The process that takes place in creating memories during the dreaming state is currently unknown. However, there are a number of theories on the subject that are providing some headway. Additional to theories on dream memory, there have been a number of changes in the current dream theory which have contributed pieces to the puzzle. In this paper, I have provided a number of examples of current theories on memory formation in dreams. This brings into the discussion topics on neurotransmitters, hormones released during sleep, theories on dream-formation, memory formation found in highly lucid states while dreaming, and other dream-like states in relation to memory formation. With these examples, we can identify some key elements of dream memory which provide us some guidance on how memory is formed in dreams. These elements continue to contribute to us further asking ourselves the difficult questions: what are dreams and how is memory involved in understanding them.
Understanding Dream Memory
Understanding memory and its involvement in the creation of dreams is a complicated subject to discuss. We look at dreams as something independent of memory, something that is created on their own and exists regardless of our ability to remember them. But do they? This question has influenced my interest in finding and understanding the mechanisms of dream memory, to try to remember my own dreams, observe their creation, and see ultimately see what dreams are, and how memory is involved in understanding them. Though the discussions on these topics are complex and can hardly be expressed in this paper entirely, I have challenged myself to express some of those key findings.
Basic Theories of Memory and Dreams
Long-Term Potentiation. To understand dream memory, we must first try to understand how basic memory is formed. Even today we still don’t fully understand the process, however, currently, one of the most highly regarded theories is based on the concept of long-term potentiation (LTP). LTP occurs when synapsis in the brain continue to fire over an extended period in a specific pattern. The continued activation creates a strengthening of that synapse to its neighboring synapsis (Cooke & Bliss, 2006). Inactivity of that synapse, on the other hand, can cause long-term depletion (LTD) and weaken the bonds that that synapse has with another synapsis around it (Massey & Bashir, 2007). This basic action creates strong bonds between the synapsis and relationship with neighboring synapsis which when collectively fire together create a memory as we know it (Cooke & Bliss, 2006).
Most research into LTP has been focused on the hippocampus as the seat of memory formation because of its involvement in long-term memory and other high-level memory formations for the human mind ([Description of the hippocampus and its function], n.d.). The hippocampus is essential to dreams because of its participation in converting short-term memories (the experience of the dream itself) into long-term memories in other regions of the brain so that when we awake, we can remember the dream (Maurizi, 1987). Specific neurotransmitters and hormones that the brain releases either allow for LTP or LTD in the hippocampus, supporting memory to be either formed or destroyed. Little is fully understood about these chemical processes, however, some recent work by Dr. Allan Hobson and his Activation-Synthesis Hypothesis has provided some direction for understanding dream memory.
Activation-Synthesis Hypothesis. Hobson, through his research, has shown that acetylcholine is most active in the Random Eye Movement (REM) sleep stage (Hobson, 2003, p. 206). We also know that acetylcholine is important in the strengthening of synapsis by the oscillation of synapse firing and in the result, this is theorized as to why we have a higher chance of remembering dreams if woken up during REM (Hasselmo, 2006). The idea that high levels of acetylcholine promote memory formation in dreams has also been adopted by the lucid dreaming community. Many of the supplements and drugs that promote lucid dreams are sought out for their ability to increase acetylcholine levels in sleep or to use acetylcholine’s counterpart, serotonin, to push REM to later parts in the night, allowing for REM rebound and increased the dream memory (Mccarthy, 2016). This is easy enough to understand in practice, however, there are some issues with this theory as we dive deeper into the complexities of dream memory.
