How Memory Works
To start off with, we need to understand how memory works. That way we can know how it could go wrong. There’s a lot we don’t know about memory. It’s incredibly hard to study at a chemical level, especially in humans. However, there have been some good animal studies, and there is an accepted model of memory formation. The basis of memory is a theory called “Long-Term Potentiation” (LTP). There are loads of articles, both scientific and popular, about LTP if you want more info on it. Essentially, LTP works on the rule of “neurons that fire together, wire together.” We know that neurons continually send signals to each other all over the brain. LTP says that if Neuron A sends a signal to Neuron B over and over again, then Neuron A and Neuron B will form a sort of link between each other. It will become easier and faster for those two neurons to send the same signal again. This is the physical basis of memory. A “memory circuit,” if you like.
So LTP allows neurons to link together which is what stores a memory, but how does that happen chemically? There was an article published in the journal “Neuron” a couple of months ago that has an excellent explanation of it. When Neuron A fires a signal to Neuron B repeatedly, Neuron B opens NMDA channels on its surface. These NMDA channels allow Calcium ions (Ca2+) ions into the cell. These Ca2+ ions activate CaMKII, which then creates AMPA channels in Neuron B’s cell membrane. More AMPA channels = easier activation when Neuron A sends a signal, which means that this pathway is more sensitive. The neurons fired together, and now they wire together, allowing for faster, more efficient activation in the future. LTP in action.
I recognize that this is all very dense, so let’s do a real-world example. Say you wanted to remember how to spell the “Colonel” since it’s so weird. You would read the word and spell it out “C-O-L-O-N-E-L.” This act would make a few neurons in your brain fire as it interpreted the information you were reading. Now, if you never looked at it again, then nothing more would happen. But if you read the same word repeatedly (like twice a day for a week), then every time you spelled it out, it would activate those same neurons in the brain. After your week of spelling out “colonel,” those neurons would have been activated in the same way several times, and so would wire together via LTP and all those chemicals I described above.
The central place this neural activity occurs in the hippocampus. This structure is primarily considered the “memory center” of the brain. Technically, memory formation does happen in other places, but the hippocampus is probably the single most crucial part. We know this because of people with hippocampal damage. Patients like HM and Clive Wearing (both of these guys can be googled for more information on their cases. They’re incredibly famous) with damage to their hippocampus can function entirely normally all day long, but they don’t remember anything that happens.
Okay. So now we know how memory usually works. Neurons in your hippocampus fire in a certain way when exposed to a particular stimulus. If this stimulus is repeated enough, that firing pattern will be stabilized via loads of chemicals and LTP, which leads to a memory being formed. That’s all well and good, but what happens when it goes wrong?
Memory Drugs and Greyouts
Drug users often report memory loss. This is a complicated, messy issue with a bunch of factors, but I’ll give you the main ones. A significant factor that is often forgotten is the impact of context. Have you ever been sitting at your desk and realized you needed something from another room? You go into the other room, but then you can’t remember what it was you needed, so you go back to your desk. As soon as you get there, you say something like “crap, *now* I remember what I needed, ” and then you have to go back to the other room again. This is primarily due to the effect of context on memory. If a memory is formed under a particular set of conditions, it will be most readily recalled when you are in those same conditions. You were at your desk when you thought about something you needed, so leaving your desk makes it harder for you to recall that thought. When you come back to your desk, the context triggers the memory, and it comes back to you.
This same phenomenon impacts drug users. If you say/do/think something while high/drunk/whatever, then trying to recall it while sober is much harder. You don’t have the same context, so the memory is less likely to come back. Of course, this is not the only reason memory loss occurs. If it was, you could just get drunk again and remember everything that happened last time you were drunk. This (apparently) is not the case. A lot of memories just fail to form at all when using drugs, but context effects do play a part. You see context pop up with “grayouts” instead of blackouts. A grayout refers to when the person has a very fragmented recall of what occurred when they were drunk, but with the help of some context clues, they can eventually recall most of what happened.
Context effects clearly aren’t enough to explain the memory loss, so the chemicals must be playing a part. You mentioned both alcohol and marijuana, both of which are regarded as Central Nervous System (CNS) depressants. As are opioids, barbiturates, and benzodiazepines. Any substance which is a CNS depressant will probably affect memory through the system I mentioned earlier. GABA is the CNS’s primary inhibitory/depressant neurotransmitter, and all of these drugs increase the body’s levels of GABA. In the hippocampus, GABA acts to stop AMPA channels from being added to neural membranes. If you recall from my discussion of LTP, this is an essential step in memory formation. If I stop the AMPA channel creation process, I stop memory formation. In this way, depressant drugs stifle recall. They chemically prevent memories from forming in the first place via GABA.
This also explains how uppers, like cocaine, nicotine, and Adderall can improve recall (at least short-term. By increasing levels of excitatory neurotransmitters, like Glutamate and Dopamine, they make the LTP process easier, which means that memories are more likely to be formed as it’s easier to do the AMPA channel process. However, they also suffer from context effects. A chronic smoker will often have sharper recall and mental faculties, but when/shortly after smoking. When not smoking, their memory is often worse than normal people, since their body doesn’t have the nicotine that was giving them a boost to their neurotransmitters and a context to their learning.
