SA Node Action Potential

This forum made possible through the generous support of SDN members, donors, and sponsors. Thank you.

izchief360

Full Member
7+ Year Member
Joined
Apr 28, 2014
Messages
44
Reaction score
26
The autorythmic cells in the SA node have Na+ leak channels that are always open, allowing the cells to undergo polarization/depolarization. Does this mean that the polarization/depolarization of these cells is opposite that of neurons?

I was watching one of Chad's videos (skip to 1:35) and when he talks about this, his hand gestures indicate that when the cell's potential difference is becoming more positive, the cell is polarizing, and when the potential difference is becoming more negative, the cell is depolarizing. This is opposite to what occurs in neurons, so I'm confused and wondering if I missed something.

Members don't see this ad.
 
  • Like
Reactions: 1 user
The autorythmic cells in the SA node have Na+ leak channels that are always open, allowing the cells to undergo polarization/depolarization. Does this mean that the polarization/depolarization of these cells is opposite that of neurons?

I was watching one of Chad's videos (skip to 1:35) and when he talks about this, his hand gestures indicate that when the cell's potential difference is becoming more positive, the cell is polarizing, and when the potential difference is becoming more negative, the cell is depolarizing. This is opposite to what occurs in neurons, so I'm confused and wondering if I missed something.

No, the SA node cells still depolarize to cause contraction.
 
  • Like
Reactions: 1 users
That's what I thought. The video is clearly incorrect then, oh well.
You have to be careful here. The cell in its resting state is polarized (there's a potential difference). Neurons have a RMP of -70 mV. Skeletal muscles approx. -90 mV. Smooth and Cardiac muscles vary but generally -60 mV. Any increase in this RMP or depolarization occurs due to influx of cations like sodium or calcium down their electrochemical gradient INTO the cell. In contrast, the efflux of potassium ions or the influx of anions like chloride would cause the cell to repolarize or hyperpolarize. We use the term repolarize as we are becoming more negative and approaching the negative RMP. We use hyperpolarize is we are exceeding RMP to a more negative value. The depolarization of sodium channels of the SA node is no different than depolarization occuring in neurons (sodium influx). The only difference here is that it's automatic, which allows for the heart to be autorhymic and contract even in the absence of outside neuronal stimulation. The specific channel is called funny ion channel named because of its unusual characteristic. It functions within a certain threshold (-60 to -45 mV) and becomes inactivated, but reactivates after repolarization once the cell reaches the -45 threshold to -60 (it acts to depolarize the cell again back to -45 to re-establish another action potential) over and over again. There is never a point where the cell maintains a steady RMP (atleast, while living).
 
Last edited:
  • Like
Reactions: 1 user
Members don't see this ad :)
@Czarcasm

What kind of ion is responsible for the depolarization in action potentials in smooth muscle?

ALL MUSCLES use Na for depolarization and release intracellular Ca2+ for contraction (though smooth muscle doesn't use troponin/tropomyosin complex; uses calmodulin instead...not important)
Edit: ALL muscles also use Ca imported from extracellular fluid via membrane Ca channels
SA node uses Ca for depolarization (and Na for reaching threshold)
 
Last edited:
@Czarcasm

What kind of ion is responsible for the depolarization in action potentials in smooth muscle?
If I recall correctly, it's a calcium channel which allows influx of calcium and acttivates calcium-induced release of the smooth ER ("RyR") Ca2+ channel, further increasing intracellular calcium.
 
@Czarcasm

Thanks. I've looked at many textbooks (and online) and I could never find that info.

Do you know if the Ca2+ is mostly from the SR or from the outside (outside the cell)?

What about depolarization? Is it the usual K+?
 
@The Brown Knight

I thought that skeletal muscle doesn't really rely on outside Ca2+.

But ok let's say all muscle cells rely on Ca2+.

Does having high extracellular Ca2+ affect muscle contraction (perhaps make it easier to contract)?
 
@The Brown Knight

I thought that skeletal muscle doesn't really rely on outside Ca2+.

But ok let's say all muscle cells rely on Ca2+.

Does having high extracellular Ca2+ affect muscle contraction (perhaps make it easier to contract)?

By SR I meant sarcoplasmic reticulum not extracellular (and smooth ER for smooth muscle).
Since most Ca comes from SR/smooth ER and since a depolarization wave is required for its release, I would guess extracellular Ca (which is naturally MUCH higher than cytoplasmic Ca) shouldn't affect muscle's ability to contract.
 
@The Brown Knight

You've made me wonder. Is the SR a specific type of smooth ER or a separate thing?

You imply that Ca2+ is stored in the smooth ER in smooth muscle but in the SR in everything else?
 
@The Brown Knight

You've made me wonder. Is the SR a specific type of smooth ER or a separate thing?

You imply that Ca2+ is stored in the smooth ER in smooth muscle but in the SR in everything else?
My bad, I just checked all muscles have SR; smooth muscles lack T TUBULES. In comparison to smooth ER, SR is probably more Ca rich and probably has a higher surface area since it forms a netlike structure around the myofibrils. Also SR is adjacent to the T tubules which are part of the cell membrane whereas in other cells the smooth ER is not adjacent to membrane.
 
@The Brown Knight

So is intracellular Ca2+ mainly released from the SR then? I guess that's it's sole purpose?

Yes, that would be its main purpose.
Though since muscle cells don't have another smooth ER, it might serve as other smaller roles that smooth ER normally serves in most cells (i.e. lipid/steroid biosynthesis, drug detox, etc.)
 
Top