More about Pain

Welcome to another blog post!

Link to First Blog Post about Pain: Pain

If you want to read the review article first: Direct Link to the Paper

Quote of the Post:

Let's Get Back to It

We are onto the next section. The reviewers state that changes in gamma waves are constantly seen when studying pain in humans and animals. Pain causes gamma waves to have a bigger amplitude (amplitude is like the height of an ocean wave, frequency is like the speed of a wave). So, maybe there are more neurotransmitters released due to the pain stimulus?

The parts of the brain that have these increased gamma oscillations in rodent models have been the somatosensory cortex and the cingulate cortex.

• This picture shows that the affective dimension of pain is handled by the cingulate cortex and the sensory dimension of pain is handled by the somatosensory cortex. In other words, how you react to the pain is processed by the cingulate cortex, and how you sense pain is processed by the somatosensory cortex.

• This picture shows you clearly where the cingulate and somatosensory cortex are. Both pictures are from this website, a great tool for learning about the brain: thebrain.mcgill

Since the reviewers seem like they don’t really understand the deal with low frequency oscillations, we’ll ignore them for now. The reviewers also discuss the technology used to measure these signals, but I’ll discuss that technology in a later post.

Now, we get to the meat of things—what scientists believe is going on in neurons that causes these brain waves.

Apparently, when dealing with rats, GABAergic interneurons (I’m guessing these are inhibitory neurons in the basal ganglia) regulate local gamma synchrony, the oscillations that are most important when we talk about pain.

We finally get some more specificity in the paper, as the reviewers give me a name for the interneurons studied: parvalbumin expressing neurons. What are these neurons? I have no clue, let’s find out. (Before you ask a question you already know the answer to, yes I am using Wikipedia. 😊)

Aside: Parvalbumin expressing neurons (https://en.wikipedia.org/wiki/Parvalbumin): These are neurons involved in calcium signaling. They are found in—Chandelier and basket cells in the cortex, the heck? Let’s get a picture of that:

• Basket and Chandelier cells, along with other neurons.

I have no idea how scientists classify these neurons, they look the exact same to me. I’m guessing it's through a combination of how many dendrites stick out from the cell body, and the neuron's location in the brain. I’m too lazy to look into this further, I’ve still got the rest of the article to finish. Back to parvalbumin…ok, they're also involved in muscle contractions.

It makes sense that these parvalbumin cells that are involved with muscle contractions are also involved with gamma, high frequency oscillations. I feel like cells that deal with high frequency oscillations will be more robust, and better equipped to handle higher stress conditions. This is important as these cells deal with important biological processes.

Pyramidal neurons are involved with parvalbumin neurons in generating local gamma synchrony. Local gamma synchrony is what it sounds like, lots of neurons act together to produce gamma waves.

Pyramidal neurons are inhibited by the parvalbumin cells to generate local gamma synchrony, but I don’t know how scientists figured this out?

I think they measured electrical impulses from different brain region, but what analysis did they use on that data in order to figure out that a set of neurons reduces the voltage of signals coming from another set of neurons? There are so many neuronal connections, and everything is so interconnected in the brain. How can you know with a high degree of certainty that the changes you observe are due to that region of the brain? Hopefully I learn that soon.

NEUROTRANMITTER ALERT: Boys and girls, we have our first neurotransmitter. Somatostatin. Here’s what it looks like: From what I can recall from my physiology class, it’s involved with inhibiting other hormones.

Okay, so I rushed to judgement. We’re not talking about somatostatin, we’re talking about somatostatin producing cells. These cells are involved with generating gamma oscillations. Unexpected. I would’ve expected them to be involved in some inhibitory pathway.

Pictures

Connexin and gap junctions are how these oscillatory signals get around the brain via interneurons, but I’m not really interested in delving too much into this right now.

The reviewers gave me some insight into the kind of experiments that are revealing oscillatory activity and the functions of different cells in the brain.

What happens is that scientists remove certain types of cells (I’m guessing optogenetically or through some form of molecular genetics) and measure the changes in wave patterns, probably using electrophysiology (EEG, etc.).

I will provide pictures of some of the channels they talk about knocking out:

Pannexin 1 (ATP fueled Glycoprotein):

Dopamine D3 Receptors:

Hyperpolarization-activated cyclic nucleotide-gated (HCN)4 channel:

Hope that provides you with some sort of insight, because it really didn’t help me at all. Fun to look at though.

Ok, we have to look in this technique: viral-based labeling. Hopefully, I talk about it in another blog post, because I really want to know how these scientists are labelling neurons. Sometimes, I feel like they’re just teaching us a bunch of complicated gibberish. You know that feeling when you look at your car’s engine and don’t understand how the hell this is what causes your car to move at 100 km/h? Unfortunately, in neuroscience, you don’t even get to see the car move. You’re just supposed to look at the engine and believe that yes, the thalamus is the relay center of the brain. How do you take all of the data you generate and form a coherent set of principles for how the brain works?

I think we’ll stop it here. Let’s finish this off in our next blog post, because this review article is just too damn long.

Link:

-Direct Link to the Paper