is a 5-HT agonist and the latter promotes DA. I thought using these amphetamine analogs might be effective in the RX of addiction and so they were. It was easy to try the precursors. I noted that when I did so some reported that their tastes varied.

    Levodopa readily oxidizes in H20.

    phitz96atgmaildotcom

  • http://neuromancy.wordpress.com/ neuromancy

    As far as I understand it, Regrave and Gurney have (although they're not explicitly linked theoretically, and the details of the phasic dopamine theory have changed slightly since the advancement of the theory of tonic dopamine) suggested that phasic dopamine release in the basal ganglia is the basis of connecting cause with effect, and the beginnings of learning behaviour and its outcomes. A burst of dopamine in response to a stimulus 'stamps' a running copy of an organism's actions and environment, and biases repetition of the actions which preceded the stimulus, with some variation. Tonic dopamine in the basal ganglia controls the 'choice' of a particular action over other potential actions.

    Parkinson's could be seen as the inability to select an action to do, whilst the positive symptoms of schizophrenia might be the result of the breakdown of the ability to determine cause and effect, and the selection of incongruous behaviours in response to environmental stimuli.

    Ref for phasic DA function: Nature Reviews Neuroscience 7, 967-975 (December 2006) | doi:10.1038/nrn2022
    The short-latency dopamine signal: a role in discovering novel actions?
    http://www.nature.com/nrn/journal/v7/n12/full/nrn2022.html

    Can't find the paper I want for tonic dopamine function.

    Any thoughts?

  • SN Kim

    Thanks for your great review! I'v studied about dopamine and its basal ganglia circuit theory. how do you think about receptor activation and its relation with behavioral states and dopamine firing? I found 2010 computational neuroscience research paper in journal of neurosciences which is about dopamine firing (tonic and phasic) and receptor activation.

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No brain. No gain.

About Neuroskeptic

Neuroskeptic is a British neuroscientist who takes a skeptical look at his own field, and beyond. His blog offers a look at the latest developments in neuroscience, psychiatry and psychology through a critical lens.

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