It is well known that as we sleep through the night, we go through a number of phases of sleep. Each phase includes a period of time that includes REM sleep. This happens on average about every ninety minutes during sleep and continues throughout the night (Gordon, 2013). The amount of sleep that we get in one phase or another also changes as we continue sleeping, increasing the amount of time we are in REM the longer we sleep (Gordon, 2013). This raises the questions if we have a number of sleep phases each night, and REM in each phase, why is it so hard to remember each REM phase and dream associated with each phase? The association with acetylcholine and dream memory is also challenged when investigating supplements that are solely based on their acetylcholine increasing features, as the results are often hit or miss and could be considered near the level of the placebo effect (Yuschak, 2006, p.101). Though memory formation in dreams does increase in late night or early morning REM stages, this shows us that this is yet a more complex process than simply the supply of acetylcholine in the brain.
Supportive Memory Medications Affecting Glutamate. Galantamine which is a medication that is provided for Alzheimer’s disease and also used avidly in the lucid dreaming community. Galantamine is provided to individuals with Alzheimer’s because of its ability to stop the breakdown of excess acetylcholine in the brain. The reason that this is important to Alzheimer’s patients is that it is theorized that Alzheimer’s disease is destructive to memory because of its breakdown in the mechanisms that produce acetylcholine in the brain and degenerates neural growth especially in the hippocampus (Kihara & Shimohama, 2004) (Mu & Gage, 2011). This loss of the acetylcholine function in the brain does seem to result in memory loss and aligns with Hobsons view of acetylcholine being the key to memory formation, but additional research into Alzheimer’s disease shows that acetylcholine is not only the affected neurotransmitter.
Glutamate is also something that is being looked at to be related to Alzheimer’s disease as it also is disrupted in the hippocampus (Francis, 2005). Galantamine also promotes glutamate in the hippocampus (Penner et al., 2003,). Glutamate is also an excitatory neurotransmitter and acts in tandem with the depressant neurotransmitter GABA. When glutamate is active in the hippocampus, GABA is lowered (Petroff, 2002). If we look at substances that bind to the GABA receptors in the hippocampus, we find the same interesting result: the inability to form new memories, much like dreams (Alcohol and GABA, n.d.). We see this effect take place in high levels of intoxication with alcohol and marijuana. Additionally, if we allow for these intoxicating substances to wear off over a period, we find an increased dream recall which seems to align with the idea of increased glutamate due to the lowering of GABA would increase memories and dream recall (Stoffels, 2015).
Glutamate also adds to the complexity by affecting the nicotinic acetylcholine receptors which are also activated by acetylcholine (Kihara et al., 204). These receptors responsibilities also align with Hobson in his view that acetylcholine promotes memory in REM. Nicotine also promotes the activation of nicotinic acetylcholine receptors and is highly regarded for its memory formation abilities in lucid dreaming, especially if combined with galantamine (Yuschak, 2006, p.78).
When we take a step back and look at all of these processes I have described, we start to form a larger picture. The picture is that though Hobson may have been right about acetylcholine being an important part of dream memory formation, there are many other essential processes taking place that when combined seem to provide us with the ability to build new memories. Galantamine with its ability to disrupt the natural forgetfulness in dreams by reducing GABA, increase glutamate, which increases nicotinic acetylcholine receptors activation, and its ability to reduce the breakdown of the acetylcholine in the brain, makes it an essential tool for lucid dreaming and dream recall.
Additional Options for Memory Formation
Out of the world of Hobson and neurotransmitters, we run into more questions revolving around dream memory. These questions revolve around the effectiveness of hormones on memory and their effects on our dreams.
