The Basics of Neuron “Firing”

Nerve cells, or neurons, are differentiated into four major parts that all contribute to it’s ability to communicate impulsively via electricity. These are the cell body (soma)dendrites (dendrons), axon, and axon terminals. The cell body is the familiar eukaryotic cell, with membrane-bound organelles and a nucleus. The other modified parts of the neuron are what make it specialized for cell-to-cell communication. The dendrites, which also go by dendrons, are named for being “tree-like”, due to their extensive branching and spreading. These  projections are essentially the inputs to the soma from other neurons’ axons. So, axons are the outputs to other neurons’dendrites (although, there are cases where they can terminate effectively at “unconventional” locations, such as the soma or axon). The axon terminal and the dendrite are connected “virtually”. What I mean here is that they do not actually touch, they are nearly touching in a zone called the synapse, where neurotransmitters pass back and forth from the axon terminal and the dendron. These neurotransmitters are molecules of communication between the neural cells which either inhibit or excite another neuron into “firing”.

[Neural Figures for Visual Aid]

Before I explain the “firing” (the electrical, action potential component that makes the brain work) there is another type of cell worth noting. A neuroglia cell called the oligodendrocyte, is also a critical part of neuron functioning. Neuroglia means neuron glue and is the structure that holds the nuerons and keeps their synapses close but not in contact. In particular, the oligodendrocyte has many extensions that reach out and wrap around the axon of a neuron. This wrapping is a type of fat which provides the insulation needed for a positive charge to flow down the axon. In detail, the fat, or myelin sheathing, does not cover the entire axon. This is necessary for an action potential to occur (a flow of electrons caused by a voltage induced in the neuron). The gaps between the fat insulation have a section called the Node of Ranvier.

At this node, saltatory conduction (of salt ions: sodium, potassium, chloride, and calcium) can occur with the contact of the axon cell membrane to the ions outside the cell. Saltatory conduction is basically a recharging of an incoming action potential; a bolstering of the flowing electrical current. As the positively charged action potential weakens and slows from nearly the speed of light (see Speed of Electricity), sodium enters at the Node of Ranvier and gives the action potential more positive charge and invigorates it back up to the speed of light. So, the action potential is a chain reaction between Nodes of Ranvier.

In order for the action potential to occur the charge on the cell membrane must depolarize. To clarify, the charge is at a negative baseline, is induced toward a neutral charge (depolarization), then overshoots slightly to a positive peak charge, then once the signal passes on it returns to it’s negative rest potential. In more detail, this membrane electrical potential will allow sodium to pass into the cell, following both the concentration gradient and voltage gradient; in other words it follows from more to less concentration of ions and from negative to positive charge. Once enough sodium enters the cell (through openings called voltage-gated ion channels) and makes it more positive – around -55 mV from the resting -70mV – and an excitation threshold is reached. The sodium channels will remain open until the inside of the cell reaches +40 mV (the overshoot from depolarization). At this point the sodium channels will close and potassium channels will open. Since there is a high concentration of potassium inside the cell the positive ions will flow out and hyperpolarize the inside of the cell once again. The hyperpolarization tends to overshoot down to around -70 or -80 mV. During this refractory period the inside of the cell will steadily depolarize back to the resting potential of around -65 mV.

Remember, the purpose of an action potential is to release a neurotransmitter from one neuron to another in order for neuron-to-neuron communication. Also, the release of neurotransmitters from one neuron to another initializes the action potential, which will be excitatory or inhibitory. This communication is accomplished through a synapse at the end of the axon to a dendrite, soma, or axon of another neuron. The end of the axon indirectly connects to the other neuron’s receptors via a space called the synaptic cleft. The axon of the pre-synaptic cell’s axon (which has a bulbous structure called the terminal bouton; which is French for “button”) contains small, bubble-like structures which contain neurotransmitters. These bulbs are synaptic vesicles and require calcium in order to function as they need to. Calcium exits the post-synaptic cell’s receptors and enters the pre-synaptic cell’s terminal bouton. The calcium causes the vesicles to bind to the pre-synaptic cell membrane. This binding basically causes the vesicle to turn inside out and dump its neurotransmitter molecules out into the synaptic cleft for the post-synaptic cell’s receptors to receive. The process of the dumping of neurotransmitters out from the vesicles is termed exocytosis and is essential for neuron voltage-based communications.

