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As Na ions enter the cell, the membrane potential is further depolarized, and more voltage-gated sodium channels are activated.
Such a process is also known as a positive feedback loop.
This includes morphology and physiological properties of single neurons.
In neuroscience, synaptic plasticity is the ability of synapses to strengthen or weaken over time, in response to increases or decreases in their activity.
Since memories are postulated to be represented by vastly interconnected networks of synapses in the brain, synaptic plasticity is one of the important neurochemical foundations of learning and memory (see Hebbian theory).
Synaptic plasticity in both excitatory and inhibitory synapses has been found to be dependent upon postsynaptic calcium release Two molecular mechanisms for synaptic plasticity (researched by the Eric Kandel laboratories) 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 Ca2 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 displaces the magnesium ions that block NMDA ion channels and allows calcium ions to enter a cell – probably causing LTP, while weaker depolarization only partially displaces the Mg2 ions, resulting in less Ca2 entering the post-synaptic neuron and lower intracellular Ca2 concentrations (which activate protein phosphatases and induce long-term depression, LTD).