NEUROPLASTICITY: BIOCHEMICAL AND NEUROPHYSIOLOGICAL ASPECTS

Facilitation, depression, and posttanic potentiation may briefly modify synaptic transmission but cannot provide the basis for memories or other manifestations of behavioral plasticity that persist for months, weeks, or years. Some patterns of synaptic activity in the central nervous system produce a prolonged increase in synaptic strength known as long-term potentiation (PLP), while other patterns of activity cause a prolonged decrease in synaptic strength, known as long-term depression.

• Neural modulation of intracellular signaling (dependent on neurotrophic factors and protein kinases) • Synaptic plasticity (modulation of basal transmission, denervation hypersensitivity, activity-dependent synaptic unmasking, dendritic sprouts) • Axonal and dendritic shoots of uninjured collaterals • Axonal regeneration (genetic expression of remodeling proteins, modulation of factors neurotrophic)

• Recovery of neuronal excitability (cellular and axonal ionic balance, reabsorption of edema and hematic debris, transynaptic reverse diaschisis). • Activity in partially undamaged neural pathways. • Representational plasticity with type neurons assemble. • Recruitment of not ordinarily active parallel networks. • Recruitment of subcomponents in networks distributed. • Modulation of the excitability of subnets by neurotransmitters.

Neuroplasticity is the flexibility of the brain to adapt to changes through neural networks. Every time something is learned, the neurons themselves form networks to communicate and give signals to one another, through synapses. When what has been learned is practiced, communications between these neurons improve, which facilitates the best development of tasks.