Neuroplasticity: The latest BUZZ word
Neuroplasticity has become one of those words that gets tossed around everywhere, from wellness blogs to neuroscience labs to psychedelic therapy retreats.
At its core, neuroplasticity simply means the brain’s resilience and ability to change: to form new connections, reorganize old ones, and adapt in response to experience, learning, or injury.
Neuroplasticity is present throughout life, with heightened sensitivity during critical periods of development, but remains active in adulthood, supporting adaptation, recovery, and learning. While the word is often used as a catch-all for brain “healing,” the science is far more nuanced.
Not All Neuroplasticity Is Equal
Neuroplasticity isn’t a monolithic process. Different drugs, therapies, and activities can induce different forms of plasticity: structural, functional, or synaptic. Exercise, meditation, cognitive behavioral therapy, music training, and, yes, even SSRIs all have neuroplastic effects (Pittenger & Duman, 2008; Draganski et al., 2004). For example, stroke rehabilitation relies on targeted training to rewire motor circuits, while antidepressants promote dendritic growth and synaptogenesis in mood-related brain regions.
Adaptive neuroplasticity underlies beneficial changes such as skill acquisition, memory formation, and recovery after brain injury, while maladaptive plasticity can contribute to chronic pain, dystonia, or epilepsy.
Where psychedelics stand out is in the magnitude and openness of plasticity they induce. Psychedelics such as psilocybin, LSD, and MDMA (in “the family” of psychedelics) have been shown to rapidly promote dendritic spine growth, synapse formation, and neural flexibility (Ly et al., 2018). More compelling is the work of Dr. Gül Dölen at Johns Hopkins, who has demonstrated that psychedelics may reopen “critical periods” in the brain, windows of heightened plasticity typically limited to early development (Nardou et al., 2019). In animal models, MDMA reactivated social learning periods long thought closed, suggesting that psychedelics may unlock modes of learning and adaptation unavailable with other interventions.
Homeostatic plasticity acts as the brain’s stabilizing force, maintaining a balance between excitation and inhibition across neuronal networks (Pozo & Goda, 2010; Chen et al., 2022). When this balance fails, it contributes to disorders such as epilepsy, schizophrenia, Alzheimer’s disease, and even chronic pain, where local circuits become persistently misregulated (Lepeta et al., 2016; Meftah & Gan, 2023; Thapa et al., 2021). Therapeutic strategies are emerging, from pharmacological agents targeting NMDA receptors to factors influencing synaptic scaling, that seek to restore this equilibrium (Nicosia et al., 2024; Wu et al., 2023).
Structural plasticity refers to the brain’s ability to physically reshape itself by forming new synapses, branching dendrites, and pruning away unused connections (Leuner & Gould, 2010; Kolb & Gibb, 2011). These changes can be highly adaptive—for example, learning a musical instrument increases dendritic complexity in motor regions, refining movement and coordination (Schlaug, 2001). But the same processes can become maladaptive: drugs like cocaine drive abnormal synapse growth in reward circuits, reinforcing addiction (Nestler & Lüscher, 2019). Pruning, too, is a double-edged sword. Normally it sharpens neural networks by eliminating weak connections, yet excessive pruning has been implicated in disorders like schizophrenia (Howes & Onwordi, 2023). Structural plasticity also plays a vital role in recovery: after stroke, neurons near damaged areas sprout new connections to restore lost functions (Campos et al., 2023). Advances in imaging, such as two-photon microscopy, now allow researchers to observe these structural changes in real time, though applying this knowledge clinically remains challenging due to the complexity and cost of such technologies (Murphy, 2015; Ayaz et al., 2022).
Neuronal plasticity is the overarching concept, while synaptic plasticity is a key mechanism within it, focused on changes at the synapse level.
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Neuronal plasticity describes how individual neurons adjust their properties in response to experience, learning, or environmental change (von Bernhardi et al., 2017). This happens in two main ways: through intrinsic plasticity, where a neuron alters its own excitability and responsiveness, and through network-level plasticity, where groups of neurons reorganize their connections and activity patterns (Oberman & Pascual-Leone, 2013; Stampanoni Bassi et al., 2019). Together, these processes allow neurons not only to fine-tune their own activity but also to integrate into broader functional networks, supporting learning, memory, and recovery after brain injury (Chen & Nedivi, 2010; Wenger et al., 2021). Yet, when dysregulated, neuronal plasticity can backfire, contributing to conditions such as epilepsy, addiction, and psychiatric disorders (Cramer et al., 2011; Marzola et al., 2023). Synaptic plasticity is a specific subtype of neuronal plasticity, referring to activity-dependent changes in the strength or efficacy of synaptic transmission between neurons. It involves molecular and cellular mechanisms such as neurotransmitter release, receptor trafficking, and structural remodeling of synapses, and is considered the primary mechanism underlying learning and memory (Kennedy MB., 2013).
