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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).The undershoot phase occurs because unlike voltage-gated sodium channels, voltage-gated potassium channels inactivate much more slowly.Nevertheless, as more voltage-gated K channels become inactivated, the membrane potential recovers to its normal resting steady state..
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.Cellular neuroscience is the study of neurons at a cellular level.This includes morphology and physiological properties of single neurons.When there is a change in voltage in the terminal bouton, voltage-gated calcium channels embedded in the membranes of these boutons become activated.
These allow Ca2 ions to diffuse through these channels and bind with synaptic vesicles within the terminal boutons.
There are two families of receptors: ionotropic and metabotropic receptors.