I know you’ve heard of it.

“Dopamine.”

It’s supposedly a chemical in the brain that causes pleasure, right?

I mean, everyone says so. Even Harvard says so, and surely we can trust Harvard, right?

No, sadly, this most perpetuated of common wisdom is perhaps the most common medical myth of our time. If you thought dopamine had anything to do with feelings of pleasure, it’s time to set the record straight.

To do that, we need to start at the beginning of the story; the story of how dopamine became so misunderstood.

Check out Part II of our myths series:

In a sterile room of a McGill University laboratory in 1954, a surgical mistake birthed a fascinating discovery.

James Olds and Peter Milner were attempting to study the neural mechanisms of learning in rats, using a microelectrode embedded into the midbrain reticular formation.

When it came time to test “rat number 34”, the electrode slipped, misaligning by a fraction of a millimetre, and embedding itself into the septal area.

Like the others, this rat was placed into their operant conditioning box and given a lever which, when pressed, delivered a fraction of a volt through the electrode into the brain. Unlike all the others, however, this particular animal became utterly transfixed by this device. It pressed the lever again, and again, and again. Soon, it was pressing it thousands of times an hour.

The rat ignored food, it ignored water, and it ignored females in heat.

It would actively stimulate its own brain until it collapsed from exhaustion, and starved to death.

Olds and Milner concluded they had stumbled upon the mammalian brain’s “pleasure centres.” The pathways radiating from these regions were rich in a specific neurotransmitter: Dopamine.

Thus began one of the most persistent biological myths, one that has survived for over 70 years despite rigorous scientific falsification, embedding itself in the popular consciousness, and even today being repeated in academic research as an axiom that “everyone knows” without any citation or reference.

Look again at that article from Harvard; do you see any citations?

This idea - that dopamine was “the brain’s pleasure chemical” - was further crystallised in 1978, when researcher Roy Wise formulated the “Anhedonia Hypothesis” after observing that administering the dopamine receptor antagonist (blocker) pimozide to rats caused them to stop working for food.

To the naked eye, the rats behaved exactly as if the food had been removed entirely.

Wise argued that blocking dopamine systematically eroded the “hedonic impact” of the reward itself. In this paradigm, dopamine was pleasure incarnate; chemically turning off dopamine meant chemically disabling the capacity for enjoyment.

It was a neat, beautifully simple and consumable theory that resonated deeply in the minds of scientists and laypeople alike, and helped to invent many of the most ridiculous pop-psychology fads we see today.

That anhedonia hypothesis held for a decade, until neuroscientists Kent C. Berridge and Terry Robinson fundamentally broke everything about the model in 1989.

Berridge reasoned that if dopamine was the quintessential chemical of pleasure, a rat stripped of all dopamine should exhibit a total absence of hedonic response. The question was: how do we really test “hedonic response” with confidence?

Using the neurotoxin 6-hydroxydopamine (6-OHDA, or “oxidopamine”), Berridge selectively destroyed 99 percent of the dopamine neurons in the rat striatum. Predictably, the rodents became entirely aphagic (refusal or inability to swallow). They refused to seek out food and would rapidly starve unless they were artificially fed via gastric tubes.

However, Berridge also introduced a novel metric originally designed by Grill and Norgren in 1978: the “taste reactivity paradigm.”

It turns out, rats give off a remarkably consistent signal of receptivity to taste through their facial expressions. It’s so consistent, in fact, it can be used as an empirical measurement.

Given something sweet and delicious, rats exhibit rhythmic tongue protrusions and relaxed facial muscles: the “positive” response.

When given something bitter and yucky, they gape with mouth open wide, jaw dropped, and corners of the mouth retracted, followed by a sequence of physical aversive reactions: the “negative” response.

When given something entirely tasteless, such as room-temperature water, only rhythmic mouth movements occur, without either the tongue protrusions of sweetness or gaping from bitterness: the “neutral” response.

If dopamine really was the chemical responsible for pleasurable sensations, blocking or destroying dopaminergic neurons should result in the total elimination of the “positive” response to sweet or delicious-tasting substances. In fact, that’s exactly what Berridge had been expecting to find: that all taste reactivity would become either “neutral” or “negative,” regardless of what was given to the rats.

So when Berridge manually pipetted a sweet sucrose solution directly into the mouths of these dopamine-depleted rats and recorded their facial micro-expressions in slow motion, the results were… confusing.

The rats still exhibited the same rhythmic tongue protrusions and relaxed facial muscles as would be found in the unmodified control rats; the positive pleasure response.

So then what, exactly, was dopamine-depletion doing to them? If they still experienced pleasure, why were they so... depressed?

Berridge and Robinson spent the subsequent decade proving an idea: that dopamine does not mediate “liking” (hedonic impact, pleasure).

Instead, it mediates “wanting”.

They believed dopamine in the mesolimbic pathway supports an unconscious tagging system that makes reward cues fundamentally attractive, propelling the organism’s behaviour toward an objective.

They called this “incentive salience.”

The dopamine-depleted rats still liked and enjoyed sugar; they merely stopped caring for it one way or another. They stopped pursuing it. They no longer particularly wanted it.

It turns out there is a distinct difference in the brain between liking something and wanting something.

