All the social construct and higher-level understanding aside, what is pain in terms of chemical and physical interactions with the neurons? For example, dopamine (and others) cause happiness…anything similar to that with pain?
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Oooo… fun question!
Nerves take signals and move them to the brain for us to process. From the vibration of your phone, to feeling the table, to groping your loved one, all go through nerves.
The difference is the location. Nerves to through ‘tracts’ that go to certain parts of your brain. Pain and temperature tend to go through the tract to your thalamus, which handles emotions.
However, that’s not the only signal! The same signal will also make a stop in the spine, and activate motor nerves, causing movement. That’s why when you touch something that’s painful and you don’t expect it, you pull your hand back. That’s called a reflex.
Hormones are very complicated, and are more like random components than actual emotions themselves. For example, oxytocin is often called “the love hormone”, but it also is released when you fire a gun, so is clearly not always to do with love. Actual sensations or thoughts are more about what pathways those signals then create in which areas of your brain.
Pain is a subset of sensation. And sensation is exactly limited by the receptor a body has. We can see because we have receptors for light, we can feel because we have receptors for touch, we can taste because we have receptors for that, we can feel pain because we have a receptor for that. It is important to remember that you can only feel something that you have receptors for. Receptors for pain are called nociceptors.
Nociceptors are receptors found mainly in skin, muscles and joints. Based on how they are activated, they are divided into different caterogies (thermal receptors, chemical receptors, mechanoreceptors) There’s also a type called “silent” nociceptors which i’ll explain later.
Nociceptor is a type of a neuron called a pseudounipolar neuron. Pseudounipolar neurons transmit sensation from the periphery to the brain. Their main difference from standard is that nociceptors end as free nerve endings which have different receptors that standars sensory neurons. For example, nociceptors that notice tissue damage caused by low pH levels have acid-sensing ion channels (ASICs) that open those ion channels when they register a low pH level. The most notable receptor is TRPV1 receptor, that activates in 2 infamous cases – high heat and capsaicin (a molecule found in spicy food).
Nociceptors that function as mechanoreceptors get activated as any other mechanoreceptor in the tissue, by having ion channels that can sense pressure and transform that into an electrical impulse. However, nociceptors have a higher activation treshold, meaning that light touch won’t activate them, but a slap would. That’s useful because we don’t want every touch to hurt, only extreme ones.
Some nociceptors can get activated more easily by the molecules that we call “the mediators of inflammation”. As the name suggests, they are released during inflammation and can help activate these nociceptors. The interesting type of nociceptors are silent nociceptors, often found in joints, that are, obviously, silent most of the time. Only after an inflamation occurs (arthritis), do the mediators of inflammation help activate these nociceptors so you feel joint pain.
Regardless of how the ion channels get opened, that opening in the cell membrane causes ions to rush through the channels changing the membrane polarity. That change in polarity creates an action potetial. An action potential is a stereotypical and fast change in a cell membrane’s polarity that is the electrical impulse that goes to the brain. It forms as follows: as positive ions enter the cell thru the ion channels that opened, the membrane becomes more positive. That is called depolarization. After the membrane becomes positive enough, a massive number of other ion channels open and an action potential is formed that travels to the spinal chord.
After it gets there, the action potential “jumps” from the nociceptor to the 2nd neuron of the pain pathway to the brain using the neurotransmitter glutamate. Note that glutamate is a generic excitatory neurotransmitter meaning that it produces an action potential on the neuron that it binds to. So, it is not special to nociceptors, other neurons also use it. Just a small caveat – although dopamine is the hormone of happiness, this is not its only role. It includes movement and memory. There’s a bunch of dopaminergic receptors in the hippocampus, a part of the brain that forms memories; you can also find them in the striatum, a part of the brain that finalizes desired movement so you can move your hands without having tremors (this function of dopamine is especially important for people with Parkinson’s disease or Huntington’s disease)
After getting into the brain, the impulse arrives at the Thalamus. The thalamus is the part of the brain that i like to describe as a secretary; it receives all kinds of information from your body, but only lets the interesting ones through. The best way to describe this is as follows: until you read this sentence, you don’t feel that you’re wearing clothes. As soon as you’ve read it, you start feeling it. The reason is that the feeling of your clother was always going to the brain, only your Thalamus didn’t let it go to the brain cortex, so it couldn’t be interpreted. Only after reading the sentence did the thalamus allow the information to pass.
Lastly, the 3rd neuron in the thalamus sends the pain information to the brain cortex and you interpret it as pain. Truth be told it also sends that to many different places which all form a higher sense of the pain, but that’s a topic worthy of another lengthy answer.
So to answer your question, in therms of chemical and physical interaction, pain is not that much different that normal touch. You have receptors for normal touch, you have receptors for pain. Albeit, they are more versitile and “resistant” to producing an impulse, but that is quite useful because again, we don’t typically want to feel pain by the lightest touch. The impulse appears just as any other would, by the opening of ion channels, and travels just as any other would. When the impulse needs to pass to another neuron, it passes just as any other would, by using a synapse, and a neurotransmitter glutamate. Glutamate is a boring, generic, neurotransmitter that excites the following neuron so it can keep forwarding the message to the brain (glutamate is very interesting, plz don’t sue)
So yeah, pain is boring so here’s a fun fact.
Contrary to what would be expected, most pain is actually slow. Meaning that when you hurt yourself, you will first feel that something happened, only after will you feel the pain. For exaple, let’s say you burn your hand on the stove. The next time you accidentally burn yourself, notice that the following will happen.
You touch a hot object.
You remove your hand as a reflex
Around the same time you notice that you’ve touched something.
You have completely removed your hand
Your hand is getting hotter and hotter
You feel that the object was hot
The heat is greater and greater and it start to hurt.
Notice that often times, you start feeling that the object was hot long after you already removed your hand.
That is about it, if you have further questions, feel free to ask.
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