The Pineal Gland Hormone Oxytocin. The pineal gland has always been an interesting key point when it comes to dreams simply by its relationship to dimethyltryptamine which has been found in the pineal gland (Barker, Borjigin, Lomnicka, & Strassman, 2013). The pineal gland also is referred to by many as the third eye and contains hormones that are involved in our sleep-wake cycle, specifically melatonin and vasotocin (oxytocin) (Maurizi, 1987). There is little research done on oxytocin when it comes to sleep, but still, its role is immense when it comes to memory and dreams. Oxytocin is released by melatonin during sleep, activates REM sleep, and has been shown to create amnesia by affecting the hippocampus (Maurizi, 1987). Additionally, oxytocin is involved in the modulation of GABA and glutamate in the hippocampus modulating our central nervous systems excitability (Qi et al., 2012). Melatonin is most active during the early night and gets less over the night as the pineal gland is converting serotonin into melatonin (Adams, 2017). Oxytocin in relationship to melatonin would be released less as the night continues, reducing its amnesia like effects. This is an exciting idea as to why we would remember our REM dreams later in the evening as oxytocin is at its lowest or early night than when oxytocin is at its highest. Could oxytocin be a contributing factor as to why we are unable to remember our dreams? We find holes in this theory when we find studies done on Non-Random Eye Movement (NREM) dreams and how dreamers are able to remember their dreams when REM is suppressed (Oudiette et. al., 2012). The interesting thing about these studies is that often they use clomipramine to suppress REM in patients, an SSRI that also interferes with oxytocin release in the pineal gland (Humble & Bejerot, 2016). This particular SSRI could be unintentionally interfering with the brain’s ability to remember NREM dreams due to its ability to reduce oxytocin which would increase the memory capacity of the hippocampus.
Cortisol and Memory. Another contributing factor to memory that is often overlooked in sleep is the hormone cortisol. Like melatonin and oxytocin, cortisol also follows a circadian rhythm and is involved in memory formation in the hippocampus (Payne, 2004). High levels of cortisol can result in hippocampus dysfunction which as we now know, can lead to memory issues during sleep (Joëls & Krugers, 2007). Cortisol as a stress released hormone is also lowered due to practices such as mindfulness meditation (Turakitwanakan, Mekseepralard, & Busarakumtragul, 2013). Practices like dream journaling, binaural beats, and reality checking, which mimics many of the features that mindfulness meditation provides, could affect the cortisol levels released into the hippocampus. This may be the reason why these practices all seem to improve dream recall as well as being an essential part of lucid dreaming (Adams, 2018).
Figure 1. This figure illustrates the activation process in relation to memory formation.
Continued Research. Further studies into the effects of cortisol and oxytocin on memory while sleeping need to be conducted to learn more about their involvement as little research has been conducted or suggested. I wrote Mark Solms, a highly regarded researcher on the subject of dreams and psychology, and asked him about these chemical processes and their influences in dream memory. His response was, “Unfortunately, there is still no consensus on the mechanism of forgetting of dreams. So, your guess is as good as everybody else’s!” (M. Solms, personal communication, November 11, 2017). This, unfortunately, was not the clarification I was looking for. This view of cortisol and oxytocin only provides us with more complexity to the discussion of dreams and memory. Dream memory is obviously not as simple as previously thought and cannot be explained only by the effects of acetylcholine on the brain alone.
If You Could Remember Dreams
Galantamine with its high effectiveness in providing the necessary compounds to support memory formations in dreams is regarded as a highly effective lucid dreaming supplement (Yuschak, 2006, pg. 62). It has the ability to allow us to become aware of the dream, to control the dream, and remember the dream after waking (Yuschak, 2006, pg. 62). I have personally used galantamine over the period of months, documented my dreams, and have noticed some interesting experiences.
One important finding that I noticed is that galantamine greatly increased my ability to be aware of the dream and remember the dream. Additionally, my memory formation in dreams seems to be linked to the quality of awareness. When I was more aware of the dream I had a much higher quality memory of the dream than when I was unaware and remembered the dream. If I was nonlucid in the dream, the vividness of the dream memory would also drop. I also noticed that my awareness in the dream affected the dream outcome, as though the dream narration changed because I was aware, causing the dialog with the dream characters to relate more to the Jungian archetype of the Wise Old Man (McDowell, n.d.). With galantamine, I was also able to remember NREM experiences such as sleep paralysis, hypnogogic hallucinations, and phenomenon like out of body experiences. I have also noticed that dream characters have acted more aggressively to my awareness in the dream, challenging me with visitation while in sleep paralysis. This provided me additional insights into the natural sleep processes that are often hidden by our inability to form memories during this phase of sleep.
