Key facts
- What it is
- The capacity of neural tissue to change structure and function with experience
- Main forms
- Synaptic strength, structural change in spines, cortical remapping, neurogenesis
- Guiding principle
- Hebb's rule (1949): repeated co-activation strengthens a connection
- Critical periods
- Windows of heightened plasticity; demonstrated in vision by Hubel and Wiesel
- It is lifelong
- But not unlimited: the adult brain is plastic, not infinitely malleable
- Brain training
- Improves the trained task; transfer to general ability is not supported
What neuroplasticity means
For much of the history of neuroscience the adult brain was considered essentially fixed. Santiago Ramón y Cajal, whose work founded the field, wrote in 1913 that in the adult centres the nerve paths are something fixed, ended, and immutable, and that everything may die, nothing may be regenerated. It was a reasonable conclusion from the evidence he had, and it was wrong.
Neuroplasticity is the umbrella term for the many ways in which nervous tissue changes with use. It is not one mechanism but a family of them, operating over timescales from milliseconds to years and at scales from a single synapse to an entire cortical map. What unites them is that experience leaves a physical trace, and that trace changes how the tissue subsequently behaves.
The word carries a great deal of unearned optimism in popular usage, and it is worth stating the boundary at the outset. Plasticity is real, it is lifelong, and it is constrained. The adult brain can learn a language, master an instrument, and partially reorganise around damage. It cannot rewrite its basic architecture, it cannot make you good at everything by drilling one thing, and it cannot regrow a destroyed cortex.
Plasticity: the ability of a system to be shaped by input and to retain that shape. In neuroscience the term covers functional change (a synapse becomes stronger) and structural change (a synapse is physically built or removed). The two are usually two views of the same event.
The forms of plasticity
Synaptic strength
The gain of an existing connection is turned up or down. Long-term potentiation strengthens synapses that are activated in the right pattern; long-term depression weakens those that are not. This is the fastest and best-understood form, and it is the cellular currency of learning.
Dendritic spines
Synapses are not just tuned; they are built and demolished. Two-photon imaging of the living cortex shows dendritic spines appearing, enlarging, shrinking, and disappearing over hours and days, with learning producing measurable increases in spine formation in the relevant cortex, and spines that survive predicting retained skill.
Cortical remapping
The functional map of the cortex is not fixed. When input from a body part is lost, neighbouring representations expand into the vacated territory; when a body part is used intensively, its representation grows. The somatosensory and motor maps are continuously renegotiated by use.
Adult neurogenesis
The generation of new neurons in the adult brain, principally in the dentate gyrus of the hippocampus. Robust in rodents. In adult humans it is genuinely disputed, with methodologically careful studies reaching opposite conclusions. See Neurogenesis for the state of that debate.
These are not independent. A synapse strengthened by LTP tends to enlarge structurally; enough structural change across a population shifts the map. Plasticity at one level is generally plasticity at every level, seen at a different magnification.
Hebb's principle, stated properly
The idea that organises all of this was set out by the Canadian psychologist Donald Hebb in The Organization of Behavior in 1949, long before anyone could observe a synapse changing. His formulation was careful:
Hebb's postulate: "When an axon of cell A is near enough to excite a cell B and repeatedly or persistently takes part in firing it, some growth process or metabolic change takes place in one or both cells such that A's efficiency, as one of the cells firing B, is increased."
The popular version, "cells that fire together, wire together", is a slogan coined decades later, and while it is a serviceable memory aid it drops two things Hebb was careful to include. First, causality and order: Hebb specified that A must take part in firing B, which means A must fire before B and contribute to it, not merely at the same time. Modern work on spike-timing-dependent plasticity confirms exactly this: if the presynaptic spike precedes the postsynaptic one by a few tens of milliseconds the synapse strengthens, and if the order is reversed it weakens. Simultaneity is not the criterion; predictive precedence is.
Second, Hebb proposed a physical growth process, not just a change in a number. He was right about that too, decades before the imaging existed to see it.
Hebb's rule is a principle rather than a complete theory. On its own it is unstable: connections that strengthen fire more, which strengthens them further, and the network saturates. Real circuits balance it with homeostatic mechanisms that scale synaptic weights as a whole, and with long-term depression, which weakens connections that fail the timing rule. Plasticity that only ever strengthens is not learning; it is a runaway feedback loop.
Critical and sensitive periods
The brain is not equally plastic at all times. During development there are windows in which particular circuits are unusually open to being shaped, and outside which the same experience has far less effect.
The definitive demonstration came from David Hubel and Torsten Wiesel, working on the visual cortex of kittens in the 1960s. In normal development, cells in visual cortex are driven by both eyes, arranged in interleaved ocular dominance columns. Hubel and Wiesel closed one eye of a kitten for a period during early life. When the eye was reopened, the animal was functionally blind in it: not because the eye was damaged, but because the cortical territory that would have served it had been taken over by the open eye. The columns had physically shifted. Critically, the same deprivation applied to an adult cat produced no such effect. The window had closed. Hubel and Wiesel shared the Nobel Prize in Physiology or Medicine in 1981 for this and related work.
The clinical parallel is direct. A child with an untreated cataract or a strabismus in one eye can develop permanent amblyopia, a loss of vision in a structurally healthy eye, if the problem is not corrected early. The same condition acquired in adulthood does not do this. It is the reason paediatric vision screening exists.
