How does the EPSP or IPSP travel towards the axon hillock?

My concepts so far:

EPSP and IPSP are membrane potentials generated due to the opening of ligand-gated ion channels.


EPSPs are membrane potentials that are well below the threshold potential, generated due to the influx of Na or Ca ions(depolarisation).


IPSP are membrane potentials that are due to hyperpolarization of the membrane caused by the influx of Cl- or efflux of K, in the cell body.

1. Now, do these potentials travel in the same way as action potential in the axon?

In case of an EPSP, say for example, a ligand-gated sodium channel got opened and Na rushed into the cytoplasm. As a result, the local positive charges (that were already in the cytoplasm) will experience a strong repulsive force and will travel away from the channel. This local flow of current will depolarise (make the membrane potential less negative) the adjacent membrane and if the potential reaches the threshold potential only then an Action Potential will be generated. But an EPSP usually doesn't generate a threshold potential. EPSPs from different synapses generate a total current which depolarises the axon hillock/ initial segment to reach the threshold potential, and an Action potential is generated.

In case of IPSP, the influx of negative charge cause the adjacent membrane to hyperpolarize in a similar way, inhibiting stimulation, as the membrane potential at Axon hillock drops far from the threshold potential.

2. During axonal propagation, the impulse once travels in forward direction. It doesn't travel backward because the Na-channels cannot be immediately excited, as they need to change from inactive to closed state to be reactivated (refractory period). But what happens in the cell body ? Do the depolarization (EPSPs) and hyperpolarization (IPSPs) travel backward?

3. Is the threshold potential at the axon hillock/initial segment less than that of the nodes of ranvier? Why is it so?
 

atyy

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1. Now, do these potentials travel in the same way as action potential in the axon?

In case of an EPSP, say for example, a ligand-gated sodium channel got opened and Na rushed into the cytoplasm. As a result, the local positive charges (that were already in the cytoplasm) will experience a strong repulsive force and will travel away from the channel. This local flow of current will depolarise (make the membrane potential less negative) the adjacent membrane and if the potential reaches the threshold potential only then an Action Potential will be generated. But an EPSP usually doesn't generate a threshold potential. EPSPs from different synapses generate a total current which depolarises the axon hillock/ initial segment to reach the threshold potential, and an Action potential is generated.

In case of IPSP, the influx of negative charge cause the adjacent membrane to hyperpolarize in a similar way, inhibiting stimulation, as the membrane potential at Axon hillock drops far from the threshold potential.
PSPs do not travel in the same way as action potentials. Action potential travel is described by the Hodgkin-Huxley equations. In contrast, as a first approximation, PSPs can be described by passive travel using the cable equation. The way in which velocity is defined in the Hodgkin-Huxley equations and passive cable equations is different. See for example the discussion of both equations in https://www.amazon.com/dp/0195181999/?tag=pfamazon01-20.

PSPs do not always travel purely passively. However, the voltage-dependent channels in the dendrites are different from those in the axon, eg.
https://www.nature.com/articles/nn0900_895
https://www.researchgate.net/publication/12354724_Somatic_EPSP_amplitude_is_independent_of_synapse_location_in_hippocampal_pyramidal_neurons

2. During axonal propagation, the impulse once travels in forward direction. It doesn't travel backward because the Na-channels cannot be immediately excited, as they need to change from inactive to closed state to be reactivated (refractory period). But what happens in the cell body ? Do the depolarization (EPSPs) and hyperpolarization (IPSPs) travel backward?
Yes and no. Yes, in the sense that in passive travel, there is no inactivation to prevent the PSPs from travelling backward. However, in practice, you will find that it is not a useful concept.

There can be backpropagating action potentials that travel from the cell body into the dendrites, eg. https://www.ncbi.nlm.nih.gov/pubmed/7658365

3. Is the threshold potential at the axon hillock/initial segment less than that of the nodes of ranvier? Why is it so?
I'm not sure off the top of my head. There are questions as to whether the action potential in certain neurons begins at the axon initial segment or the first node of Ranvier. Maybe the issues are resolved now, but here a couple of papers some time ago that looked at the issue and disagreed.
https://www.ncbi.nlm.nih.gov/pubmed/15665877
https://www.ncbi.nlm.nih.gov/pubmed/16481425
 

BillTre

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#1: sounds good.

#2: Yes, normally the action potentials don't travel backwards. However, this can be done experimentally by stimulating an axon, but not after it has just propagated an action potential (when the Na-channels are inactive).

Action potentials are often said to be actively propagated because additional Na-channels are recruited to their open state by the change on membrane potential in an ever enlarging region of the cell membrane.
The IPSPs and EPSPs effects on membrane potential are often said to spread passively. They open where the receptors are stimulated and the neighboring membrane potential is affected but additional channels of the same type are not opened.
All of these membrane potential changes can go in all directions. Only the action potentials are actively conducted by recruiting additional neighboring channels to open so it can travel to distant locations.

#3: The axon hillock, where the cell body joins the axon, is a transition between the two. The channel proteins (including receptors and other channels) can differ between the two locations. This results in different membrane properties (electro-physiologically speaking) for the two areas. The axon hillock itself may have its own set of special channels, I don't know.
Voltage gated Na-channels (used in action potentials) are not usually located in the cell body, so Na based action potentials are not usually propagate there. That would start at the axon hillock.
After an action potential is initiated, additional unopened Na-channels open, injecting new current into the cell, making the signals propagation more robust. This may account for the impression that the nodes of Ranvier have a different threshold of activation. Not sure if that is true.
Not all axons that can generate action potentials have myelin and nodes of Ranvier. Some just have the neuronal membrane with voltage gated channels in it. This can also conduct action potentials, just not as fast.

Besides voltage gated Na-channels there can be voltage gated Ca-channels which can also produce action potentials, but usually with a slower longer time course. Among other places they are found in synapses and heart muscle.
 

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