Action potentials in pacemaker cells

Last updated: February 23, 2023

Action potentials in pacemaker cells

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Action potentials are the really rapid electrical changes that occur across the membrane of certain cells, and often propagates from one cell to an adjacent cell. Cells in the heart communicate this way. That signal’s gotta start somewhere, so some of these cells, called pacemaker cells, have the responsibility of setting the rhythm and the pace of the heartbeat. They’ve got this really important job, but they’re a relatively tiny group -- only about 1% of the heart cells -- and they’re able to continually generate new action potentials that get conducted to the rest of the heart -- the other 99% -- and that’s what tells the heart pump. Now, pacemaker cells also listen to which usually come from neighboring pacemaker cells. But if those don’t come, then a pacemaker cell will simply launch its own and that action potential will then spread around. This is called automaticity, and that’s easy to remember because it’s got “automatic” right in it.

So let’s start by mapping out those pacemaker cells. The first clump of pacemaker cells is tucked up here into the corner of the right atria, and that’s the sinoatrial node, which sometimes gets called the SA node. We’ve also got pacemaker cells in internodal tracts between nodes, in the atrioventricular, or AV node, the Bundle of His, and the Purkinje fibers, and that’s our electrical conduction system.

And all around these pacemaker cells are heart muscle cells or cardiomyocytes and they pick up the action potential too, but that happens just a tiny bit more slowly -- we can think of these bands of pacemaker cells as highways that carry the action potential to its destination super fast, and then the muscle cells are like little side roads where it’s slower. That’s important because we want all of the myocytes to pick up that action potential and contract at the same time. We call this whole system a functional syncytium, which means that the mechanical, chemical, and electrical connections between these cells allow them to act as one unit in some ways, and it’s the pacemaker cells that make that happen.

Okay, now let’s take a closer look at the chemistry that gets that action potential moving. Action potentials are initiated by depolarization, which is the opposite of polarization. Polarization is when there’s a higher negative charge inside the cell relative to outside the cell, and that difference in charge is called the membrane potential. So if the membrane potential is negative the inside of the cell is more negative than the outside, if it’s positive the inside is more positive than the outside, and if it’s 0mV, then the inside and outside have the same charge - there’s 0mV of difference. Ok -- so, the key here is understanding how the membrane potential changes, and it all comes down to the movement of ions. Specifically, two factors -- which ion wants to move across the membrane, and how permeable the membrane is to that ion. So, depolarization is when ions move across the membrane and the membrane potential becomes less negative or even slightly positive.

Think of a really pessimistic negative cell throwing his hands up and enjoying a moment of joy. When one cell depolarizes enough - it can cause some ions to flow into neighboring cells and trigger them to depolarize as well. If one cell after another depolarizes, then there’s a depolarization wave which you can imagine would look like a wave moving through a crowd at a football stadium. Each depolarization wave causes heart muscle contraction, so the rate at which depolarization waves ripple through the heart actually sets the heart rate. So if depolarization waves are going through about once per second, that means that your heart beats once per second, or sixty times in a minute.

Key Takeaways

Action potentials are voltage changes that propagate along the surface of cells. In the heart, they are generated by specialized cell structures called pacemaker cells, which use them to control the rhythmic contraction of muscles.

In cardiac pacemaker cells, action potentials occur when specialized channels in the cell membrane open and allow ions to flow into or out of the cell. This change in electric charge makes the cell more positive on the inside, which attracts more ions from neighboring cells and triggers a chain reaction that propagates the action potential along the heart muscle. This eventually leads to the contraction of the heart and pumps blood around our bodies.

Sources

  1. "Medical Physiology" Elsevier (2016)
  2. "Physiology" Elsevier (2017)
  3. "Human Anatomy & Physiology" Pearson (2017)
  4. "Principles of Anatomy and Physiology" Wiley (2014)
  5. "How does the shape of the cardiac action potential control calcium signaling and contraction in the heart?" Journal of Molecular and Cellular Cardiology (2010)
  6. "The Role of the Funny Current in Pacemaker Activity" Circulation Research (2010)
  7. "Impact of Sarcoplasmic Reticulum Calcium Release on Calcium Dynamics and Action Potential Morphology in Human Atrial Myocytes: A Computational Study" PLoS Computational Biology (2011)