Quantum Effects in neuroscience
When Classical Physics Cannot Explain Neural Data
Quantum biology is an emerging scientific discipline that studies the possible role of quantum phenomena (such as tunneling coherence, entanglement) in biological processes and in particular essential biological functions. Quantum coherence has been measured in photosynthesis, quantum tunnelling in enzyme catalysis, radical pair mechanisms in avian magnetoreception. These are established findings (Marais, A., et al., 2018).
In neurosicence, the concept of quantum mechanics was introduced in a speculative way as “quantum consciousness”, by physicist Roger Penrose and anaesthesiologist Stuart Hameroff, positing that consciousness would arise from “quantum computations within microtubules”. As the reader will see later in this post, I am quite open to new concepts and theories, but I never considered this theory as serious, for the following reasons: (1) no experimental evidence has never been provided to credit or discredit this microtubule related mechanism, (2) this purely speculative theory is unable to explain what classical neural theories of consciousness can explain. There are other reason and objections, but the main one is that I have never seen any equation containing Planck's constant (the signature of quantum physics equations) that connects quantum-level processes to conscious experience, behaviour, or brain activity. Despite frequent claims about "quantum consciousness," no such model has been proposed with empirical validation.
The question examined here will be narrower: whether quantum effects operate in neural systems at the level of cellular mechanisms and signalling. I would like to present and discuss four cases where classical neuroscience models face temporal, anatomical, or substrate impossibilities—and where quantum mechanisms offer experimentally testable explanations.
1. The VTA dopamine response timing problem
The Ventral Tegmental Area (VTA) is a midbrain region rich in dopamine neurons. This structure is essential in the generation, learning, reinforcement and monitoring of goal-directed behaviours and cognitive control sequential processes. VTA dopaminergic neurons fire in response to unexpected primary rewards, or to stimuli that will predict the occurence of a reward. Importantly, VTA neurons show characteristic phasic bursts of 50-110ms onset latency and ~200ms duration in response to reward-predicting stimuli, in many species.
Electrophysiology reveals a temporal coordination problem that classical sequential processing cannot explain.
The timing measurements:
VTA phasic response onset: 50-110ms post-stimulus (Wang et al., 2011)
Yet, the temporal cortex (part of ventral visual stream) neuronal activity involved in object category discrimination peaks at:
Mid-level categories (faces, bodies): 105-125ms
Superordinate categories (animate/inanimate): 149ms
(Dehaqani et al., 2016)
The correlation problem:
It is important to note that VTA phasic responses occur on correct trials but are absent on incorrect trials (Totah et al., 2013). This means VTA activity correlates with successful object discrimination.
Yet VTA's phasic response begins at 50-110ms—overlapping with the period when temporal cortex is still computing reliable discrimination information (peak at 105-149ms).
Classical sequential processing would require:
Temporal cortex completes discrimination (105-149ms)
Signal propagates through prefrontal cortex to VTA
VTA generates phasic response
But VTA responds during the same time window when discrimination information is reaching peak reliability in temporal cortex. The response timing doesn't allow for sequential transmission through the known anatomical pathways.
Anatomical constraints:
While the prefrontal cortex (PFC) connects to both VTA and sensory cortices, the polysynaptic pathway (temporal cortex → PFC → VTA) requires transmission time. VTA's early response onset (50ms) and its correlation with discrimination outcomes that are computed over 105-149ms creates a coordination problem: how does VTA activity track discrimination success when the timing doesn't permit classical information flow?
fMRI studies, commonly used in Human cognitive neuroscience, with a 1-2 second temporal resolution, average over these millisecond-scale temporal relationships. Electrophysiology, with millisecond precision, exposes them.
2. Biochemical signalling speed problem: the neuromodulator paradox
Another challenge of classical neuroscience model pertain to neural signalling. Neural networks exhibit rapid, coherent dynamics—gamma oscillations at 40Hz, sharp-wave ripples at 200Hz—requiring millisecond-scale coordination across distributed populations of neurons (Brunel 2000, Brunel & Wang 2003). Yet the chemical messengers supposedly orchestrating these dynamics operate on fundamentally incompatible timescales.
Fast neurotransmitters like glutamate and GABA clear from the synaptic cleft within 0.1-1 milliseconds, providing rapid but strictly local signalling confined to individual synapses. Neuromodulators like dopamine, acetylcholine, and norepinephrine—which originate from specialised nuclei in the brainstem, coordinate network-wide state changes—diffuse through extracellular space over hundreds of milliseconds to seconds, reaching receptors micrometers away from release sites through volume transmission.
