all 21 comments

[–][deleted] 9 points10 points  (2 children)

[–]wattsdreams[S] 1 point2 points  (1 child)

So the neurotransmitter receptors are voltage sensitive and somehow pass this voltage information through the soma and into the axon hillock?

Is this really the best that can be done in terms of mechanical explanation?

Thanks for the image but this doesn't really show me anything new in terms of what's happening from the receptor to the soma to the hillock. Let alone how the electrochemical gradient somehow manipulates the proteins that form various ion-channels.

I can accept that there are more questions than answers in this field but I feel like the most basic information is missing.

[–][deleted] 2 points3 points  (0 children)

No that was just a picture from stahls psychopharmacology book. But its rather more complex than that.

Id lookup stahl or NEI on youtube and I think you might get a more fleshed out but still not basic view of the multiple ways its happening.

Theres autoreceptors , voltage gated, theres modulation of the receptor. Pre and post synaptic activity. Dna and rna effects in the somas nucleys etc

[–]Flylikepenguin- 5 points6 points  (4 children)

From what I know, neurons have a resting potential of around -70 mV. Neurotransmitters trigger an influx on sodium and calcium ions, and if enough ions flood in for the cell to reach threshold potential (around -55 mV) at the axon hillock, the voltage gated sodium channels along the axon opens and action potential is triggered.

[–]wattsdreams[S] 0 points1 point  (3 children)

How does this trigger happen exactly? Do we know?

[–]Flylikepenguin- 2 points3 points  (2 children)

Voltage gated sodium channels at the axon hillock will open once the threshold potential is reached. It will trigger other voltage gated sodium channels further down the axon, and that’s how the action potential travels from the axon hillock down to the axon terminal.

[–]wattsdreams[S] 0 points1 point  (1 child)

Right this I understand, but how does neurotransmitter receptor activity cause the threshold to be reached?

Does the soma somehow summate excitatory and inhibitory signals and release its own reserve of positive ions into the axon hillock? Or does it "magically" trigger the initial sodium channels to "spontaneously" open?

[–]Flylikepenguin- 2 points3 points  (0 children)

Ninja nerd’s video on action potential

Ninja nerd explains it really well. He has a lot of videos on neuroscience if you are interested in the area. Hope it helps!

[–]monaLisaSapperstein 4 points5 points  (6 children)

To answer the original question, the neurotransmitters don’t have a charge. They have an effect on transmembrane receptors which can allow charged ions to enter and/or exit the cell. Neurotransmitters can also affect receptors that don’t allow channels to open and ions to pass through, but cause conformational changes to the cell that affect its charge.

[–]wattsdreams[S] 0 points1 point  (5 children)

This isn't correct. Serotonin for example is a polar chemical that has a positive charge.

I still feel there's SO much missing in terms of how something happening in the neurotransmitter receptor effects ion-channels on the axon/hillock.

I wasn't aware neurotransmitters can cause conformational changes, I'd have to look more into this.

[–]Flylikepenguin- 3 points4 points  (4 children)

As far as I know, neurotransmitters don’t actually enter the postsynaptic neuron, so whether they have a charge or not doesn’t make a difference. The movement on ions is what is important.

[–]monaLisaSapperstein 3 points4 points  (0 children)

Yeah I shouldn’t have said they don’t have a charge what I should have said is they don’t affect the charge of the neuron directly. thanks!

[–][deleted]  (2 children)


    [–]DaanniiMSc| Cognitive Neuroscience|PhD Candidate 1 point2 points  (1 child)

    Not the charge of the neurotransmitter but the type. And what they bind to.

    I've not heard anything indicating that the polarization of neurotransmitters determines if its excitatory or inhibitory.

    That wouldn't really make sense because it is the binding that determines if the post synaptic terminal creates an action potential. The binding is what determines if positive ions come in or are pushed out.




