The Alkaloid #7: Why You See What You See

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Abstract spiral galaxy painting with warm orange and teal tones suggesting psychedelic visual experience
When psychedelics quiet the brain's visual input system, memory takes over — and the brain begins to dream while awake.

THE ALKALOID

Science, culture and capital — one dose at a time.

Issue #7 — May 5, 2026


THE DOSE

Why You See What You See

There is a question that has puzzled curious minds for as long as people have eaten mushrooms or chewed peyote buttons. Why do psychedelics produce such elaborate, structured, often beautiful visual experiences? The kaleidoscopic geometry. The breathing walls. The faces emerging from wood grain. The sense, sometimes overwhelming, that a familiar room has become a living, watching, intricate place. None of this corresponds to anything actually entering the eyes. So where is it coming from?

A team of neuroscientists at the Ruhr-University Bochum in Germany published findings in Communications Biology this February that offer the clearest answer the field has ever produced. The study, led by Callum White and Dirk Jancke, used optical brain imaging in mice given a 5-HT2A serotonin receptor agonist, the same receptor class psilocybin and LSD activate. What they found is that the psychedelic experience visually is, quite literally, the brain dreaming while awake.

The mechanism is elegant. Under normal waking conditions, the brain's visual cortex is dominated by signals coming in from the eyes. Sensory input wins. The rhythmic brain waves that fire when the eyes are processing real-world information operate at a frequency around ten cycles per second. These waves act like a gatekeeper, prioritizing external signals over internal ones.

Under psychedelics, that frequency shifts. The visual cortex begins generating slower oscillations at around five cycles per second, the same frequency the brain produces during REM sleep. The gate that normally privileges external input begins privileging internal content instead. Memory, imagination, and stored visual associations stop being filtered out. They begin appearing as if they were perceptions.

This is why psychedelic visions feel real rather than imagined. The brain is using the same machinery it uses for actual seeing, but pointing it inward instead of outward. The sensory input system has been temporarily quieted, and the brain replaces what is missing with vivid fragments from memory and association. The resulting experience is, technically, hallucination. But it is hallucination produced through the visual system functioning more like it does during dreams.

Andrea Benucci, professor of biology and experimental psychology at Queen Mary University of London who studies neural mechanisms of visual processing, summarized the implication elegantly. Psychedelics push the brain to dream while awake.

The finding is more than a curiosity. It changes how researchers think about the therapeutic mechanism of these compounds. If the visual phenomena are produced by the same neural process that generates dream content, then the entire psychedelic experience may be best understood as a controlled, conscious, waking dream state. The therapeutic value of dreaming itself, in dream-based therapies and grief integration practices that have existed for millennia, suddenly maps onto a biological framework that was previously mysterious.

The brain on psychedelics is not malfunctioning. It is doing something it already knows how to do, in a state it does not normally permit itself to enter.


QUICK HITS

  • The 5-Hz frequency matters. The slow brain rhythm psychedelics induce in the visual cortex matches the frequency the brain produces during REM sleep, when most vivid dreaming occurs. The same wave that gates dream content appears to gate psychedelic visions.
  • The retrosplenial cortex lights up. The Bochum team also documented increased 5-Hz oscillations in the retrosplenial cortex, a brain region involved in spatial memory, navigation, and self-referential thinking. This may help explain why psychedelic experiences often involve vivid memories and shifts in the sense of self.
  • A psilocybin without hallucinations is being designed. Researchers at multiple institutions are now developing modified versions of psilocin, the active form of psilocybin, that may retain therapeutic effects while reducing visual side effects. The Bochum findings sharpen this work by clarifying which neural mechanisms produce the visuals specifically.
  • Closed-eye visuals are the strongest evidence. Some of the most consistent reports across psychedelic compounds describe vivid geometric patterns visible with eyes closed in total darkness. These cannot be perceptual distortions of incoming light. They are pure internal generation, exactly what the new research predicts.
  • DEA boosts research production quotas. The Drug Enforcement Administration has proposed nearly tripling the legal production quota for 5-MeO-DMT for research purposes in 2026, from 11,000 grams to 30,000 grams. Psilocybin and psilocyn quotas were also increased. The research infrastructure is finally catching up to the demand.

SCIENCE DESK

The 5-HT2A receptor and what it actually does

Almost every classical psychedelic, from psilocybin and LSD to DMT and mescaline, works by activating the same receptor in the brain. The 5-HT2A serotonin receptor is one subtype of receptor that ordinarily binds serotonin, the neurotransmitter associated with mood, appetite, and sleep regulation. Psychedelics fit the same binding site as serotonin but produce much more dramatic and prolonged effects.

What 5-HT2A activation actually does at a cellular level is excite pyramidal neurons in the cortex, the main output neurons of the brain's outer layer. When these neurons become more excitable, the dynamics of cortical processing change. Networks that normally communicate through tightly regulated channels begin firing more freely. The April 2026 Nature Medicine mega-analysis from McGill University, covered in Issue #3 of The Alkaloid, confirmed that this loosening produces a consistent neural signature across multiple psychedelic compounds.

