Neurotransmitters are a confidence game

You might have heard people often talk about the ‘reward neurotransmitter’ or the ‘love hormone’ or the ‘happiness molecule’ and so on.

Remarkable stuff—that one molecule in our brain is responsible for making us happy, and another for our social bonding. Makes you wonder why we need all this extra stuff in our heads. Molecules are tiny, and our brain takes up so much space. Seems wasteful. Almost as if it doesn’t make sense…

Fact is, although we know about some actions of these neurotransmitters, we actually have very little idea about how those actions play out in behaviour. So let me tell you a bit about them, a bit about what we do know, and then show you how anyone using them to explain behaviour to you is running some kind of con.

¶What is a neurotransmitter?

A neurotransmitter is the catch-all term we use for any chemical that nerve cells use to communicate with each other. In the brain, or elsewhere in your nervous system, whenever one cell wants to influence another, it needs a method of doing so. As I write in the article I linked there:

There are two sort-of stages to a neuron’s communication: a chemical part and an electrical part. In the cell body, specialised organelles create vesicles: little bubbles full of chemical messengers called neurotransmitters. The vesicles get transported towards the [end of the cell closest to its neighbors]. Eventually, these vesicles will be ‘popped’, releasing the neurotransmitters … to float over to neighbouring neurons. This sharing of the released neurotransmitters between neurons is the chemical part.

The neurotransmitters are gobbled up by the neighbouring neurons, and then, when one of the neighbours:

recieves enough neurotransmitters … it will open some channels in its skin (the cell membrane) to allow in some of the electricity that’s washing through your body. This will lead to a sort-of overcharge … and this electrical energy will whiz down the [cell to the place where it keeps its vesicles] … the trigger for the ‘popping’ of the vesicles … kicking off the process once more for the neighbouring neurons.

That’s basically it. The neurotransmitters are just the thing which tells a neuron that it need to release more neurotransmitters. Eventually the cell that receives this signal won’t be connected to other neurons, but instead to muscle fibres, and instead of making more neurotransmitters happen, it’ll make you do stuff.

Which raises a couple of questions. Firstly, if this is all neurotransmitters are doing, why are there different types of them? And why would different types be involved in different stuff?

If you have those questions, you’re in good company.

¶What are all the different types of neurotransmitter doing?

Neurotransmitters can be wildly different to each other, because any molecule could be a neurotransmitter. If anything was a case for evolution, it’d be this, because it really looks like the nervous system was just grabbing whatever information it could, from wherever it could, to work out what it was supposed to be doing.

So, for example, when we think about neurotransmitters, we usually think about more traditional small molecules—amino acids like glutamate, and monoamines like dopamine and serotonin. These things are usually derived from metabolic processes, which is pretty sensible—grab the byproducts of other body processes, and use them to help you communicate about what you should be doing while the body is doing those processes. This helps explain how a lot of neurotransmitters double as hormones, like adrenaline and oxytocin. Hormones basically do what neurotransmitters do, but for other organs, so if these chemicals can be used by one communication system, why not another? In a similar vein, we have lipids like endocannabinoids and anandamide, which are derived from fatty substances. Again, using byproducts of stuff that’s already floating around to help figure out what’s going on, and what needs to be going on. And all these things are usually associated with more transient events. So, you know, dopamine seems like it’s really important for the little reward signals we get when we’re expecting something good to happen. Adrenaline often follows our little frissons of fear, amping up our system for some problematic event.

But sometimes we need something that’s going to support more slow, sustained stuff. So, the nervous system has co-opted some peptides too—big molecules, like endorphins and substance P. These are often involved in more complex pathways, which makes sense because they’re bigger and sturdier. And endorphins seem like they’re often related to pain, and substance P often related to mood. Both of these are ongoing and more complicated process, so it makes sense that the body is using chemicals and pathways that are bigger, slower, and more complex.

And, sometimes, we need something that can go a bit farther, faster, so we also have neurotransmitters that are gases, like nitric oxide and carbon monoxide. These don’t do the usual thing of living in vesicles until they’re ‘popped’, but instead just get synthesised and released instantly when the cell overcharges. These molecules also get through cell skin really quickly, so in general they just speed up the process. And you find these things involved in really fast changes, like the rapid adjustment of blood flow or neuron firing in reflex pathways.

This isn’t comprehensive. But the picture here I’m trying to paint is one of the nervous system just grabbing whatever chemicals are nearby in order to do what it needs to do. Like a patchwork of solutions to all the different problems it needs to solve. And to really make the idea clear, dopamine is one of the most well understood neurotransmitters, involved very heavily in reward signalling pathways. But not in all animals. In invertebrates, like the humble honeybee, dopamine is much less important for this—they use octopamine to fill this role instead. You’ve never heard of octopamine, because no one cares about it in humans. But we have it too, and it largely does different stuff than dopamine for us. Two different evolutionary pathways, two different methods of solving the same problems. Their nervous system just happened to grab something else instead.

