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The pruning that is associated with learning is known as small-scale axon terminal arbor pruning. Axons extend short axon terminal arbors toward neurons within a target area. Certain terminal arbors are pruned by competition. The selection of the pruned terminal arbors follow the "use it or lose it" principle seen in synaptic plasticity. This ...
Activity-dependent plasticity is a form of functional and structural neuroplasticity that arises from the use of cognitive functions and personal experience. [1] Hence, it is the biological basis for learning and the formation of new memories.
The principles of STDP can be utilized in the training of artificial spiking neural networks. Using this approach the weight of a connection between two neurons is increased if the time at which a presynaptic spike ( t p r e {\displaystyle t_{pre}} ) occurs is shortly before the time of a post synaptic spike( t p o s t {\displaystyle t_{post ...
Humans have varying degrees of neuroplasticity due to their genetic makeups, which affects their ability to adapt to conditions in their environments and effectively learn from experiences. [1] The degree to which intelligence test scores can be linked to genetic heritability increases with age. There is presently no explanation for this ...
Neuroplasticity, also known as neural plasticity or just plasticity, is the ability of neural networks in the brain to change through growth and reorganization. Neuroplasticity refers to the brain's ability to reorganize and rewire its neural connections, enabling it to adapt and function in ways that differ from its prior state.
The hippocampus regulates memory function. Memory improvement is the act of enhancing one's memory. Factors motivating research on improving memory include conditions such as amnesia, age-related memory loss, people’s desire to enhance their memory, and the search to determine factors that impact memory and cognition.
Despite the common use of Hebbian models for long-term potentiation, Hebb's principle does not cover all forms of synaptic long-term plasticity. Hebb did not postulate any rules for inhibitory synapses, nor did he make predictions for anti-causal spike sequences (presynaptic neuron fires after the postsynaptic neuron).
Two molecular mechanisms for synaptic plasticity involve the NMDA and AMPA glutamate receptors. Opening of NMDA channels (which relates to the level of cellular depolarization) leads to a rise in post-synaptic Ca 2+ concentration and this has been linked to long-term potentiation, LTP (as well as to protein kinase activation); strong depolarization of the post-synaptic cell completely ...