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Plastic change often results from the alteration of the number of neurotransmitter receptors located on a synapse.

There are several underlying mechanisms that cooperate to achieve synaptic plasticity, including changes in the quantity of neurotransmitters released into a synapse and changes in how effectively cells respond to those neurotransmitters.

As the rising phase reaches its peak, voltage-gated Na channels are inactivated whereas voltage-gated K channels are activated, resulting in a net outward movement of K ions, which repolarizes the membrane potential towards the resting membrane potential.

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Neurons are diverse with respect to morphology and function.

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).

Several techniques such as intracellular recording, patch-clamp, and voltage-clamp technique, pharmacology, confocal imaging, molecular biology, two photon laser scanning microscopy and Ca2 imaging have been used to study activity at the cellular level.

Cellular neuroscience examines the various types of neurons, the functions of different neurons, the influence of neurons upon each other, how neurons work together.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.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 .When ionotropic receptors are activated, certain ion species such as Na to enter the postsynaptic neuron, which depolarizes the postsynaptic membrane.