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.
After neurotransmitters are synthesized, they are packaged and stored in vesicles.
These vesicles are pooled together in terminal boutons of the presynaptic neuron.
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.
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.
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 .
Metabotropic receptors on the other hand activate second messenger cascade systems that result in the opening of ion channel located some place else on the same postsynaptic membrane.