As René Descartes said, “I think therefore I am” (Burns, 2001, p.84). It makes me wonder if awareness and the ability to form memories in dreaming states creates the dream itself, or if the experiences themselves existed before the memory. Would we dream if we were unable to remember the dream? Did the dream exist if we did not remember it? With LTP we could say that the act of synapsis firing creates not only the experience but also creates the memory of the experience. Without the firing of those synapsis and the strengthening of those connections, we would never have the memory of the experience. This seems to conclude that memory and experience are one in the same.
When it comes to dreaming memory, I have shown that there are a number of key chemical process that occurs in the mind to allow for memory to be formed. These chemicals involve neurotransmitters and hormones that not only affect our dream state but also our waking state. These processes are complex and interact with each other to the point that its hard to truly understand what process causes what. If anything, I have shown that memory in sleep is more complex than simply identifying one neurotransmitter and its involvement in our minds.
We may never know the answer to the question of what causes memory or how memory is influenced by sleep as the systems that take place are complex and hard to research. As science advances and we are better able to provide real-time imaging of the brain, better understand the actions of LTP and LTD, as well as understand chemical processes and their involvement with synaptic firing, I am confident that we will have tools available to remember more of our dreams and continue to learn from them allowing us to better understand consciousness as a whole. Until then we can continue to use the tools and systems that we have available and update models to align closer to the personal experience each of us has in dreams.
Adams, L. (2018, January 04). How to Lucid Dream – A easy to follow guide on lucid dreaming. Retrieved February 26, 2018, from https://taileater.com/2018/01/04/how-to-have-a-lucid-dream/
Adams, L. (2017, December 19). Dreaming and DMT | A Connection to Psychedelic Theory. Retrieved February 26, 2018, from https://taileater.com/2017/10/17/dreaming-dmt-connection-psychedelic-theory/
Alcohol and GABA | Does Alcohol Increase GABA? (n.d.). Retrieved February 26, 2018, from https://www.therecoveryvillage.com/alcohol-abuse/alcohol-and-gaba/#gref The Recovery Village
Barker, S. A., Borjigin, J., Lomnicka, I., & Strassman, R. (2013). LC/MS/MS analysis of the endogenous dimethyltryptamine hallucinogens, their precursors, and major metabolites in rat pineal gland microdialysate. Biomedical Chromatography,27(12), 1690-1700. doi:10.1002/bmc.2981
Burns, William E. (2001). The scientific revolution: an encyclopedia. Santa Barbara, California: ABC-CLIO. p. 84. ISBN 0-87436-875-8.
Cooke, S. F. (2006). Plasticity in the human central nervous system. Brain,129(7), 1659-1673. doi:10.1093/brain/awl082
[Description of the hippocampus and its function] (n.d.) Retrieved from: http://www.caam.rice.edu/~cox/wrap/hippocampus.pdf
Francis, P. T. (2005). Neuroanatomy/pathology and the interplay of neurotransmitters in moderate to severe Alzheimer disease. Neurology,65(Issue 6, Supplement 3). doi:10.1212/wnl.65.6_suppl_3.s5
Gordon, A. M. (2013, July 26). Your Sleep Cycle Revealed. Retrieved February 26, 2018, from https://www.psychologytoday.com/blog/between-you-and-me/201307/your-sleep-cycle-revealed
Hasselmo, M. E. (2006). The role of acetylcholine in learning and memory. Current Opinion in Neurobiology,16(6), 710-715. doi:10.1016/j.conb.2006.09.002
Hobson, J. A. (2003). The dream drugstore: chemically altered states of consciousness. Cambridge, MA: MIT Press.