When your body is getting a chemical from the outside environment (exogenously), it stops creating as much of that chemical on its own. Let’s use Dopamine as an example. Dopamine is a massively important chemical. It acts in memory formation, learning, decision making, value judgments, etc. It’s also one of the main chemicals which provides a sense of reward/satisfaction in the brain. Many drugs act to increase levels of dopamine (alcohol, cocaine, nicotine, pretty much any other drug out there…), which is a key reason why these drugs are pleasurable. They’re activating the pleasure chemical. However, the brain is lazy. If it’s getting its dopamine exogenously, it’s going to quit making dopamine on its own and just rely on the external supply. This is easy to visualise as a step-by-step process:
• Brain functions normally with 100% dopamine creating by the brain itself
• Use cocaine and dopamine shoots up to 200% normal. Awesome rush
• Cocaine wears off, dopamine down to 50% normal
• Feel like total shit (coming down)
• Dopamine works back up to 100% over time
Now you’re back to normal but what if you used cocaine over and over again? What if you did it so often that the brain relied on it for its dopamine? What does that look like?
• 100% normal dopamine
• Use cocaine and dopamine shoots to 200%
• Cocaine wears off, down to 50% dopamine
• Feel like crap, do more cocaine
• Dopamine up to 150%
• Wears off, down to 25% dopamine
• Do more cocaine, up to 115% dopamine
You can see how this process would continue. This is a big reason drug addicts do progressively higher and higher doses. They have basically stopped producing dopamine on their own and so they need to get ALL of their dopamine from drugs. Except no matter how much they take, it’s incredibly hard to get as high as they used to get since there’s no internal dopamine. This doesn’t just happen with dopamine, either. Your brain can come to rely on external sources for pretty much anything, like GABA, Glutamate, Serotonin, etc.
The brain exists in a delicate balance. To function optimally, it needs 100% of each of its different transmitters. When any of them get out of whack, normal function is next to impossible. Think about how people with depression have low levels of serotonin, so they have lowered mood, energy, and ability to engage with their surroundings. By using drugs of any kind, you throw your system out of balance. Especially something like alcohol. Using alcohol impacts serotonin, GABA, dopamine, endogenous opioids, and probably some other stuff I’m forgetting. If you just get drunk once, then your levels of all those chemicals shoot up past 100%, then fall down below it. Over the course of a day or so, they come back into balance and normal function is restored. If you’re an alcoholic, however, the levels get permanently altered and can no longer reach 100% on their own. This is why severe alcoholics are angry, non-functional, in pain, and can actually die during alcohol withdrawal. To give you a concise answer, the fluctuation in neurotransmitter levels is going to be the biggest culprit in why alcohol causes memory (and other) problems. Whether levels are too high or too low, the body just doesn’t function properly with incorrect levels of these chemicals
Memory and dreams
This section will be a lot shorter for the simple reason that it’s a lot more unknown. We don’t actually know *why* dreaming occurs. Let alone all the chemicals and pathways involved. However, using the information I gave up above, we can piece together a few reasons it’s hard to remember dreams. For one, when sleeping, your levels of GABA will increase as your body function lowers and you need to depress your system for rest. Higher levels of GABA make it less likely for you to form memories since it interrupts LTP. For two, LTP requires a repetitive firing of neurons, right? If I want to remember how to spell “colonel,” I have to do it over and over again to store that memory. Most dreams last five minutes or fewer and are never repeated. This means that you’re trying to remember an event that happens one time instead of several, and you’re trying to do it with higher levels of GABA than you normally have. Basically, it’s nearly impossible for LTP to occur with memories.
So if everything I just said is true, how on earth do we ever remember dreams? For one, sometimes dreams do repeat. Like if you’re scared of an upcoming talk you have to give, you may have a very similar dream about public speaking several nights in a row. This makes it more likely you’ll remember that dream (or at least that type of dream). For two, it’s a numbers game. You will typically have 5-7 dreams a night, which means you can almost 50 dreams a week. Even if it’s hard to remember dreams, you get about 50 chances a week, which greatly raises the odds that at least one will be remembered.
As for how to aid dream recall, there’s not a whole you can do. Like I said, dreams are pretty poorly understood and very hard to study. There are two ways I can think of that have been shown to improve dream recall. The first one is to keep a dream journal next to your bed. As soon as you wake up, make it a habit to write anything you can remember in your dream journal. Often, we can remember dreams the second we wake up, but once we go to the bathroom and start getting ready, the memory disappears. By writing it down before you do anything else, you make it more likely that you’ll retain the memory. The other way to remember dreams is to practice lucid dreaming. There are loads of strategies to trigger lucid dreams, like binaural sounds as you go to sleep or practicing some kind of visual cue to recognize you’re in a dream. I’m by no means an expert on lucid dreams, but there are loads and loads of online sources. If this interests you, I would just google around and try a few different strategies until you see if you find one that works for you.
Lee is the creator of taileater.com as well as author of a number of published articles that deal with sleep, sleep paralysis, and lucid dreaming. Lee has a Bachelor of Science in Psychology and is currently studying at John F. Kennedy University for his Masters in Consciousness and Transformative Studies.
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