True pleasure, or “liking,” is actually fragile and remarkably localised in the brain. It is mediated by isolated “hedonic hotspots” predominantly driven by opioid and endocannabinoid signalling in the nucleus accumbens shell and ventral pallidum. By contrast, the dopamine-driven “wanting” system is massive, robust, and highly susceptible to sensitisation.

This neurological divergence explains the bleak reality of severe addiction. As Berridge noted, the dissociation of wanting and liking means a drug addict can reach a neurobiological state where their mesolimbic system, driven by dopamine, is so heavily sensitised to a particular sensory cue - in this case, a drug - that they possess a desperate, overwhelming want for it, even if subjective tolerance is so high that they no longer like the experience of taking it.

Furthermore, in 2025, Berridge was able to demonstrate conclusively that it is possible for an organism to want something that they severely dislike by directly manipulating the mesolimbic pathway with electrical stimulation: using this mechanism they were able to cause rats to feel an overwhelming motivation to bite on an electrified rod, causing them pain and discomfort.

Clearly, we can like things we don’t want, and want things we don’t like.

It has been scientifically proven that you both want and like articles just like this one; subscribe!

Here’s another fact about dopamine you probably didn’t know: your eyes use dopamine to signal the brightness of light entering the retina.

Your brains motor cortex uses dopamine to gate movement signals for fine motor control.

In fact, dopamine is used in lots of completely different ways throughout the brain and body; it makes no sense whatsoever to pin any one function on it.

Suggesting dopamine is the brain’s pleasure chemical is not only specifically wrong, it’s also wrong in general.

It would be like suggesting radio waves are how software engineers communicate cat videos with each other. Sure, if you follow enough reductionist reasoning, you can reach a level where cat videos are indeed carried across the internet which sometimes includes radio waves, but would anyone describe “the internet” explicitly as a “system for transmitting images and videos of cats?”

Don’t answer that.

(On that subject, this is one of my earliest youtube videos:)

Anyway, you get my point. Sometimes people watch other sorts of videos on the internet, too.

Not me, though I’ve heard rumours of it happening.

So, if dopamine really isn’t relevant to the phenomenon of pleasure, why has the myth been so persistent?

My only guess is that it lets us quickly and easily explain away things like addiction, ADHD, depression, “youths” (get off my lawn.)

It makes it easy to say that drug addicts are just out to get “high”, that it is a choice they make  - choosing to seek pleasure even to the detriment of all else  -  which they could change if they really wanted to, if they simply “took responsibility for themselves.”

It allows us to pretend ADHD isn’t real, that such people need to “be responsible”, as if it’s all just a choice they make to pursue only “enjoyable things”, or that it’s only a childhood phase one grows out of: because, you know, being a “grown up” means you start making “good choices” and “doing the hard things” which is the antithesis of ADHD, right?

It makes it easy to wave away depression as merely an absence of joy, to say “come on, it’s not that bad”, as though the cure were merely to realise that butterflies and rainbows exist, and allow all the joy to flow back into the brain just like that.

These simplistic explanations may allow us to forget about the complexities of the world around us, and especially our own brains. We don’t like things being too complicated; part of being human is trying to simplify and explain things, even things we don’t understand.

We also don’t like to believe anything which suggests a lack of human control, especially over our choices. To believe it’s all just some chemical reaction makes it seem like it’s not really a conscious choice, doesn’t it? (It isn’t)

The illusion of the ethereal conscious self as being in absolute control over our physical bodies, like an external puppet-master, is indeed a very powerful and very useful one to our sense of a unified identity, despite the fact that our bodies are an amalgamation of uncountable numbers of other micro-organisms.

What’s more, it’s no doubt comforting to believe our choices are made by some fully integrated and consciously aware entity, as though we design the choices we make with intent.

We don’t.

It’s all just chemistry.

Don’t forget to check Part II:

References:

Positive reinforcement produced by electrical stimulation of septal area and other regions of rat brain. | J. Olds and P. Milner | 1954 | Journal of Comparative and Physiological Psychology, 47(6), pp. 419-427.

“the electrical stimulus in the septal area has a positive reinforcing effect of a very high order”

Neuroleptic-induced “anhedonia” in rats: pimozide blocks reward quality of food. | R.A. Wise, J. Spindler, H. deWit and G.J. Gerberg | 1978 | Science, 201(4352), pp. 262-264.

“Pimozide appears to selectively blunt the rewarding impact of food and other hedonic stimuli.”

Taste reactivity analysis of 6-hydroxydopamine-induced aphagia: implications for arousal and anhedonia hypotheses of dopamine function. | K.C. Berridge, I.L. Venier and T.E. Robinson | 1989 | Behavioral Neuroscience, 103(1), pp. 36-45.

“The persistence of normal taste reactivity argues against... an anhedonia... hypothesis”

What is the role of dopamine in reward: hedonic impact, reward learning, or incentive salience? | K.C. Berridge and T.E. Robinson | 1998 | Brain Research Reviews, 28(3), pp. 309-369.

The incentive sensitization theory of addiction: some current issues. | T.E. Robinson and K.C. Berridge | 2008 | Philosophical Transactions of the Royal Society B, 363(1507), pp. 3137-3146.

Wanting what hurts: D1 dopamine neuronal stimulation in CeA is sufficient to induce maladaptive attraction | Nguyen and Berridge | 2025 | Nature

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