Humble, M. B., & Bejerot, S. (2016). Orgasm, Serotonin Reuptake Inhibition, and Plasma Oxytocin in Obsessive-Compulsive Disorder. Gleaning From a Distant Randomized Clinical Trial. Sexual Medicine,4(3). doi:10.1016/j.esxm.2016.04.00227. Mark Solms email.
Joëls, M., & Krugers, H. J. (2007). LTP after Stress: Up or Down? Neural Plasticity,2007, 1-6. doi:10.1155/2007/93202
Kihara, T., Sawada, H., Nakamizo, T., Kanki, R., Yamashita, H., Maelicke, A., & Shimohama, S. (2004). Galantamine modulates nicotinic receptor and blocks Aβ-enhanced glutamate toxicity. Biochemical and Biophysical Research Communications,325(3), 976-982. doi:10.1016/j.bbrc.2004.10.132
Kihara, T., & Shimohama, S. (2004). Alzheimer’s disease and acetylcholine receptors. Acta Neurobiol Exp,64(1), 99-105.
Massey, P. V., & Bashir, Z. I. (2007). Long-term depression: multiple forms and implications for brain function. Trends in Neurosciences,30(4), 176-184. doi:10.1016/j.tins.2007.02.005
Maurizi, C. (1987). The function of dreams (REM sleep): Roles for the hippocampus, melatonin, monoamines, and vasotocin. Medical Hypotheses,23(4), 433-440. doi:10.1016/0306-9877(87)90064-8
Mccarthy, A., Wafford, K., Shanks, E., Ligocki, M., Edgar, D. M., & Dijk, D. (2016). REM sleep homeostasis in the absence of REM sleep: Effects of antidepressants. Neuropharmacology,108, 415-425. doi:10.1016/j.neuropharm.2016.04.047
McDowell, M. (n.d.). Jungian therapy jungian analysis new york. Retrieved February 26, 2018, from http://www.jungny.com/lexicon.jungian.therapy.analysis/carl.jung.209.html
Mu, Y., & Gage, F. H. (2011). Adult hippocampal neurogenesis and its role in Alzheimers disease. Molecular Neurodegeneration,6(1), 85. doi:10.1186/1750-1326-6-85
Oudiette, D., Dealberto, M., Uguccioni, G., Golmard, J., Merino-Andreu, M., Tafti, M., . . . Arnulf, I. (2012). Dreaming without REM sleep. Consciousness and Cognition,21(3), 1129-1140. doi:10.1016/j.concog.2012.04.010
Payne, J. D. (2004). Sleep, dreams, and memory consolidation: The role of the stress hormone cortisol. Learning & Memory,11(6), 671-678. doi:10.1101/lm.7710423. https://www.ncbi.nlm.nih.gov/pubmed/23724462
Penner, J., Rupsingh, R., Smith, M., Wells, J. L., Borrie, M. J., & Bartha, R. (2010). Increased glutamate in the hippocampus after galantamine treatment for Alzheimer disease. Progress in Neuro-Psychopharmacology and Biological Psychiatry,34(1), 104-110. doi:10.1016/j.pnpbp.2009.10.007
Petroff, O. A. (2002). Book Review: GABA and Glutamate in the Human Brain. The Neuroscientist,8(6), 562-573. doi:10.1177/1073858402238515
Stoffels, T. (2015, March 04). Why Your Dreams Are Suddenly So Intense After You Stop Smoking Weed. Retrieved February 26, 2018, from https://www.vice.com/en_us/article/7b7gn4/why-are-your-dreams-suddenly-so-intense-when-you-stop-smoking-weed-876
Turakitwanakan, W., Mekseepralard, C., & Busarakumtragul, P. (2013). Effects of mindfulness meditation on serum cortisol of medical students. J Med Assoc Thai,96(1), 90th ser.,
Yuschak, T. (2006). Advanced Lucid Dreaming: The Power of Supplements. Lulu Enterprises.
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.Lee Adams
Join the Discussion
Want to discuss more about this topic and much more? Join our discussion group online and start exploring your consciousness with others like yourself