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I am trying to understand the mechanisms underlying action potential generation on the cellular level.

Typically, there is an emphasis on voltage-dependent permeability changes of Potassium (K+) and Sodium (Na+) channels which lead to the respective changes of the membrane potential.

Also typically, synapses in the brain are chemical synapses (in contrast to the smaller fraction of electrical synapses, e.g. in the hippocampus, which make use of gap junctions for signal transmission).

My confusion is now this: Chemical synapses depend on neurotransmitters to trigger permeability changes. The canonical explanation of action potentials is with reference to voltage-gated channels -- how do these two things go together?

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  • $\begingroup$ Have you learned about what neurotransmitters bind to? $\endgroup$
    – Bryan Krause is on strike ♦
    Jul 14, 2019 at 21:39
  • $\begingroup$ Yes, so I think to understand that they bind to the receptors/ion channels on the neuron's membrane - but then again, it is the NT binding and not the voltage-changes which affect these channels permeability? $\endgroup$
    – Pugl
    Jul 14, 2019 at 21:40
  • $\begingroup$ Yes. Those are called ligand-gated channels. $\endgroup$
    – Bryan Krause is on strike ♦
    Jul 14, 2019 at 21:42
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    $\begingroup$ When you learn about voltage gated channels and APs, you probably started with resting conditions and then with some depolarization of undescribed origin: it could be by an experimenter or it just "happens". Next you learn about ligand gated channels, which it turns out provide that initial "kick". $\endgroup$
    – Bryan Krause is on strike ♦
    Jul 14, 2019 at 23:37
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    $\begingroup$ I see, thanks! So what you are saying is that the change in membrane potential which "kicks off" the VGICs is in a first step induced by the ionotropic/metabotropic channels? $\endgroup$
    – Pugl
    Jul 14, 2019 at 23:38

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