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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.
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).After neurotransmitters are synthesized, they are packaged and stored in vesicles.These vesicles are pooled together in terminal boutons of the presynaptic neuron.When ionotropic receptors are activated, certain ion species such as Na to enter the postsynaptic neuron, which depolarizes the postsynaptic membrane.If more of the same type of postsynaptic receptors are activated, then more Na will enter the postsynaptic membrane and depolarize cell.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.
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).
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..
As Na ions enter the cell, the membrane potential is further depolarized, and more voltage-gated sodium channels are activated.