The temporal mismatch is stark: networks synchronise, oscillate, and shift states on 5-25 millisecond timescales, yet the neuromodulatory systems that gate these transitions operate orders of magnitude slower. Classical diffusion models cannot explain how dopaminergic signals from substantia nigra coordinate rapid network reconfigurations across striatum, or how VTA projections modulate dynamics in anterior cingulate cortex and prefrontal cortex—targets even more distant—when the chemical messenger itself requires hundreds of milliseconds to diffuse meaningful distances.
Nicolas Brunel's biophysical models of network dynamics reveal that oscillation frequency in the fast regime is "almost fully controlled by the synaptic time scale"—yet synaptic transmission via diffusing neurotransmitters appears too slow to generate the observed dynamics. The models work mathematically by assuming instantaneous or near-instantaneous synaptic communication, but the underlying biochemistry suggests otherwise.
This is where pilot wave models might offer resolution: if information propagates via electromagnetic fields rather than molecular diffusion, coordination occurs at wave speeds, not diffusion speeds. The chemical messengers may serve as triggers or modulators of field-based signalling rather than as the primary information carriers themselves.
Pilot wave mechanisms:
Louis de Broglie's pilot wave theory (de Broglie-Bohm mechanics) proposes that particles are guided by quantum wave functions. If biochemical signalling involves pilot waves rather than purely molecular diffusion:
Information propagates at wave speeds, not diffusion speeds
Non-local coordination becomes possible
Temporal gaps resolve
Experimental support:
Geesink & Meijer (2016) conducted a meta-analysis of 175 articles (1950-2015) on electromagnetic radiation effects in biological systems. They found electromagnetic frequency patterns in cells matching pilot-wave structures interpretable as "hidden variables" in Bohm's causal quantum field theory.
Their conclusion: Cells operate "under the influence of active wave fields of internally induced EM oscillations and are at the same time driven in concert by pilot waves."
This is not speculation about future possibilities—it's analysis of existing experimental data showing that classical diffusion-based models fail to predict observed cellular response times.
3. Ion channel quantum mechanics
Ion channels are the fundamental units of neural signalling. Recent mathematical modelling reveals quantum behaviour at the single-channel level.
Classical model failure:
Traditional models assume ions move randomly and independently through channels (Markovian process, where the past does not influence present/future), like balls bouncing through a tube. These models predict how fast ions should move, but measurements show they don't match reality (Liebovitch & Sullivan, 1987; McManus et al., 1988).
The actual movement is more complex: ions oscillate as they pass through channels, and each movement depends on what happened before—the system has memory (Vaziri & Plenio, 2010). When researchers model this accurately, they need quantum mechanics equations. Specifically, Planck's constant—the fundamental constant that distinguishes quantum from classical physics—appears in the equations describing how single ion channels work.
In other words, the numbers don't work without quantum mechanics. This is not analogical or metaphorical quantum mechanics. The equations governing ion channel behaviour contain ħ (Planck's constant) because the system exhibits memory-dependent dynamics that classical diffusion equations cannot capture.
When the fundamental units of neural computation require quantum mechanical descriptions, the question shifts from "could quantum effects matter in neuroscience?" to "how extensively do they matter?"
4. The NDE Memory Problem: Verified Perceptions During Cardiac Arrest
Near-death experience research has documented cases where individuals report accurate, verifiable perceptions of events occurring during periods of documented cardiac arrest, sometimes lasting several long minutes—when brain activity should be absent or severely compromised. The AWARE study (AWAreness during REsuscitation), a prospective investigation of cardiac arrest survivors, identified cases of apparently veridical perception during clinically confirmed periods of unconsciousness (Parnia et al., 2014). Systematic compilations of such cases reveal a consistent pattern: patients describe specific details of resuscitation procedures, conversations, events in adjacent rooms or in the hospital, that they could not have perceived through normal sensory channels whilst unconscious (Rivas, Dirven, & Smit, 2016). Three decades of investigation have yielded sufficient documented cases of verified out-of-body perceptions during cardiac arrest that the phenomenon cannot be dismissed as anecdotal (Holden, Greyson, & James, 2009).
The challenge to classical neuroscience is straightforward: if memories form during periods of absent or minimal brain activity, where is the substrate? Synaptic consolidation requires neuronal firing. Pattern completion requires hippocampal replay. Yet these patients encode detailed, accurate memories when the neural machinery supposedly necessary for memory formation is offline. Classical models assuming memory storage solely in synaptic weights and neuronal connectivity cannot account for information acquisition and subsequent retrieval under these conditions.
The NDE phenomenon doesn't prove consciousness is quantum, but it demonstrates that neural activity alone is insufficient to account for perception and memory formation.