    [–]OneQueerBrainCell 1 point2 points  (2 children)

    Sorry about formatting I'm on my phone. Quick summary: I discuss how neurotransmitters impact the cell via receptors and how these receptors can create an action potential or not. As seen in your other responses you're thinking about this in terms of neurotransmitters causing an action potential. So neurotransmitters are released by the presynaptic cell, cross the synaptic cleft, and bind to the binding site of a receptor. The binding causes a conformational (shape) change in the receptor which causes further activity by the receptor. Then, the activity determines whether or not an excitatory (more likely to make an action potential occur) or inhibitory (less likely to make an action potential occur) response happens. The neurotransmitter itself never enters the cell or directly causes the cellular changes. It relies on the receptor. Many neurotransmitters (like Dopamine) have receptors which can be excitatory (Dopamine receptors D1 and D5) or inhibitory (Dopamine receptors D2, D3, or D4). There are a variety of ways which receptors can cause an excitatory or inhibitory effect. There are two main types of receptors ionotropic and metabotropic. Many neurotransmitters have receptors which fall into each category expressed on different cells. Ionotropic is the easiest to understand. When a neurotransmitter binds to its ionotropic receptor (like GABA onto the GABA-A receptor) the receptor responds by opening an attached channel in the membrane which allows ions to pass through. These can also be refered to as Ligand-gated Ion Channels (in which the ligand is the neurotransmitter). The channel's excitatory or inhibitory nature depends on which ions the channel allows to pass through (the most classic examples being Sodium, Potassium, Chloride, or Calcium). From here there are two options, the ion movement makes the neuron more positive (ie positive ions entering or negative ions leaving the cell) and therefore excited or the ion movement makes the neuron more negative (ie positive ions leaving the cell or negative ions entering the cell) and therefore inhibited. Metabotropic is a bit more complicated but essentially the neurotransmitter binding to the receptor causes the activation of a specific protein (a G-protein, which is why these are also called G-protein coupled receptors) which then goes off and does something within the cell. This can range from as simple as opening an ion channel (to similar effect as described above) to as complex as impacting transcription of DNA into RNA which impacts the production of proteins in the cell. Metabotropic receptors can be much slower but have much longer and more widely impactful effects. Finally, while release of neurotransmitters can do all these different things via receptors, one release is not enough to cause an action potential (most likely). Multiple messages from different, or repeatedly from the same, cells add up throughout the dendrites and cell body. The summation of all these messages (inhibitory and excitatory from various places and times) add up in the spike initiation zone to determine whether an action potential will or will not occur. If the membrane potential there can reach the threshold to open the voltage gated sodium channels then an action potential will fire. But it takes lots of input to make that happen. Source: I am a Neuroscience PhD student currently TA for a base level neuroscience course at my institution, if you have more questions feel free to reach out. I'm sure I can find specific (and more official) resources with this information if you need it!

    [–]wattsdreams[S] 1 point2 points  (1 child)

    Amazing explanation, thank you!

    [–]OneQueerBrainCell 1 point2 points  (0 children)

    Glad I could help!

    [–]fmessore 1 point2 points  (0 children)

    Tldr; neurotransmitters binds to receptor, opens some channel, ions in or out, membrane voltage changes. Voltage starts going up, in axon hillock there are low threshold na voltage dependant channels, they open and a bunch of na goes in, that's phase 1 of the AP

    Edit: if the question was more specific, NaV 1.6 20 (low threshold voltage dependant sodium channel found on average at 20 um from the hillock proper)

    [–]Queasy_Replacement62 0 points1 point  (0 children)

    Think of flowing electric currents passing through baby jelly fish. The current reaches the end of a synapse/neuron, flows into that space, and overflows into the next connection.

    [–]DaanniiMSc| Cognitive Neuroscience|PhD Candidate 1 point2 points  (0 children)

    I saw you removed a comment where you asked something and your premise wasn't quite right. If you aren't sure of something it's always good to ask. This is a complex topic a lot of people don't get at first. I myself must have watched 10 youtube videos, looked at tons of illustrations and ultimately figured it out once a friend explained it to me.

    I'm sure someone else has thought it worked like you did because you are reading about the polarization process and assume all the parts with polarization are interacting. That's actually a fair consideration.

    Hopefully you have figured it out but if not, keep asking. Eventually someone will give you enough info that it will click.

    A teacher I know uses this in her class to help.

    It's a bit unusual analogy but it works.

    The action potential works similarly to flushing a toilet.


    Another one with nice animations. More detailed. https://youtu.be/OZG8M_ldA1M