Summary
Neurons have charged membranes because there are different concentrations of ions inside and outside of the cell. Voltage-gated ion channels control the movement of ions into and out of a neuron. When a neuronal membrane is depolarized to at least the threshold of excitation, an action potential is fired. The action potential is then propagated along a myelinated axon to the axon terminals. In a chemical synapse, the action potential causes release of neurotransmitter molecules into the synaptic cleft.
Through binding to postsynaptic receptors, the neurotransmitter can cause excitatory or inhibitory postsynaptic potentials by depolarizing or hyperpolarizing, respectively, the postsynaptic membrane. In electrical synapses, the action potential is directly communicated to the postsynaptic cell through gap junctions—large channel proteins that connect the pre-and postsynaptic membranes. Synapses are not static structures and can be strengthened and weakened. Two mechanisms of synaptic plasticity are long-term potentiation and long-term depression.
Glossary
action potential
self-propagating momentary change in the electrical potential of a neuron (or muscle) membrane
depolarization
change in the membrane potential to a less negative value
excitatory postsynaptic potential (EPSP)
depolarization of a postsynaptic membrane caused by neurotransmitter molecules released from a presynaptic cell
hyperpolarization
change in the membrane potential to a more negative value
inhibitory postsynaptic potential (IPSP)
hyperpolarization of a postsynaptic membrane caused by neurotransmitter molecules released from a presynaptic cell
long-term depression (LTD)
prolonged decrease in synaptic coupling between a pre- and postsynaptic cell
long-term potentiation (LTP)
prolonged increase in synaptic coupling between a pre-and postsynaptic cell
membrane potential
difference in electrical potential between the inside and outside of a cell
refractory period
period after an action potential when it is more difficult or impossible for an action potential to be fired; caused by inactivation of sodium channels and activation of additional potassium channels of the membrane
saltatory conduction
“jumping” of an action potential along an axon from one node of Ranvier to the next
summation
process of multiple presynaptic inputs creating EPSPs around the same time for the postsynaptic neuron to be sufficiently depolarized to fire an action potential
synaptic cleft
space between the presynaptic and postsynaptic membranes
synaptic vesicle
spherical structure that contains a neurotransmitter
threshold of excitation
level of depolarization needed for an action potential to fire