Plasticity at the smallest scale
Brain plasticity is a broad term, and one way to make it concrete is to look at a single synapse, the junction where one neuron signals to another. At the synapse, the sending cell releases chemical messengers and the receiving cell responds through receptor proteins. How large that response is can go up or down depending on past activity. This changing efficiency is called synaptic plasticity, and it is considered one of the main cellular foundations of learning and memory. Larger-scale effects, including recovery after injury, are discussed in the article on rewiring the brain.
Cells that fire together
In 1949, the psychologist Donald Hebb proposed that when one cell repeatedly helps to fire another, the connection between them is strengthened. The idea has been summarized as cells that fire together wire together. It is a simplification, but it captured an enduring principle: connections reflect patterns of coincident activity.
Experimental support came later. In the early 1970s, researchers Tim Bliss and Terje Lomo reported that brief, high-frequency stimulation of a pathway in the rabbit hippocampus produced a lasting increase in the response of the receiving cells. This phenomenon, long-term potentiation, or LTP, became a leading model of how memory traces might be stored. A complementary process, long-term depression, or LTD, weakens synapses after other patterns of activity. The word depression here has no connection to the mood disorder; it just means a decrease in strength.
How strengthening seems to work
Details differ across brain regions, but some general features have been described, particularly in studies of the hippocampus.
- Receptors play a key role. One type of glutamate receptor, the NMDA receptor, acts like a coincidence detector: it opens only when the receiving cell is already active and the sending cell releases glutamate. This allows the synapse to register that the two cells were active together.
- Calcium acts as a trigger. Entry of calcium ions into the receiving cell starts chemical cascades that alter the synapse.
- Early and late changes. Early changes can include adding more receptors to the synapse or modifying existing ones, and they can last minutes to hours. Longer-lasting changes appear to require new protein production and can involve structural changes in the synapse.
- Weakening works in reverse. Different patterns of activity can lead to the removal of receptors and shrinking of connections.
These mechanisms are best characterized in experimental preparations such as brain slices and animals. Showing that the same processes underlie particular memories or skills in intact brains is more difficult, and researchers continue to test how closely lab models match real learning.
Why weakening matters
It would be a mistake to think plasticity is only about strengthening. If synapses only grew stronger, the system would saturate and lose the ability to discriminate. Weakening and pruning let the brain refine its wiring and forget what is not useful. During development, an initial overproduction of connections is followed by pruning, with those used often tending to be retained. A balance of strengthening, weakening and stability is thought to support both learning and reliable function. Forgetting and its causes at the behavioral level appear in the article on the forgetting curve.
Homeostasis: keeping things stable
Neurons also have mechanisms that adjust overall sensitivity to prevent activity from becoming too high or too low. This kind of regulation, often called homeostatic plasticity, helps keep networks in a workable range as individual synapses change. It is an active research topic, and details of how it interacts with learning are still being worked out.
Critical periods
During early development, some brain systems are especially sensitive to experience during limited windows called critical or sensitive periods. The best-known experimental evidence comes from research on vision by David Hubel and Torsten Wiesel in the 1960s. When one eye of a young kitten was kept closed during an early window, the brain’s visual areas became biased toward the open eye, and the effect was hard to reverse later. This helped explain why children with untreated problems such as a misaligned or cloudy eye in early life can have lasting vision difficulties, and why such problems are typically treated promptly.
Other abilities show sensitive periods too. Language is a commonly discussed case: those who learn a language in early childhood usually reach native-like fluency more reliably than those who start as adults, though the exact timing and strength of any window are debated, and adults can still learn languages to a high level. Researchers do not agree on how strictly the term critical period should apply to human language and other cognitive abilities, and many prefer the softer term sensitive period.
Studies in animals suggest that the end of a critical period involves molecular brakes, such as changes in inhibitory circuits and the structures around neurons, and that under some conditions these brakes can be partly released. This is intriguing, but it is research in progress and has not yielded established treatments for people.
Limits and cautions
- Most mechanistic knowledge is from animals and laboratory tissue.
- Strengthening a synapse is only one component of how memories are thought to be stored; circuits and networks matter as well.
- Plasticity can contribute to unhelpful outcomes as well as helpful ones.
- Claims that a supplement or device can boost synaptic plasticity and thereby learning should be treated cautiously unless backed by solid human evidence.
The bigger picture
Synaptic plasticity connects the molecular and behavioral levels: practice changes activity, activity changes synapses, and changed synapses change future activity. This loop, along with the larger question of how adult experience reshapes the brain, is part of what the discussion of new perspectives on the brain describes as a shift from a fixed to an adaptable organ.