For decades, we’ve understood that the brain learns by strengthening connections between neurons that fire together – Hebb’s famous learning rule. This “cells that fire together, wire together” principle has been the bedrock of our understanding of learning and memory[i]. However, new research[ii] is revealing a complementary and equally crucial mechanism: a neural “delete” button that allows for remarkably rapid unlearning when associations become irrelevant. This phenomenon, which aligns with Split-Second Unlearning[iii], finds compelling evidence in the recently discovered principle of “Stentian plasticity”[iv] and holds significant promise for understanding and treating conditions like stress, anxiety, and even chronic pain.
While Hebb’s rule explains how we form associations, the ability to quickly discard outdated or incorrect ones is equally vital for navigating a constantly changing world. This is particularly relevant when considering the impact of past traumatic experiences. The “Split-Second Unlearning” (SSU) model proposes that a traumatic event can become linked with a specific physiological response in the body. Subsequently, even subtle “reminders” of this past trauma, whether consciously perceived or not, can re-trigger that physiological response. While each re-triggering might be a weaker “echo” of the original intense reaction, its recurrent nature leads to a cumulative effect of low-level yet persistent physical and psychological stress. Over time, SSU suggests, this chronic stress can manifest as a wide array of symptoms, including common mental health issues like stress and anxiety, as well as more complex conditions such as unexplained pain or fibromyalgia (chronic primary pain).
The key insight of the SSU model lies in the potential to sever the connection between the trigger memory, or “reminder,” and the associated physiological response. If this link can be neutralised, the cumulative burden of psychophysiological distress may be significantly reduced, leading to an improvement in symptoms. The ability to effectively dampen or eliminate the stress response linked to traumatic memories has profound implications for an individual’s allostatic load – the cumulative wear and tear on the body caused by chronic stress[v] – and consequently for a wide range of physical and mental health conditions.
Enter the groundbreaking research from the Montreal Neurological Institute-Hospital at McGill University. By observing the developing visual systems of tadpoles at a cellular level, scientists have provided compelling evidence for “Stentian plasticity,” a rule that operates in reverse to Hebb’s: “fire out of sync, lose their link.”ii
Using ingenious techniques involving fluorescently labelled neurons and advanced 3-dimensional microscopy, researchers tracked the behaviour of individual axons. What they discovered was remarkable. When a specific axon fired consistently out of step with its neighbouring neurons, it didn’t just fail to strengthen its connections; it appeared to actively retract or weaken them. This suggests that the brain isn’t just passively building connections; it’s actively pruning those that don’t contribute to coherent, synchronous activity within a neural network.
This “fire out of synch, lose their link” principle offers a compelling biological mechanism that could underlie the “unlearning” process proposed by the SSU model. Consider how a seemingly innocuous sensory cue might act as a “reminder” of a past trauma, triggering a stress response. According to Stentian plasticity, if therapeutic interventions can help decouple this cue from the original traumatic memory and its associated physiological reaction – essentially causing the neurons involved in the trigger-response link to fire out of synchrony – then the connection itself might weaken and eventually dissolve.
The tadpole studyii provides a vivid illustration of this principle in action during neural development. However, the implications for therapeutic interventions targeting maladaptive learned responses are significant. By understanding the brain’s inherent ability to “unlearn” through mechanisms like Stentian plasticity, we can potentially develop strategies that promote the decoupling of traumatic memories from their physiological echoes. This could involve techniques that help individuals process and re-contextualise past experiences, thereby reducing the likelihood of triggers firing simultaneously with the original stress response and facilitating the “losing of the link” at a neural level.
This doesn’t negate the importance of Hebb’s rule in forming new, healthier associations. Rather, it suggests a more nuanced and dynamic model of brain plasticity. Healing from trauma and chronic stress may involve both the strengthening of new, adaptive neural pathways and the active weakening of maladaptive ones through mechanisms like Split-Second Unlearning. This dual mechanism, with the brain possessing an inherent “delete” function for outdated or harmful associations, offers a promising new lens through which to understand and treat a wide range of debilitating mental and physical health conditions. The discovery of Stentian plasticity provides a crucial piece of the puzzle in understanding the brain’s remarkable ability to learn, unlearn, adapt, and ultimately, to heal.
References
[i] Hebb, D. O. (1949). The organization of behavior: A neuropsychological theory. John Wiley & Sons
[ii] Rahman, A., Deister, C. A., Raval, M., Hokanson, K. C., Zhang, Y., Meabon, J. S., … & Cline, H. T. (2020). Stentian structural plasticity in the developing visual system. Proceedings of the National Academy of Sciences of the United States of America, 117(22), 12319–12329. https://doi.org/10.1073/pnas.2001107117
[iii] Hudson, M., & Johnson, M. I. (2021). Split-second unlearning: Developing a theory of psychophysiological dis-ease. Frontiers in Psychology, 12, 716535. https://doi.org/10.3389/fpsyg.2021.716535
[iv] Somaiya, R. D., & Feller, M. B. (2024). Visualizing synaptic pruning in the mammalian brain. Science, 385(6710), 711-712.
[v] Peters, A., McEwen, B. S., & Friston, K. (2017). Uncertainty and stress: Why it causes diseases and how it is mastered by the brain. Progress in Neurobiology, 156, 164–188. https://doi.org/10.1016/j.pneurobio.2017.05.004