Can it really be measured?
Measuring neuroplasticity remains a challenge. Researchers typically rely on indirect markers such as changes in cortical thickness or connectivity on MRI, electrophysiological measures like long-term potentiation (LTP) and EEG patterns, or behavioral outcomes such as improved learning or motor recovery. Yet, these approaches capture only fragments of the larger picture. Current research emphasizes the need for improved biomarkers,molecular, imaging, and physiological, that can reliably track plasticity in humans. Such advances are essential for translating laboratory findings into clinical strategies, particularly in fields like neurorehabilitation and neurodevelopmental disorders (Zatorre et al., 2012; Grefkes & Fink, 2011).
The opportunity
The hype around neuroplasticity often makes it sound like a cure-all. In reality, plasticity is value-neutral; it can strengthen maladaptive pathways as easily as beneficial ones. The question is not whether a therapy induces plasticity, but how it is directed and integrated. This is why pairing psychedelics with structured therapy, or exercise with rehabilitation, matters so deeply. Without context, plasticity can reinforce the very patterns we are trying to change.
So yes, psychedelics may represent the most powerful tools we currently have for inducing broad, rapid, and therapeutically useful neuroplasticity. But they are part of a larger landscape: antidepressants, behavioral therapies, physical exercise, stimulating conversation, learning new information, and even contemplative practices all sculpt the brain in measurable ways.
Neuroplasticity is the language of how the brain learns and adapts. The key is harnessing it wisely.
References:
Draganski, B. et al. (2004). Neuroplasticity: Changes in grey matter induced by training. Nature, 427, 311–312.
Ly, C. et al. (2018). Psychedelics promote structural and functional neural plasticity. Cell Reports, 23(11), 3170–3182.
Nardou, R., et al. (2019). Oxytocin-dependent reopening of a social reward learning critical period with MDMA. Nature, 569, 116–120.
Pittenger, C., & Duman, R. (2008). Stress, depression, and neuroplasticity: A convergence of mechanisms. Neuropsychopharmacology, 33, 88–109.
Nardou, R., Lewis, E. M., Rothhaas, R., Xu, R., Yang, A., Boyden, E., & Dölen, G. (2019). Oxytocin-dependent reopening of a social reward learning critical period with MDMA. Nature, 569(7754), 116-120. DOI:10.1038/s41586-019-1075-9
Nardou, R., Sawyer, E., Song, Y. J., Wilkinson, M., Padovan-Hernandez, Y., de Deus, J. L., Wright, N., Lama, C., … & Dölen, G. (2023). Psychedelics reopen the social reward learning critical period. Nature, 618, 790-798. DOI:10.1038/s41586-023-06204-3
The Neuroplastic Brain: Current Breakthroughs and Emerging Frontiers. Gazerani P.Brain Research. 2025;1858:149643. doi:10.1016/j.brainres.2025.149643.
Harnessing Neuroplasticity for Clinical Applications. Cramer SC, Sur M, Dobkin BH, et al.
Brain : A Journal of Neurology. 2011;134(Pt 6):1591-609. doi:10.1093/brain/awr039.
Cerebral Plasticity: Windows of Opportunity in the Developing Brain.Ismail FY, Fatemi A, Johnston MV. European Journal of Paediatric Neurology : EJPN : Official Journal of the European Paediatric Neurology Society. 2017;21(1):23-48. doi:10.1016/j.ejpn.2016.07.007.
Synaptic Signaling in Learning and Memory. Kennedy MB. Cold Spring Harbor Perspectives in Biology. 2013;8(2):a016824. doi:10.1101/cshperspect.a016824.
Cerebral Plasticity as the Basis for Upper Limb Recovery Following Brain Damage. Lotze M, Ladda AM, Stephan KM. Neuroscience and Biobehavioral Reviews. 2019;99:49-58. doi:10.1016/j.neubiorev.2019.01.027.
The Times They Are a-Changin': A Proposal on How Brain Flexibility Goes Beyond the Obvious to Include the Concepts of "Upward" and "Downward" to Neuroplasticity. Diniz CRAF, Crestani AP. Molecular Psychiatry. 2023;28(3):977-992. doi:10.1038/s41380-022-01931-x.
The Combined Influences of Exercise, Diet and Sleep on Neuroplasticity. Pickersgill JW, Turco CV, Ramdeo K, et al. Frontiers in Psychology. 2022;13:831819. doi:10.3389/fpsyg.2022.831819.
Environment and Brain Plasticity: Towards an Endogenous Pharmacotherapy. Sale A, Berardi N, Maffei L. Physiological Reviews. 2014;94(1):189-234. doi:10.1152/physrev.00036.2012.
The pons, a region involved in movement and implicated in consciousness.
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