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03-Dec-2016 12:59

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).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 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.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.

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The neurotransmitters then diffuse across the synaptic cleft and bind to postsynaptic receptors embedded on the postsynaptic membrane of another neuron.Cellular neuroscience is the study of neurons at a cellular level.