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.
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.
Thus, not all neurons correspond to the stereotypical motor neuron with dendrites and myelinated axons that conduct action potentials.
Some neurons such as photoreceptor cells, for example, do not have myelinated axons that conduct action potentials.
Repolarization of the membrane potential continues, resulting in an undershoot phase or absolute refractory period.
The undershoot phase occurs because unlike voltage-gated sodium channels, voltage-gated potassium channels inactivate much more slowly.
Cellular neuroscience examines the various types of neurons, the functions of different neurons, the influence of neurons upon each other, how neurons work together.
When ionotropic receptors are activated, certain ion species such as Na to enter the postsynaptic neuron, which depolarizes the postsynaptic membrane.
Although slower than ionotropic receptors that function as on-and-off switches, metabotropic receptors have the advantage of changing the cell's responsiveness to ions and other metabolites, examples being gamma amino-butyric acid (inhibitory transmitter), glutamic acid (excitatory transmitter), dopamine, norepinephrine, epinephrine, melanin, serotonin, melatonin, and substance P.