Neuroplasticity
The brain's ability to reorganise its structure and connections throughout life, underlying learning, memory, and recovery from injury. Neuroplasticity involves synaptic strengthening/weakening, dendritic remodelling, and limited neurogenesis. Neurotrophic factors such as BDNF are key regulators.
Technical Context
Neuroplasticity mechanisms: synaptic plasticity (LTP — strengthening of synaptic connections through repeated activation, mediated by NMDA receptor-dependent calcium influx → CaMKII activation → AMPA receptor insertion; LTD — weakening of connections through low-frequency stimulation → phosphatase activation → AMPA receptor removal), structural plasticity (dendritic spine growth/retraction — new spines form at sites of potentiated synapses, providing structural basis for memory), adult neurogenesis (new neurons generated in hippocampal dentate gyrus and subventricular zone — exercise, learning, and enriched environments promote neurogenesis; stress and ageing reduce it), and large-scale cortical reorganisation (remapping of cortical representations after injury or training). BDNF is a key molecular mediator of neuroplasticity — it promotes LTP, dendritic growth, neuronal survival, and neurogenesis. Exercise increases BDNF levels and enhances neuroplasticity, partly explaining the cognitive benefits of physical activity.