Spine plasticity is implicated in motivation, learning, and memory.
In particular, long-term memory is mediated in part by the growth of new dendritic spines (or the enlargement of pre-existing spines) to reinforce a particular neural pathway.
Because dendritic spines are plastic structures whose lifespan is influenced by input activity, spine dynamics may play an important role in the maintenance of memory over a lifetime.

Age-dependent changes in the rate of spine turnover suggest that spine stability impacts developmental learning.
In youth, dendritic spine turnover is relatively high and produces a net loss of spines.
This high rate of spine turnover may characterize critical periods of development and reflect learning capacity in adolescence—different cortical areas exhibit differing levels of synaptic turnover during development, possibly reflecting varying critical periods for specific brain regions.
In adulthood, however, most spines remain persistent, and the half-life of spines increases.
This stabilization occurs due to a developmentally regulated slow-down of spine elimination, a process which may underlie the stabilization of memories in maturity.

Experience-induced changes in dendritic spine stability also point to spine turnover as a mechanism involved in the maintenance of long-term memories, though it is unclear how sensory experience affects neural circuitry.
Two general models might describe the impact of experience on structural plasticity.
On the one hand, experience and activity may drive the discrete formation of relevant synaptic connections that store meaningful information in order to allow for learning.
On the other hand, synaptic connections may be formed in excess, and experience and activity may lead to the pruning of extraneous synaptic connections.

In lab animals of all ages, environmental enrichment has been related to dendritic branching, spine density, and overall number of synapses.
In addition, skill training has been shown to lead to the formation and stabilization of new spines while destabilizing old spines, suggesting that the learning of a new skill involves a rewiring process of neural circuits.
Since the extent of spine remodeling correlates with success of learning, this suggests a crucial role of synaptic structural plasticity in memory formation.
In addition, changes in spine stability and strengthening occur rapidly and have been observed within hours after training.

Conversely, while enrichment and training are related to increases in spine formation and stability, long-term sensory deprivation leads to an increase in the rate of spine elimination and therefore impacts long-term neural circuitry.
Upon restoring sensory experience after deprivation in adolescence, spine elimination is accelerated, suggesting that experience plays an important role in the net loss of spines during development.
In addition, other sensory deprivation paradigms—such as whisker trimming—have been shown to increase the stability of new spines.

Research in neurological diseases and injuries shed further light on the nature and importance of spine turnover.
After stroke, a marked increase in structural plasticity occurs near the trauma site, and a five- to eightfold increase from control rates in spine turnover has been observed.
Dendrites disintegrate and reassemble rapidly during ischemia—as with stroke, survivors showed an increase in dendritic spine turnover.
While a net loss of spines is observed in Alzheimer's disease and cases of intellectual disability, cocaine and amphetamine use have been linked to increases in dendritic branching and spine density in the prefrontal cortex and the nucleus accumbens.
Because significant changes in spine density occur in various brain diseases, this suggests a balanced state of spine dynamics in normal circumstances, which may be susceptible to disequilibrium under varying pathological conditions.

There is also some evidence for loss of dendritic spines as a consequence of aging.
 One study using mice has noted a correlation between age-related reductions i
Spine plasticity is implicated in motivation, learning, and memory. In particular, long-term memory is mediated in part by the growth of new dendritic spines (or the enlargement of pre-existing spines) to reinforce a particular neural pathway. Because dendritic spines are plastic structures whose lifespan is influenced by input activity, spine dynamics may play an important role in the maintenance of memory over a lifetime.
Age-dependent changes in the rate of spine turnover suggest that spine stability impacts developmental learning. In youth, dendritic spine turnover is relatively high and produces a net loss of spines. This high rate of spine turnover may characterize critical periods of development and reflect learning capacity in adolescence—different cortical areas exhibit differing levels of synaptic turnover during development, possibly reflecting varying critical periods for specific brain regions. In adulthood, however, most spines remain persistent, and the half-life of spines increases. This stabilization occurs due to a developmentally regulated slow-down of spine elimination, a process which may underlie the stabilization of memories in maturity.
Experience-induced changes in dendritic spine stability also point to spine turnover as a mechanism involved in the maintenance of long-term memories, though it is unclear how sensory experience affects neural circuitry. Two general models might describe the impact of experience on structural plasticity. On the one hand, experience and activity may drive the discrete formation of relevant synaptic connections that store meaningful information in order to allow for learning. On the other hand, synaptic connections may be formed in excess, and experience and activity may lead to the pruning of extraneous synaptic connections.
In lab animals of all ages, environmental enrichment has been related to dendritic branching, spine density, and overall number of synapses. In addition, skill training has been shown to lead to the formation and stabilization of new spines while destabilizing old spines, suggesting that the learning of a new skill involves a rewiring process of neural circuits. Since the extent of spine remodeling correlates with success of learning, this suggests a crucial role of synaptic structural plasticity in memory formation. In addition, changes in spine stability and strengthening occur rapidly and have been observed within hours after training.
Conversely, while enrichment and training are related to increases in spine formation and stability, long-term sensory deprivation leads to an increase in the rate of spine elimination and therefore impacts long-term neural circuitry. Upon restoring sensory experience after deprivation in adolescence, spine elimination is accelerated, suggesting that experience plays an important role in the net loss of spines during development. In addition, other sensory deprivation paradigms—such as whisker trimming—have been shown to increase the stability of new spines.
Research in neurological diseases and injuries shed further light on the nature and importance of spine turnover. After stroke, a marked increase in structural plasticity occurs near the trauma site, and a five- to eightfold increase from control rates in spine turnover has been observed. Dendrites disintegrate and reassemble rapidly during ischemia—as with stroke, survivors showed an increase in dendritic spine turnover. While a net loss of spines is observed in Alzheimer's disease and cases of intellectual disability, cocaine and amphetamine use have been linked to increases in dendritic branching and spine density in the prefrontal cortex and the nucleus accumbens. Because significant changes in spine density occur in various brain diseases, this suggests a balanced state of spine dynamics in normal circumstances, which may be susceptible to disequilibrium under varying pathological conditions.
There is also some evidence for loss of dendritic spines as a consequence of aging.  One study using mice has noted a correlation between age-related reductions i
Dendritic spine