Long term neuroplasticity refers to the sustained, enduring capacity of the central nervous system to reorganize its structure and function by forming new synaptic connections, strengthening existing ones, and even generating new neurons. This fundamental biological process is the basis for lasting learning, memory formation, and recovery from neurological insult. Unlike transient functional changes, long-term neuroplasticity involves structural modifications, including changes in dendritic spine density and axonal sprouting, which are crucial for cognitive longevity. Optimal hormonal signaling, particularly by estrogens and androgens, is essential for maintaining this adaptive capacity throughout the lifespan.
Origin
The term combines ‘neuro,’ relating to the nervous system, and ‘plasticity,’ derived from the Greek plastikos, meaning capable of being molded. The concept gained widespread acceptance in the late 20th century, challenging the older dogma that the adult brain was fixed and incapable of significant structural change. It is a core tenet of modern neuroscience and rehabilitation.
Mechanism
The process is fundamentally mediated by molecular signaling pathways that regulate gene expression and protein synthesis, leading to structural changes at the synapse. Key mechanisms include Long-Term Potentiation (LTP) and Long-Term Depression (LTD), which strengthen or weaken synaptic transmission, respectively. The release of neurotrophic factors, such as Brain-Derived Neurotrophic Factor (BDNF), is a critical driver, promoting the survival, differentiation, and growth of neurons and synapses.
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