Action potentials in myocytes

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Action potentials in myocytes

MSK Module Content

MSK Module Content

Resting membrane potential
Action potentials in myocytes
Neuron action potential
Neuromuscular junction and motor unit
Sliding filament model of muscle contraction
Cholinergic receptors
Lambert-Eaton myasthenic syndrome
Neuromuscular junction disorders: Pathology review
Myasthenia gravis
Myalgias and myositis: Pathology review
Pediatric orthopedic conditions: Clinical
Muscle weakness: Clinical
Slow twitch and fast twitch muscle fibers
Muscle spindles and golgi tendon organs
Muscle contraction
Skeletal muscle histology
Muscular system anatomy and physiology
Lower back pain: Clinical
Back pain: Pathology review
Systemic lupus erythematosus (SLE): Clinical
Osteoporosis
Child abuse: Clinical
Non-steroidal anti-inflammatory drugs
Rheumatoid arthritis
Physiological changes during exercise
Polymyositis
Lordosis, kyphosis, and scoliosis
Spinal disc herniation
Acetaminophen (Paracetamol)
Osteochondroma
Scleroderma
Skeletal system anatomy and physiology
Bone remodeling and repair
Legg-Calve-Perthes disease
Genu varum
Inflammatory myopathies: Clinical
Muscular dystrophies and mitochondrial myopathies: Pathology review
Mitochondrial myopathy
Inclusion body myopathy
Monoclonal antibodies
Spondylolysis
Spondylosis
Spondylitis
Bone disorders: Pathology review
Muscular dystrophy
Mixed connective tissue disease
Cartilage histology
Raynaud phenomenon
Scleroderma: Pathology review
Osteoarthritis
Cartilage structure and growth
Fibrous, cartilage, and synovial joints
Septic arthritis
Slipped capital femoral epiphysis
Bone tumors
Osgood-Schlatter disease (traction apophysitis)
Achondroplasia
Rheumatoid arthritis: Clinical
Developmental dysplasia of the hip
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Spinal cord reflexes
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Paget disease of bone
Bone histology
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Anatomy clinical correlates: Bones, joints and muscles of the back
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Clostridium perfringens
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Brachial plexus
Anatomy of the brachial plexus
Klumpke paralysis
Anatomy clinical correlates: Wrist and hand
Muscles of the hand
Achilles tendon rupture
Rotator cuff tear
Somatosensory receptors
Carpal tunnel syndrome
Patellar tendon rupture
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Alport syndrome
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Antigout medications
Nucleotide metabolism
Joint pain: Clinical
Lesch-Nyhan syndrome
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Introduction to the muscular system
Introduction to the skeletal system
Development of the muscular system
Torticollis
Pigeon toe
Neuromuscular blockers
Myotonic dystrophy
Development of the axial skeleton
Development of the limbs
Muscles of the back
Anatomy of the arm
Anatomy clinical correlates: Clavicle and shoulder

Transcript

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Action potentials are the really fast electrical changes that happen across the membrane of certain cells, and often propagate from one cell to an adjacent cell. And cells in the heart communicate this way. Now, that signal’s gotta start somewhere, so some of these cells, called pacemaker cells, have the responsibility of setting the rhythm and pace of the heartbeat. So they’ve got this really important job, but they’re a relatively tiny group, and make up only about 1% of the heart cells. But they’re able to continually generate new action potentials that get conducted to the rest of the heart, or the other 99%, and so these are what tell the heart to pump. The cells that receive that signal are called myocytes because they make up the myocardium, which is the muscular middle layer of the heart. Myocytes are also called contractile cells because they contract to allow the heart to pump blood. Myocytes are different from skeletal muscle cells though, which get their action potential signals directly from neurons. Cardiac myocytes receive signal from pacemaker cells causing them to contract.

Now let’s focus on a single myocyte cell going through a single action potential. The action potential of a myocyte is broken into five phases. Often they’re shown on a graph of membrane potential vs. time. We’re going to start with Phase 4, because why not.

In phase 4, or the resting phase, our little myocyte friend is at rest, hanging out with an overall charge or membrane potential of -90 mV. Now, the interesting thing is that it has gap junctions which are openings between two myocytes. So when the myocyte’s neighbour depolarizes, some ions - mainly calcium ions - start leaking through the gap junctions and that makes the membrane potential go up to about -70 mV. -70mV is called the threshold potential and it marks the start of phase 0.

Phase 0 is known as the depolarization phase. Basically, some voltage gated sodium channels open up when they sense that the membrane potential is -70mV, and they allow sodium to rush into the cell, creating an inward current. This rapid influx of sodium causes the myocyte’s membrane potential to go all the way up to +20mV. 

Now, if only a few ions leaked through from the neighboring cell, and the membrane potential didn’t get to the threshold potential of -70 mV, then those voltage-gated channels wouldn’t open and there’d be no depolarization. Essentially there’s nothing in-between, which is why we say that an action potential is an all-or-none process.

Key Takeaways

An action potential (AP) is a voltage change that propagates along the membrane of a myocyte (muscle cell) or other cells such as a nerve cell. The AP is generated by the movement of positively charged ions, mainly Na+ and K+, across the plasma membrane. This generates an electrical current that travels down the length of the myocyte.

The AP triggers the release of Ca2+ from intracellular stores, which in turn activates contractile proteins within the myocyte. This ultimately leads to muscle contraction.

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. "Sinoatrial node dysfunction induces cardiac arrhythmias in diabetic mice" Cardiovascular Diabetology (2014)
  6. "How does the shape of the cardiac action potential control calcium signaling and contraction in the heart?" Journal of Molecular and Cellular Cardiology (2010)
  7. "Ionic events responsible for the cardiac resting and action potential" The American Journal of Cardiology (1982)