When a person is plunged into general anesthesia, the electrical life of their brain is radically reconfigured. Individual neurons fall quiet, like orchestral players who have stopped their solo lines. At the same time, the brain begins to generate large, slow, synchronized waves — the electrical signature of the unconscious state. This phenomenon has been reproduced in the laboratory for the first time in human brain assembloids — miniature three-dimensional models of neural circuits grown from stem cells in the laboratory at UCLA. On the results of the study, published in the authoritative journal British Journal of Anaesthesia, the institution announced on 1 October 2026.
The head of the study, assistant professor of neurology Ranmal Samarasinghe, and lead author Daniel Toker, together with the team, created small neural networks from reprogrammed stem cells, linking excitatory neurons, inhibitory neurons and glial cells into functioning three-dimensional circuits. When propofol — one of the most common anesthetics in surgery — was added to this microscopic model, exactly what happens in the living brain of a patient under anesthesia occurred: individual cells markedly reduced their activity, while at the same time the entire network began to produce bright, synchronized slow waves.
The paradox of anesthesia is simple, but at first it seems contradictory: the neurons “fall silent,” yet the brain “shouts” louder. Imagine an orchestra in which each musician plays their own melody at a different time — chaos resounds, and the individual instruments are barely distinguishable. Then the sounds become sparser, but it is precisely at that moment that all the instruments enter synchronously into a barely perceptible slow rhythm. Each musician plays noticeably more quietly, but when they sound simultaneously, the combined sound becomes, on the contrary, sharper and clearer. Anesthesia works in a similar way: the coordination of neural spikes amplifies the brain’s total electrical signal even as the activity of individual cells drops sharply. To test the mechanism, the researchers blocked the receptors on which propofol acts — the characteristic waves disappeared instantly. Moreover: it was precisely inhibitory neurons that were required for this pattern to arise; models without them produced no waves.
The results take on fundamental significance thanks to the minimalism of the model: the assembloids contain only cortical, that is, cortical, circuits, while the thalamus — a structure located deep in the brain and long considered necessary for the emergence of slow waves — is entirely absent from them. This means that a simple cortical network on its own, without the help of more primitive structures, is capable of generating this remarkable pattern of activity. This resolves a long-standing neuroscientific dispute: the role of the thalamus in the living brain remains an important question, but it is now clear that the thalamus is not an obligatory condition for the emergence of anesthetic waves.
An important clarification: in their properties, assembloids are closer to developing fetal brain tissue than to the mature brain of an adult human. The study brilliantly reveals the electrical mechanisms of anesthesia’s action at the molecular and network levels, but the question of subjective experience — why we remember nothing and feel no pain — remains beyond the data obtained. Nevertheless, the results open for neuroscience a path from the molecular level of the drug’s action straight to the behavior of an entire neural network.
This means that science now has an experimental tool for more precise study not only of anesthesia, but also of epilepsy, the consequences of traumatic brain injuries and other disorders of brain function in which normal electrical activity is disrupted.
