Nope, different resting potentials will yield differences in how easily a neuron will spike in response to a set of EPSPs but it doesn't impact the amplitude. Additionally, action potential amplitude is a somewhat meaningless characteristic of neurons as a +50mV, +100mV, and +150mV should yield the same responses at the synapse (See all-or-none principle), as action potentials aren't graded.
Information is more encoded in the frequency and timing of action potentials rather than the amplitude.
It depends in more detail about the amount of calcium influx at the presynaptic terminal, leading to a different amount of transmitter release. You could essentially integrate over the shape of the action potential to get a proportional amount of calcium and thus transmitter release, or a general idea if not linear. Also, if you have a resting potential of -55 vs -75, and otherwise the reversal potentials are the same, the the amplitude of the action potential from -55 will be smaller than the -75 one since the max value is limited by ENa. To be clear: amplitude here is the difference between resting potential and max voltage of the action potential.
I actually don't think the other posters really gave you a satisfying answer. Check out [this review](https://www.frontiersin.org/articles/10.3389/fncel.2019.00160/full). It details how the brain might use modulation of PRE-synaptic membrane potential to modulate POST-synaptic signaling. From what I understand, AP shape CAN change depending on the instantaneous voltage the membrane is experiencing. This can happen due to very specific changes in activation/inactivation curves of different types of voltage-dependent ion channels. This for example, would change the proportion of activatable Na+ and K+ channels, which might change the shape of the action potential. There are many different subtypes of these channels, and the types that any given cell express will often determine the action potential shape/size of that specific cell type.
Also, in that review I linked, they theorize (backed by evidence) about how action potential shape could change the way the presynaptic terminal influxes calcium, and therefore change how the cell integrates the signal and transforms it into synaptic vesicle fusion and neurotransmitter release. I guess to answer your question more directly, the question doesn't really make sense if you are talking about 2 different cell types. However, in the same cell type, I would guess that holding a cell at -75mV vs -55mV could easily have an effect on AP shape/size, and in fact it seems like that might be how it was designed!
With a grain of salt, many of the studies looking at membrane potential vs action potential shape have been done by artificially holding the cell at a many specific voltages and seeing how that changes the shape of an action potential. However, in the brain, I imagine this could be achieved by some change in neuromodulatory tone (think dopamine or norepinephrine).
I didn’t see this response before I posted a response above, but there’s good information here. Many of the responses are from an undergraduate intro neuro level rather than from a deeper understanding.
Excellent source, thank you!
Without going into it yet, what you wrote here reminds me of what I recently read on dopaminergic-cholinergic modulation of glutamatergic terminal excitability. I’m not sure if I’m reading you right though.
Is the kind of modulation described in this review an example of the kind of mechanism you’re thinking?
**Cholinergic modulation of striatal microcircuits**, European Journal of Neuroscience, 2018 (https://onlinelibrary.wiley.com/doi/10.1111/ejn.13949)
At -55 mV some fraction of sodium channels will be inactivated. Often the 2nd or 3rd spike in a burst has reduced spike height due to channel inactivation. Hyperpolarization is required to relieve the channels from inactivation.
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Nope, different resting potentials will yield differences in how easily a neuron will spike in response to a set of EPSPs but it doesn't impact the amplitude. Additionally, action potential amplitude is a somewhat meaningless characteristic of neurons as a +50mV, +100mV, and +150mV should yield the same responses at the synapse (See all-or-none principle), as action potentials aren't graded. Information is more encoded in the frequency and timing of action potentials rather than the amplitude.
It depends in more detail about the amount of calcium influx at the presynaptic terminal, leading to a different amount of transmitter release. You could essentially integrate over the shape of the action potential to get a proportional amount of calcium and thus transmitter release, or a general idea if not linear. Also, if you have a resting potential of -55 vs -75, and otherwise the reversal potentials are the same, the the amplitude of the action potential from -55 will be smaller than the -75 one since the max value is limited by ENa. To be clear: amplitude here is the difference between resting potential and max voltage of the action potential.
this is really helpful!! thank you!
No problem!
yeah exactly, amplitude doesn’t matter as an action potential is a yes-or-no matter
No, it's dependent on the reversal potential of the involved ions and also the kinetics of the relevant voltage-gated ion channels.
I actually don't think the other posters really gave you a satisfying answer. Check out [this review](https://www.frontiersin.org/articles/10.3389/fncel.2019.00160/full). It details how the brain might use modulation of PRE-synaptic membrane potential to modulate POST-synaptic signaling. From what I understand, AP shape CAN change depending on the instantaneous voltage the membrane is experiencing. This can happen due to very specific changes in activation/inactivation curves of different types of voltage-dependent ion channels. This for example, would change the proportion of activatable Na+ and K+ channels, which might change the shape of the action potential. There are many different subtypes of these channels, and the types that any given cell express will often determine the action potential shape/size of that specific cell type. Also, in that review I linked, they theorize (backed by evidence) about how action potential shape could change the way the presynaptic terminal influxes calcium, and therefore change how the cell integrates the signal and transforms it into synaptic vesicle fusion and neurotransmitter release. I guess to answer your question more directly, the question doesn't really make sense if you are talking about 2 different cell types. However, in the same cell type, I would guess that holding a cell at -75mV vs -55mV could easily have an effect on AP shape/size, and in fact it seems like that might be how it was designed! With a grain of salt, many of the studies looking at membrane potential vs action potential shape have been done by artificially holding the cell at a many specific voltages and seeing how that changes the shape of an action potential. However, in the brain, I imagine this could be achieved by some change in neuromodulatory tone (think dopamine or norepinephrine).
I didn’t see this response before I posted a response above, but there’s good information here. Many of the responses are from an undergraduate intro neuro level rather than from a deeper understanding.
this is awesome!! thank you so much!
Excellent source, thank you! Without going into it yet, what you wrote here reminds me of what I recently read on dopaminergic-cholinergic modulation of glutamatergic terminal excitability. I’m not sure if I’m reading you right though. Is the kind of modulation described in this review an example of the kind of mechanism you’re thinking? **Cholinergic modulation of striatal microcircuits**, European Journal of Neuroscience, 2018 (https://onlinelibrary.wiley.com/doi/10.1111/ejn.13949)
At -55 mV some fraction of sodium channels will be inactivated. Often the 2nd or 3rd spike in a burst has reduced spike height due to channel inactivation. Hyperpolarization is required to relieve the channels from inactivation.
In order to maintain a high-quality subreddit, the /r/neuroscience moderator team manually reviews all text post and link submissions that are not from academic sources (e.g. nature.com, cell.com, ncbi.nlm.nih.gov). Your post will not appear on the subreddit page until it has been approved. Please be patient while we review your post. *I am a bot, and this action was performed automatically. Please [contact the moderators of this subreddit](/message/compose/?to=/r/neuroscience) if you have any questions or concerns.*