If thinking happy thoughts/experiencing “good” things releases dopamine and serotonin in the brain, what exactly happens to the brain for us to feel “bad” when we think bad thoughts/experience “bad” things?

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Emotions seem complex but kinda really are nothing more than just chemical reactions in the brain. If I take a bite out of a delicious burger, I feel satisfied simply because of a near instant boost of serotonin/dopamine in the brain. But what chemical reaction in the brain happens that I feel a near instant feeling of being bummed when I receive bad news, like if I miss a train and curse in disappointment?

So if happiness is merely a chemical reaction of having too much serotonin/dopamine than usual, does being bummed or pissed off sort of… like *drain* the brain of these? or are there hormones that are released that achieve the “opposite” effect of feel good hormones like dopamine/serotonin?

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Anonymous 0 Comments

I apologize, because this will be more like an ELI15. Feel free to ask questions though.

What’s missing from how you’re thinking about this is that the chemicals only have meaning in the context of where they are released.

Your brain makes all kinds of molecules to act as special signalling molecules for very specific brain purposes. While typical neuron-to-neuron communication happens at the nanoscale because the synapses are tightly bound to eachother, some of the special molecules leak out of the synapse, and that’s on purpose — their general concentration in an area (say the limbic system, since we’re talking emotions) can regulate the general behavior of neurons “listening” for that kind of transmission. Think of it like a text message versus a radio transmission if the radio for an area was composed of news entirely written and produced by the residents of the area. Neurons send their texts on the same “frequency” (molecule) as they receive their radio transmissions, and there are many, many neurons that listen to many frequencies and make complex decisions based on those transmissions.

This is important to mention because it’s a common misconception to equate a boost in serotonin with a good mood. We see rises in serotonin text messages and radio transmissions when people have good experiences and a good mood — we also see a rise in serotonin text messages and radio transmissions when people are engaged in visual tasks, and we also see a rise in serotonin text messages in the anterior cingulate cortex of people who are depressed (but in few other places — this probably correlates to an increase in error analysis and rumination). For happiness and other positive experiences, we see the rise in activity happen in limbic circuits and other places involved in emotion. For visual tasks, it’s the optic radiation, which is heavily serotonergic — and many other optic processing areas “speak” serotonin too.

(This is why LSD and other hallucinogens alter visual experience — they mess with a whole host of serotonergic text messaging!)

When it comes to the emotional center of our brain, the limbic system, we see text messages sent in a few different “languages” — GABA (gamma-aminobutyric acid; inhibitory, meaning it decreases activity), glutamate (excitatory, increases activity), and NMDA (N-methyl-D-aspartate; excitatory) as well as the ones you already know; serotonin and dopamine can serve both purposes here and in most places (typically excitatory at the text message level, often inhibitory at the radio level, and different receptor subtypes can defy the trend). At a very high level, we typically see increased transmission in the limbic system (particularly in specific areas of it that differ by emotion, that is currently above my pay grade) as correlating to positive experiences and moods, while decreased transmission correlates with negative experiences and moods. Inhibitory “languages” / transmitters are thus used to induce bad feelings.

The overwhelming majority of these neurons in the limbic system speak almost-exclusively GABA + glutamate/NMDA (NMDA is kind of like a language that budded off from glutamate, which allows it to serve interesting roles in some circuits). They can listen to both and then modify their activity in a relatively simple way, firing more or less, with the complexities of emotion mostly arising from how these “meat and potatoes” neurons are interconnected. They connect to maybe 2-5 neurons, receiving inputs from about the same number. Nevertheless, serotonin and dopamine loom, and they loom large. While not “spoken” by many neurons, the neurons that speak it are hugely influential, often being able to modify the activity of hundreds or even in some cases thousands of neurons, typically inducing them to fire more or less, much like GABA or glutamate from their more dear neighbors would compel. The “boost” in serotonin (related to happiness based on location) on a biochemical level is probably an order of magnitude (or 2 or 3, I’m too tired to google, I’d bet it’s 2) smaller than the boost in glutamate, but serotonin is nonetheless responsible for much of the change in behavior. But as you know now, it can be very easily correlated to depression when seen in excess in specific areas, just as it can be correlated to poor digestion and poor sleep (and good sleep) and inflammation and a whole host of other things when you narrow your analysis to specific areas of the body or brain.

At the end of the day, it can likely be said that GABA and to a lesser extent glycine are the “bad” chemicals, but in 10 years when you’re no longer 5, you’ll appreciate the complexity afforded by looking at it like this — particularly because an equal amount of happy serotonergic activity and depressing GABAergic activity will never correlate to feeling mixed emotions, it will correlate to sitting on your couch and staring at the wall; and because alcohol, which increases the effectiveness of GABA text messages, is often (but not always!) a mild euphoriant that makes you chatty and feel somewhat pleasant. We still have much to learn.

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