The Bochum study extends this picture by showing what happens specifically in the visual cortex. When 5-HT2A receptors are activated there, the cortex shifts from external-input mode into a state resembling REM sleep dynamics. Sensory gating loosens. Memory content, normally suppressed during waking perception, begins coloring the visual field.

This is part of why psychedelic experiences feel so meaningful. The visual content is not random noise. It is drawn from the brain's own stored material, the same material dreams are made of, presented with the realism that the visual system normally reserves for actual seeing. People often describe the experience as showing them something true about themselves. From a neuroscience perspective, that report makes sense. The content really is being generated from their own memory and association networks, not from external stimulation.

The receptor target also explains why pharmaceutical developers can engineer compounds that activate 5-HT2A in different ways. Some activate it strongly and broadly, producing the full psychedelic experience. Others bind more selectively, potentially preserving therapeutic mechanisms while reducing the intensity of perceptual effects. This is the design space companies like Compass Pathways and Cybin are working in as they engineer next-generation compounds.


MARKET WATCH

The Bochum findings have specific implications for the next-generation psychedelic compound market. Pharmaceutical developers have spent years trying to engineer 5-HT2A agonists that retain antidepressant and anti-anxiety effects while minimizing the intense subjective experience. The challenge has been determining which neural mechanisms drive therapeutic outcomes versus which drive the hallucinatory phenomenology.

A clearer picture of how the visual phenomena are generated, separate from the broader cross-network communication that the McGill mega-analysis documented, gives drug designers more precise targets. If the 5-Hz oscillation in visual cortex is what produces the visions, and the broader connectivity changes are what produce the therapeutic mechanism, the two could potentially be uncoupled. This is exactly what newer compound classes including some neuroplastogens are attempting.

The DEA's proposed expansion of research quotas for 5-MeO-DMT, methylone, and psilocybin signals where regulatory infrastructure is moving. Larger legal supply means more clinical trials, more academic research, and faster development timelines for the compounds furthest along in the pipeline. Compass Pathways' priority voucher for COMP360 in treatment-resistant depression remains the closest near-term catalyst, with full FDA review now potentially compressing to weeks rather than months.

Cannabis markets remain in regulatory limbo as the November hemp THC deadline approaches without legislative resolution. Federal rescheduling continues to be slow-walked. Capital flows to psychedelic biotech remain healthy following the executive order, with the gap between psychedelics and cannabis investment narratives widening rather than narrowing.


THE LAST WORD

There is a recurring pattern in how Western science discovers what indigenous traditions have already understood for centuries. Ayahuasca traditions across the Amazon describe the visions as visits from spirits and ancestors, journeys to the past, encounters with knowledge stored in the plant. Mazatec mushroom ceremonies describe the visions as the language of nature speaking through the body. Mexican peyote traditions describe them as memory itself made visible.

These descriptions are not metaphorical. They are precise phenomenological reports of what people experience. The brain, on these compounds, generates content from its own stored material and presents it with the realism of perception. People see their dead. They revisit their childhood. They watch their lives unfold from outside. They encounter beings that feel more real than the room they are sitting in.

What the Bochum researchers have now described in technical neuroscientific terms, as a shift from 10-Hz sensory-dominated visual cortex activity to 5-Hz memory-dominated visual cortex activity, is the biological substrate of those reports. The traditions were never wrong about what was happening. They simply lacked the vocabulary of receptor pharmacology and oscillation frequencies. Indigenous medicine described psychedelic visions as dreams brought into waking awareness, sometimes literally. The neuroscience is now confirming the description.

This is part of why the contemporary commercialization of psychedelic medicine matters so much. The compounds being licensed and synthesized and sold for hundreds of dollars per session are revealing exactly what the traditional cultures said they would. The science is extraordinary. The framework that made the science possible is older.

— The Alkaloid


Sources

  1. Communications Biology — Psychedelic 5-HT2A agonist increases spontaneous and evoked 5-Hz oscillations in visual and retrosplenial cortex: https://doi.org/10.1038/s42003-025-09492-9
  2. ScienceDaily — Psychedelics may work by shutting down reality and unlocking memory: https://www.sciencedaily.com/releases/2026/02/260213223910.htm
  3. The Conversation — How psychedelics push your brain to dream while awake: https://theconversation.com/how-psychedelics-push-your-brain-to-dream-while-awake-new-study-276708
  4. ScienceAlert — Scientists Discover How Psychedelics Make The Brain 'Dream' While Awake: https://www.sciencealert.com/scientists-discover-how-psychedelics-make-the-brain-dream-while-awake
  5. Medical Xpress — How psychedelics push your brain to dream while awake: https://medicalxpress.com/news/2026-03-psychedelics-brain.html
  6. Marijuana Moment — DEA Moves To Boost Production Of Psychedelics: https://www.marijuanamoment.net/dea-moves-to-boost-production-of-psychedelics-to-explore-therapeutic-potential-for-ptsd-and-depression
  7. Andrea Benucci's Lab at Queen Mary University of London: https://www.seresearch.qmul.ac.uk/cbb/people/abenucci/

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