From this semester, the one striking idea portrayed was the discovery that the lateral posterior nucleus (LPN), a higher-order thalamic visual nucleus that takes part of a specific role in REM sleep regulation. Guerrero and Cavanaugh’s conduct of this study demonstrates that silencing the LPN selectively leads to the reduction of REM sleep in mice. In a way, initiating this method leaves non-rapid eye movement (NREM) sleep almost intact. Going along the same idea, selective circuits lead to governing sleep function, which is applied to NREM sleep, the critical phase of deep memory consolidation. This proposes the fact that REM may rely on targeted support from sensory-related thalamic circuits instead of whole-brain sleep mechanisms. In another sense, REM isn’t just “dreaming turned on” but appears to be an adapted situation, in which the neural structures are working all around and stepping in at the right time needed. This finding raises the question of whether REM is supported by specialized neural circuits, and could altering REM change memory, emotion, or even dream content?
A 2021 study from Northwestern University was widely covered in news outlets such as NPR and Science Daily. They examined the occurrence called target memory reactivation (TMR), which is the process of activating the brain with keen sounds during sleep to either strengthen dreams or to modify them. With this study presented, the participants practiced a melody on a keyboard while also listening to a specific sound. The scientists replayed that cue during sleep, which led to the factor the participants performing the melody significantly better. The results acquired from these participants the next morning were better than allowing that cue to be replayed overnight. The key point of this research displayed how specifically REM and light NREM stage sleep are not submissive, therefore is considered an active state. That is because the specific brain circuits present selectively alter what we perceive and how well we remember it. This study resonates with Guerrero and Cavanaugh’s work. If REM sleep needs the LPN to maintain its normal structure, then damaging that specific circuit could interfere with the neural cycle that TMR relies on. There could be an indication of an “entry point” for comprehending how sensory information, dreams, and memory consolidation could interact at a circuit level.
In the TMR study done at Northwestern, memories are reinforced by activating certain cortical pathways during sleep. Looking into the mouse in the REM study, by selectively silencing a visual thalamic structure, it weakened REM, which supports memory consolidation. There is the idea of distinct brain circuits that may play a role, determining what kinds of information get processed during sleep. These studies have opened the door to a new interpretation of sleep, how it's a series of regulated brain modes in which each is linked and supported by distinct neural structures with special functions. Sleep ultimately becomes less like a blanket covering for the brain but more like a series of subtly tuned spotlight beams that illuminate the different neural pathways, all at different times. As the continuation of learning proceeds, on how sleep interacts with memory and perception. The idea that one day we may influence how we dream seems to be realistic, not just being able to know whether we dream or not. The conclusion from the studies of Guerrero and Cavanagh suggests how these possibilities begin in the cortex but also how surprisingly powerful thalamic circuits can shape the landscape of our sleeping minds.
References
Guerrero, J.R., & Cavanaugh, J. (2025). Silencing the lateral posterior nucleus produced a highly selective reduction in mouse REM sleep. Neurobiology of Sleep and Circadian Rhythms. No DOI available. https://www.sciencedirect.com/science/article/pii/S2451994425000136
Anthony, J. W., Cheng, L. Y., Brooks, P. P., Paller, K. A., & Norman, K. A. (2021). Sleep spindle refractoriness segregates periods of memory reactivation. eLife, 10, e70068. https://doi.org/10.7554/eLife.70068
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