The Simple Summary:

1. The axon membrane is at it’s polarized resting potential (~ -65mV).
2. It receives neurotransmissions via another neuron’s axon(s) that are excitatory (inhibitory neurotransmissions will not cause an action potential).
3A. Depolarization (~ 0 mV) waves flow down the axon, getting bolstered at the nodes of Ranvier; and insulated by myelin sheath.
3B.  A positive overshoot follows behind (~ +40 mV), then the membrane voltage negates back to it’s resting potential (i.e. re-polarization)
5. The impulse reaches the terminal bouton and a neurotransmission occurs.

10 Comments

  1. This is amazing. It is really above my head in a lot of ways but I can get the gist of it. And I know that when my electrolytes were messed up I almost died because it messed this situation up. Also, the brain likes fat from what I have read and I did not know that the myelin sheath involves fat. But I do know that multiple sclerosis or muscular dystrophy or maybe both have something to do with the myelin sheath getting messed up.

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    1. Yeah your on point there. Exceptionally low body fat can lead to loss of myelin and so deficiency of the insulation of the axon. That’ll lead to a cascade of neural degenerative possibilities.

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  2. I think my biggest problem with all this is, as David Chalmers puts it, the “hard problem ” of consciousness.http://consc.net/papers/facing.pdf
    The really hard problem of consciousness is the problem of experience.
    We may see the mechanistic operation of the brain but at the moment are nowhere near understanding how the mechanics gives rise to experience.
    These guys are very interesting on the topic: https://qualiaresearchinstitute.org/

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    1. I ease my confused and curious amazement by believing our brains are quantum biocomputers. From there we can get past the issues of why we can have consciousness and experience, and get over how it’s possible, and get into what its components and systems are. It’s far more than biochemistry as we know it. It’s going to require an aggregate field of biophysics that combines and advances neuroscience, quantum mechanics, and metalogic with the necessary experimental physics and quantum computing to observe, test theory, and test human knowledge and perception limits.

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  3. I’m not familiar with any quantum theories at all. However, due my medical writing and research work, I get to do a lot of digging in the brain. It is way too early to say we will ever understand 100% how the brain works. Should we? It would make sense in order to cure brain disorders.
    I don’t think we would be happier having manuals on how to use the brain in order to maintain neurons and synapses.
    The brain and the beginning of a human from the cells that carry all the information: these are 2 things which I adore. Even if I had 10 times more knowledge, I’d still see it as something absolutely incredible.
    Well, brain diseases (I’m not referring to oncology or cerebro-vascular issues) are the most difficult to treat, and with so many pharmaceutical companies giving up on Alzheimer’s, it would be wonderful to not only explain many functions (I do not believe we can include yet all functions of all substances and components that contribute to the brain activity, can we?), but also do something. We literary cannot treat cognitive and functional brain disorders yet. It is a totally dark area with all kinds of assumptions which eventually are proven wrong or ineffective.
    Your explanation was pretty much the best I have seen in the recent years.
    Well, when I will be stuck again with some brain-related term which does not have an equivalent in any other language, I will have to turn to you. Lots of people know a lot about the brain, it is just so, that not many are able to describe it without getting lost in extreme terminology. English has the most developed terminology, but when I’m trying to convey the same idea into, for instance, Latvian, I search for hours for one single world. I cannot translate it wrong, I am not allowed to add extra descriptions or more words, and I have to come up with the word that means the same and does not sound weird.

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    1. Indeed, the brain is analogous to astronomy, in that it’s nature is perplexing and at times deceiving, and likewise it probably will never be known because the information required to understand it fully exceeds human potential. Regardless, the brain or the cosmos are great frontiers of exploration that give impetus to discover things we could have never predicted.

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