Most windows are better described as sensitive periods than strict critical periods: plasticity does not switch off, it declines. Second languages can be learned in adulthood, but native-like accent acquisition becomes markedly harder after childhood. Absolute pitch appears to depend on early musical exposure. The developmental picture is one of a gradient of closing doors, not a single slammed one.
Experience-dependent plasticity
The adult brain remains modifiable by sustained, demanding experience, and the structural signature is measurable.
The best-known human finding comes from Eleanor Maguire and colleagues, published in 2000. London licensed taxi drivers must pass "the Knowledge", a notoriously gruelling examination requiring them to hold the layout of some twenty-five thousand streets in mind and navigate between any two points without aids. Maguire's group scanned them and found that the posterior hippocampus was significantly larger in taxi drivers than in matched controls, and that its volume correlated with years spent driving a cab. The anterior hippocampus was correspondingly smaller.
Reading this result correctly: the original study was cross-sectional, so on its own it could not exclude the possibility that people with larger posterior hippocampi are simply more likely to become taxi drivers. Maguire's group addressed this directly in a later longitudinal study that scanned trainees before they began the Knowledge and again years later, comparing those who qualified with those who did not. Only the qualifiers showed the posterior hippocampal increase. That converts the finding from a correlation into good evidence that the training caused the change. Note also what the result does not say: their general memory was not superior, and they were somewhat worse than controls at learning new visuospatial information. The brain reallocated, it did not simply upgrade.
Comparable structural findings appear elsewhere. Professional musicians show differences in motor and auditory cortical structure that scale with training intensity, and juggling training produces transient grey-matter increases in visual motion areas that recede when practice stops. The general lesson is consistent, and it is a modest one: intensive, sustained, specific practice produces specific structural change in the circuits that do the work. Nothing in this literature supports the idea of a general upgrade.
Plasticity after injury, and its limits
After a stroke or a traumatic injury, some function typically returns. Part of that recovery is the resolution of swelling and the restoration of blood flow to tissue that was impaired but not destroyed. The remainder is plasticity: surviving regions, often in the perilesional cortex or the corresponding area of the opposite hemisphere, take on some of the lost function, and spared pathways are strengthened by use.
This is the rationale for intensive rehabilitation, and for approaches such as constraint-induced movement therapy, in which the unaffected limb is restrained so that the impaired one is forced into use. The principle is Hebbian: the circuits that are driven are the circuits that are strengthened, and an unused limb is a circuit that is not driven.
But the limits are real and should not be soft-pedalled. Cortical tissue that has died does not regenerate. Long axonal tracts in the central nervous system do not meaningfully regrow, which is why a complete spinal cord injury remains permanent. Recovery is generally greatest in the first weeks and months and then plateaus. And plasticity is not intrinsically benign: maladaptive plasticity is a real phenomenon, implicated in phantom limb pain following amputation, in focal dystonia in musicians who overtrain a movement, and in the entrenchment of chronic pain. A brain that changes with use will also faithfully encode a bad pattern.
The brain-training claims
"Neuroplasticity" has become the scientific fig leaf for an industry. The argument runs: the brain can change, therefore this app will change it, therefore you will become smarter. The first clause is true. The rest does not follow, and it has been tested.
Claim: brain-training games improve general cognitive ability.
In a large trial led by Adrian Owen and published in Nature in 2010, more than eleven thousand participants trained on cognitive tasks several times a week for six weeks. They got better at the tasks they trained on. On untrained tests of reasoning, memory, and general cognitive function, including tests closely related to the trained tasks, the trainers did no better than a control group that simply browsed the internet answering questions. In 2014 a group of around seventy cognitive psychologists and neuroscientists issued a consensus statement concluding there was no compelling scientific evidence that brain games reduce or reverse cognitive decline. Later regulatory action against several brain-training companies for unsubstantiated advertising claims followed the same reading of the evidence.
Claim: you can "rewire your brain" in thirty days with the right routine.
Rewiring is not a switch, and it is not general. Structural change follows sustained, effortful, specific practice, and it changes the circuits that do that practice. The taxi drivers spent years on the Knowledge to grow a posterior hippocampus that helped them navigate London and did not make them better at anything else. Any programme promising broad, rapid transformation is selling the word, not the finding.
Claim: the "far transfer" problem is just a matter of designing better games.
Far transfer, improvement on tasks unlike the trained one, is the thing that would make brain training worth doing, and it is precisely the thing that repeatedly fails to appear. Near transfer to very similar tasks is sometimes found; far transfer is not, and meta-analyses that control for active control groups and publication bias shrink the effects further. This is a robust pattern across decades, not a design flaw awaiting a fix.
None of this means practice is futile. It means practice is specific. If you want to be better at chess, play chess. If you want to be better at a language, use the language. The honest version of neuroplasticity is not a promise of unlimited transformation; it is a guarantee that whatever you actually do, repeatedly and with effort, is what your brain will get better at.
Sources
- Hebb DO. The Organization of Behavior: A Neuropsychological Theory. Wiley; 1949.
- Maguire EA, Gadian DG, Johnsrude IS, et al. Navigation-related structural change in the hippocampi of taxi drivers. Proceedings of the National Academy of Sciences. 2000;97(8):4398-4403.
- Owen AM, Hampshire A, Grahn JA, et al. Putting brain training to the test. Nature. 2010;465(7299):775-778.
This page is an educational reference. It is not medical advice and does not diagnose or treat any condition.