¶Talking in more depth about neurotransmitters is a confidence game

Beyond this, I’d be pretty nervous trying to use neurotransmitters to make any useful claims about human behaviour. No neurotransmitter is just involved in one thing, as you’d expect from such a patchwork system of solutions. Oxytocin might be the ‘love hormone’, but all the social bonding stuff also comes with plenty of dopamine and serotonin and various other neurotransmitters too. And when you do try to solve problems with neurotransmitters, you end up with really weird results.

So, for example, serotonin is known as the ‘happiness molecule’. We know it has a relationship to mood. Interesting evidence suggests this is so. For example, we think that the despondent ‘come down’ after taking drugs like MDMA is related to a depletion of serotonin in the brain.

But if you just flood the brain of a depressed person with serotonin, they don’t necessarily get happier. We know this because one of our main anti-depressants does this, and it only improves symptoms for something like a third of people. A similar number to simply providing a placebo pill instead. More interestingly, people taking these drugs have an increased likelihood that they’ll try and kill themselves.

I wouldn’t draw too many conclusions from this, because many other factors are at play there. It’s not clear who will have this increased likelihood, or why, just that in general the rate is higher. And I’m not saying there’s a relationship to the placebo effect, just that it has equivalent performance.¹ But it certainly means that calling serotonin the ‘happiness molecule’ is overstating the case. Really, the role of serotonin, like all the other neurotransmitters, is confusing and complex. To illustrate, I bet you also didn’t know that the two most common hallucinogenics, magic mushrooms and LSD, are serotonergic in nature. Long before we started concentrating on it for investigating mood, we exclusively concentrated on it for it’s potential to reveal this aspect of the human experience to us.

Mostly, I suspect, the problem is one of scale. You have all these tiny molecules whizzing around your body and sometimes this whizzing corresponds to stuff and sometimes it doesn’t, but there is so many things whizzing that it’s hard to pin down what’s actually going on. It’s kind of like looking at the dust in the nose of the sneezing person on the 45th floor to determine something about that company’s supply chain. It might be asbestos, making everyone ill and driving down productivity. Or it might just be dust.

Which leads me to the confidence game that’s played with neurotransmitters. You will often hear people say something like ‘doing x thing releases y neurotransmitter which has z psychological benefit’. I have never once heard a construction like that where the reference to the neurotransmitter was anything more than cosmetic. To say ‘going for a run will trigger a release of dopamine, which will make you feel good’, has precisely the same informational content as ‘going for a run will make you feel good’. You haven’t learned anything because dopamine was included in there. Indeed, that’s not even how dopamine works, and I’d be surprised if anyone noticed because including the word dopamine made absolutely zero difference to the sentence’s meaning. You just hear ‘running means brain things which means running good’.

¶What we can conclude about neurotransmitters

All anyone really needs to know about neurotransmitters, outside of very select circles, is that changes in the concentrations of these molecules across populations of neurons have difficult to understand effects on the way we learn and respond to the world. They mediate how we respond, but talking about them doesn’t particularly help us understand our responses better.

So, for example, we have excitatory neurotransmitters, like glutamate, which increase the activity of neurons. And alcohol is known to impair the ability for neurons to gobble up glutamate. So maybe all the bad stuff that happens when we’re drinking has something to do with the fact that our neurons aren’t firing as well as they should be. Or, maybe, since the brain adds more glutamate receptors if you drink a lot to compensate for the fact that they get inhibited when you drink, alcohol withdrawal symptoms are caused by the fact that your brain cells are gobbling up too much glutamate. Interesting, yes, but informative? Not really.

Or you also have inhibitory neurotransmitters, like GABA, which decrease the activity of neurons. Benzodiazapines (opiods like Valium and Xanax) encourage GABA production, so maybe the pleasant slowness and reduction in stress they create is partially due to your cells firing more slowly. Slow nervous system, slow person. Again, I’m sure you now have something interesting to say down the pub, but did it really deepen your understanding of human behaviour?

Maybe the best known effects of neurotransmitters are related to simple learning mechanisms. Changes in modulatory neurotransmitters, like dopamine and serotonin, signal to our neurons that they should change their connections to other neurons. That the neural pathways which currently exist might need to be updated. We call this neuroplasticity—the brain’s ability to reorganise itself by forming new neural connections. You can read about the effects of those changes in these articles on classical and operant conditioning. But notice that nowhere in those articles do I mention neurotransmitters, because it serves no practical purpose to do so.

The only value in stretching those two kinds of learning—operant and classical conditioning—into the brain comes from discovering that we are developing neural pathways that map the statistical structure of the environment we live in and our habitual responses to that environment. Put a different way, that certain perceptions usually have certain consequences, and that often certain responses are best when dealing with those consequences.

This is a level of brain science that we can actually understand when it comes to parsing our behaviour. That our brain helps us to link these causes and consequences together.

Less comprehensible is the idea that somehow, an enormous ecosystem of tiny little molecules are engaging in some uncountable number of transactions every second, all day, changing your brain in miniscule increments to eventually produce a reliable preference for, say, eating when you’re hungry, or hugging your sad companion. These just aren’t sensible levels of comparison.

So, do me a favour. Next time you’re inclined to talk about neurotransmitters, just don’t. And if you hear someone else dropping neuromodulators into the conversation, you might as well just ask upfront how much their e-book is. It’ll save everyone a bunch of time.