Basic mechanism of neuroplasticity

Abstract

Neuroplasticity, a concept recognised about 50 years ago, is now considered the core mechanism of brain function. Neuroplasticity is defined as a durable change in the way neurons respond to a stimulus. At the cellular level, synaptic plasticity is the leading mechanism of modification of synaptic strength, operating via long-term potentiation and long-term depression. It operates according to Hebb’s principle of simultaneous activation of preand postsynaptic neurons. Synaptic plasticity leads to structural changes of synapses, dendritic spines, and axonal modifications. An additional form of plasticity, homeostatic plasticity, changes neuronal reactivity in a less specific way, in response to intensive input or input elimination. On a macroscopic level, neuroplasticity modifies neural pathways, strengthening those with strong and correlated activity. In a developing brain, neuroplasticity serves developmental adjustments triggered by external stimuli and allows learning. In an adult brain, neuroplastic changes are the basis of learning and memory, i.e. formation of new neuronal circuits dedicated to the memory engram. Such changes also underlie modifications of sensory and motor representations by activity or by denervation. Neuroplasticity in brain repair after stroke acts via coordination of activation of weak connections, axonal sprouting, and synaptogenesis, which can result in functional recovery of lost abilities – motor, sensory, and cognitive.