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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.
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.Some neurons such as photoreceptor cells, for example, do not have myelinated axons that conduct action potentials.Other unipolar neurons found in invertebrates do not even have distinguishing processes such as dendrites.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.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 .
After neurotransmitters are synthesized, they are packaged and stored in vesicles.
These vesicles are pooled together in terminal boutons of the presynaptic neuron.
Moreover, the distinctions based on function between neurons and other cells such as cardiac and muscle cells are not helpful.
Thus, the fundamental difference between a neuron and a nonneuronal cell is a matter of degree.
When ionotropic receptors are activated, certain ion species such as Na to enter the postsynaptic neuron, which depolarizes the postsynaptic membrane.