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There are many steps detailing the depolarization and repolarization of axon nodes to describe how an action potential is transmitted from a neuron. But, after looking at many different sources, I still see one clear thing missing: what causes the action potential in the first place? Every source simply says something vague like "stimulus" or the ever redundant "depolarizing current." But, how is this stimulus generated, and what exactly does it do to which chemical to start the chain reaction of moving sodium ions to create the depolarization in the first place?

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  • $\begingroup$ In addition to my answer, I would add that there is absolutely nothing redundant about the phrase "depolarizing current." $\endgroup$ – Bryan Krause Feb 16 '18 at 17:16
  • $\begingroup$ "how is this stimulus being generated" -- have you heard of neurotransmitters? $\endgroup$ – Oct18 is day of silence on SE Feb 16 '18 at 17:18
  • $\begingroup$ @BryanKrause Yes there is, simply explaining what triggers depolarization as a "depolarizing current" does not explain much. $\endgroup$ – John Joe Feb 16 '18 at 17:25
  • $\begingroup$ I disagree somewhat, but please see my answer. $\endgroup$ – Bryan Krause Feb 16 '18 at 17:30
  • $\begingroup$ That answer requires wayyyyy more detailed than "depolarizing current." $\endgroup$ – John Joe Feb 16 '18 at 17:37
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There are several possible answers, which is partly why the sources you are reading are being vague: they are discussing the chain of events that happen after the initial depolarization, the source of which doesn't matter much for that chain of events.

Receptor potentials

Sensory receptors consist of some machinery that eventually lead to ion channels opening, often cation channels. This machinery can be direct, where a stimulus directly opens an ion channel, or it can me mediated through g-protein coupled receptors. There are many many examples, but one favorite toy example is the TRPV1 receptor, part of the ["transient receptor potential"] family(https://en.wikipedia.org/wiki/Transient_receptor_potential_channel).

TRPV1 channels open when exposed to high temperatures or chemical agonists like capsaicin (which gives chili peppers their 'heat').

There are mechanically gated channels in the inner ear that are stretched open as sound waves pass; there are G-protein coupled receptors in the retina that are activated in response to light - when they are activated, they close channels which reduces neurotransmitter release and therefore changes the amplitude of the post-synaptic polarization.

Ligand-gated ion channels

Synaptic transmission between neurons is often mediated by ion channels that are gated by neurotransmitters. A presynaptic cell releases a neurotransmitter, for example glutamate, and that neurotransmitter binds glutamate receptors on the post-synaptic cell, for example AMPA receptors. These receptors are non-specific cation channels, and when they open sodium comes in and depolarizes the cell. Other neurotransmitters, including inhibitory ones, work a similar way.

Gap junctions/eletrical synapses

Although they only occur between particular populations of neurons in mammalian nervous systems (for example, some inhibitory networks in the brain and between cardiac myocytes), some cells are coupled through channels that allow ions to pass between cells. Therefore, depolarization in one cell can be transmitted by ions flowing through that gap junction and begin to depolarize the adjacent cell.

Intrinsic conductances

It doesn't really apply in the context of a "stimulus" but in some types of cell there are intrinsic conductances that can bring a cell to threshold and trigger an action potential. One example would be in the pacemaker cells of the sinoatrial node that initiate cardiac contractions.

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