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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.
It is both the growth of new branches or extensions from existing neurons in response to injury or disease. This process is a form of neuroplasticity, which allows the brain to rewire itself and adapt to changes in the environment. Neural sprouting is thought to play an important role in recovery from brain injury, where the brain compensates ...
[1] [2] Activity-dependent plasticity is a form of neuroplasticity that arises from intrinsic or endogenous activity, as opposed to forms of neuroplasticity that arise from extrinsic or exogenous factors, such as electrical brain stimulation- or drug-induced neuroplasticity. [1]
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.
Neuroplasticity is the process by which neurons adapt to a disturbance over time, and most often occurs in response to repeated exposure to stimuli. [27] Aerobic exercise increases the production of neurotrophic factors [note 1] (e.g., BDNF, IGF-1, VEGF) which mediate improvements in cognitive functions and various forms of memory by promoting blood vessel formation in the brain, adult ...
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 ...
[1] [2] [3] This phenomenon is a result of neuroplasticity, including Hebbian learning [4] [5] and synaptic pruning. [2] Through these mechanisms, neural pathways that are more consistently used are strengthened, making them more efficient, while those pathways that are unused become less efficient.
STDP is a form of neuroplasticity in which a millisecond-scale change in the timing of presynaptic and postsynaptic spikes will cause differences in postsynaptic Ca 2+ signals, inducing either LTP or LTD. LTD occurs when postsynaptic spikes precede presynaptic spikes by up to 20-50 ms. [24]