Neurons have 3 different kinds of potentials - resting, graded, and the action potential. The neuron maintains a resting potential of -70 mV due to differences in permeability of ions on either side of its cell membrane, as well as the sodium potassium pump. The ions contributing to the charges on either side of the membrane are proteins, chloride, sodium, and potassium.
Several kinds of channels found in cell membranes, allowing for the transport of substances from one side to the other. Two kinds are important for action potentials - leaky channels and voltage-gated channels. Leaky channels allow the free flow of substances through them. Voltage-gated channels only open at certain voltages.
Back to the ions - chloride and the proteins stay put. However, the neuron has leaky sodium and potassium channels. These are always open and allow flux of these ions.
There’s a lot more potassium in the cell than outside the cell. The potassium wants to rush out because of the chemical gradient but wants to stay in the cell because of the electrical gradient. Similarly, there is a lot more sodium outside the cell than in it, and it has its own electrochemical gradient.
A graded potential is a change in potential that can vary in size, with magnitude depending on the intensity of the stimulus, and occurs when the neurons get excitatory post-synaptic potentials or inhibitory post-synaptic potentials.
Dendrites are a neuron’s input zone. The neuron cell body is like a calculator, integrating these signals. When the summation of graded potentials results in a potential of -55 mV at the axon hillock, an action potential occurs. Hence, EPSPs make it more likely that an action potential will occur, while IPSPs make it less likely. Unlike graded potentials, which are changes in potential varying in size, action potentials are all or nothing. More intense stimuli simply mean a higher frequency of firing.
At resting potential, voltage-gated sodium and potassium channels are closed. A stimulus causes some voltage-gated sodium channels to open. Once we get to the threshold of -55 mV, the action potential begins, with lots of other voltage-gated sodium channels opening. With sodium channels open, depolarization occurs - sodium rapidly rushes into the cell, and the voltage soars up to +30 mV, at which point the voltage-gated sodium channels close. Potassium channels now open, as repolarization occurs as potassium rapidly rushes out of the cell. The voltage zooms down and overshoots the -70 mV before the potassium channels can close. Finally, the sodium potassium pump restores the resting membrane potential. It does a conformational change thanks to an ATP molecule being hydrolysed. Again, this conformational change results in 3 sodium atoms being shuttled out of the cell, and two potassium atoms being shuttled in.
We’ve now seen what happens locally at one segment of the axon, but how does the action potential propagate? Well, when the sodium ions are rushing in during depolarization, they repel each other and so they spread out. This makes the next section of the axon reach threshold and also have an action potential. Why doesn’t the action potential travel backwards though? At the same time as the first section is depolarizing, the section of axon behind it is experiencing repolarization, and the potassium rushing out results in a refractory period. There is an absolute and relative refractory period. During the absolute refractory period, which coincides with most of the action potential’s duration, you can’t trigger another action potential, because the sodium channels are briefly inactivated - the membrane needs to be hyperpolarized before that can happen. During the relative refractory period, only a very strong stimulus can cause an action potential, since the membrane is below the resting potential and you need a stronger EPSP to get to threshold.
Another important point - action potential propagation is slow. That’s why most of your neurons have myelin sheaths, with are rich in lipids. Myelin sheaths are made by oligodendrocytes in the central nervous system and schwann cells in the peripheral nervous system. They insulate the axon and prevent leakage of charged ions. Instead, you get what’s called “saltatory conduction”, in which action potentials only occur in the spaces between the myelin, called “nodes of Ranvier”. In addition to myelin sheaths, neurons with larger diameters also have faster transmission speeds.
Once the action potential reaches the end of the axon, there are terminal buttons there. The depolarization triggers the opening of voltage-gated calcium channels on the presynaptic membrane, and calcium rushes into the terminal button. This causes exocytosis of vesicles full of neurotransmitter molecules, and neurotransmitter is released into the synaptic cleft, where the neurotransmitters attach to the receptors.