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The Hodgkin–Huxley model of an action potential in the squid giant axon has been the basis for much of the current understanding of the ionic bases of action potentials.Briefly, the model states that the generation of an action potential is determined by two ions: Na and K .An action potential can be divided into several sequential phases: threshold, rising phase, falling phase, undershoot phase, and recovery.Following several local graded depolarizations of the membrane potential, the threshold of excitation is reached, voltage-gated sodium channels are activated, which leads to an influx of Na ions.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).Cellular neuroscience is the study of neurons at a cellular level.

Thus, not all neurons correspond to the stereotypical motor neuron with dendrites and myelinated axons that conduct action potentials.

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).

Once bounded with Ca2 , the vesicles dock and fuse with the presynaptic membrane, and release neurotransmitters into the synaptic cleft by a process known as exocytosis.

The neurotransmitters then diffuse across the synaptic cleft and bind to postsynaptic receptors embedded on the postsynaptic membrane of another neuron.

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