Conclusion: Evidence Accumulates for Quantum Effects in Neuroscience
We are witnessing slow but steady accumulation of evidence that quantum mechanics operates at biologically relevant scales and may account for phenomena in life sciences, medicine, and neuroscience that classical models cannot explain.
The evidence is not uniform in quality or certainty. Some findings are experimentally robust: quantum coherence in photosynthesis is demonstrated, macromolecular matter-wave interference is measured, ion channel behaviour requires quantum equations to match observations. These are facts, not speculation.
Other phenomena remain at the threshold of acceptability: near-death experiences with verified perceptions during cardiac arrest, the VTA timing impossibility, biochemical signalling speeds incompatible with observed network dynamics. These observations challenge classical assumptions but do not yet constitute proof of quantum mechanisms—they constitute failures of classical explanations.
The pattern is suggestive: wherever classical physics predicts one outcome and biology exhibits another, quantum effects appear as plausible—sometimes necessary—explanations. Pilot wave models resolve timing paradoxes that molecular diffusion cannot. Quantum field coherence offers coordination mechanisms that classical chemistry lacks. Non-local information transfer provides substrates for memory formation when neural activity is absent.
Near-death experiences are well documented. Three decades of systematic investigation have established veridical perceptions during cardiac arrest as reproducible phenomena, not anecdote. Additionally, a statistically significant proportion of NDErs—predominantly female—demonstrate verified mediumship abilities post-experience (Holden, J. M., Foster, R. D., & Kinsey, L., 2014). Classical neuroscience has no framework for these observations. Quantum models at least offer potential mechanisms: if consciousness involves quantum coherence or field effects not reducible to neuronal firing, then perception without functional brain activity becomes physically possible rather than miraculous.
References
Quantum Biology - General:
Marais, A., et al. (2018). "The future of quantum biology." Journal of the Royal Society Interface, 15: 20180640.
Cao, J., et al. (2020). "Quantum biology revisited." Science Advances, 6(14): eaaz4888.
Macromolecular Matter-Wave Duality:
Arndt, M., et al. (2020). Nature. [Full citation needed]
Pilot Wave Models & Biological Frequencies:
Geesink, H.J.H., & Meijer, D.K.F. (2016). "Quantum Wave Information of Life Revealed: An Algorithm for Electromagnetic Frequencies that Create Stability of Biological Order, With Implications for Brain Function and Consciousness." NeuroQuantology, 14(1), 106-125.
Ion Channel Quantum Mechanics:
[Citations needed - papers showing oscillatory diffusion at non-Markovian limit requiring Schrödinger-Langevin equations]
Near-Death Experience Research:
van Lommel, P., et al. (2001). "Near-death experience in survivors of cardiac arrest: a prospective study in the Netherlands." The Lancet, 358(9298), 2039-2045.
Holden, J.M., Greyson, B., & James, D. (Eds.). (2009). The Handbook of Near-Death Experiences: Thirty Years of Investigation. Praeger Publishers.
Rivas, T., Dirven, A., & Smit, R.H. (2016). The Self Does Not Die: Verified Paranormal Phenomena from Near-Death Experiences. IANDS Publications.
Parnia, S., et al. (2014). "AWARE—AWAreness during REsuscitation—A prospective study." Resuscitation, 85(12), 1799-1805.
Holden, J. M., Foster, R. D., & Kinsey, L. (2014). Spontaneous mediumship experiences: A neglected aftereffect of near-death experiences. Journal of Near-Death Studies, 33(2), 69-85.
VTA Timing & Visual Processing:
Wang, D.V., & Tsien, J.Z. (2011). "Convergent Processing of Both Positive and Negative Motivational Signals by the VTA Dopamine Neuronal Populations." PLoS ONE, 6(2): e17047.
Totah, N.K., Kim, Y., & Moghaddam, B. (2013). "Distinct prestimulus and poststimulus activation of VTA neurons correlates with stimulus detection." Journal of Neurophysiology, 110(1), 75-85.
Dehaqani, M.R., et al. (2016). "Temporal dynamics of visual category representation in the macaque inferior temporal cortex." Journal of Neurophysiology, 116(2), 587-601.
Hou, G., et al. (2024). "The Formation and Function of the VTA Dopamine System." International Journal of Molecular Sciences, 25(7): 3875.
Marc Henry - Consciousness & Water:
Henry, M. (2020). "Consciousness, Information, Electromagnetism and Water." Substantia, 4(1).
Gerbaulet, J.P., & Henry, M. (2019). "The 'Consciousness-Brain' relationship." Substantia, 3(1), 113-118.
