Going Under the Knife: A Case on Membrane Structure and Function Twenty-year-old

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Going Under the Knife: A Case on Membrane Structure and Function

Twenty-year-old Kevin groaned and clutched his abdomen as he lay on the emergency room gurney. He had just been diagnosed with acute appendicitis and was waiting to be taken to the operating room (OR). Although he desperately wanted the pain to stop, Kevin was terrified of having general anesthesia. He hoped his fear wasn’t obvious to his older brother Cole, who was finishing medical school and thought he knew everything.

“Hang in there,” Cole said, for what seemed like the eighteenth time. “I’m sure they’ll get you upstairs as soon as they can. They don’t want that thing to burst.”

Kevin grunted. “I know…but does that anesthesia stuff work all the time? How can I not wake up when someone’s slicing my gut open?”

Cole assumed a professorial air, and Kevin wished he’d kept his mouth shut. However, Cole didn’t get a chance to say anything before an aide arrived to take Kevin to the OR.

In the OR, someone placed a mask over Kevin’s face and when he blinked, he suddenly found himself in a hospital room with Cole waiting in a chair by the bed. “Welcome back to consciousness, little brother. How’s your abdomen feel?”

Kevin frowned. “Not as bad as it did. So it’s over? How did I get here already?”

“You’ve been out for a few hours,” Cole chuckled, and then launched into the wonders of general anesthesia. “Certain neurons have to depolarize and undergo an action potential to maintain consciousness, but some anesthetics can hyperpolarize them and produce unconsciousness. The anesthetic binds to and opens a certain kind of potassium channel, which increases the “leak” current of potassium. However, it doesn’t affect the voltage-gated potassium channels. This inhibits the neurons, and therefore you aren’t conscious of the surgeons performing the procedure. Amazing!”

Kevin groaned again, but not from pain this time. Cole was undoubtedly right but he sounded like a textbook. “I’m just glad the stuff worked. Now when can I go home?”

Short answer questions

1. At resting membrane potential, why does a small amount of sodium leak into the cell instead of out?

2. Define depolarization and hyperpolarization and their relationship to threshold.

3. Kevin is conscious when certain neurons in his brain are active—they depolarize and undergo action potentials. Describe the process of depolarization of a neuron to threshold.

4. What does Cole mean when he says that anesthesia “inhibits the neurons?”

5. Is Cole correct when he assumes that leak potassium channels are different than voltage-gated potassium channels? Explain your answer.

6. If the anesthesia opens more potassium leak channels, why are Kevin’s neurons less likely to produce action potentials?

7. Suppose Kevin’s pre-op blood work indicates that his extracellular potassium concentration is much higher than usual. This condition is known as hyperkalemia and must be corrected before he can undergo surgery. One of the dangers of hyperkalemia is that it makes neurons and muscle cells more excitable. Why does elevated extracellular potassium have this effect?

8. Similar types of potassium channels are found in skeletal muscle cell (plasma) membranes. Predict the effect of general anesthesia on Kevin’s skeletal muscle contraction during surgery.

Explanation / Answer

1.

The concentration of sodium is higher outside the cell. The inward diffusion of Na+ ions can be prevented by applying a positive charge to the inside of the cell. When this positive charge counterbalances the force that drives Na+ into the cell, there will be no net movement of Na+ into the cell. This is called as electrochemical equilibrium.

The equilibrium potential (the membrane potential required to produce electrochemical equilibrium) for sodium is +52 mV. The resting membrane potential is -90 mV. There is a difference of -142 mV between the equilibrium potential and membrane potential. This (-142 mV) represent the electrochemical force that drives sodium ions into the cell at resting membrane potential.

The permeability of membrane to sodium is very low, and sodium can enter into the cell at high rates only through sodium channels. However, the very high electrochemical driving force makes a small amount of Na+ to leak into the cell.

2.

Depolarization is the rush of sodium ions into the cell, which causes an increase in Na+ ions inside the cell. This makes the membrane more positive than it was before. The graded membrane potential reaches the threshold to become an action potential.

Hyperpolarization is closing of the Na+ channels and opening the K+ channels to make the cell more negative. The K+ channels allow leakage of K+ ions out from the cell. Thus, the cell restores the membrane to the original resting potential.

Initial opening of Na+ ions drives the interior potential from a more negative value to less negative value. This value is called the action threshold. Once action threshold is reached, more Na+ channels open and drive the influx of Na+ ions into the cell to reach the potential to above +30 mV.

Hyperpolarization overshoots the resting potential to about -90 mV (the actual resting potential is -70 mV). This ensures that the neuron will not receive another stimulus during hyperpolarization, or it raises the threshold for a new stimulus. It prevents any stimulus that has been already sent up an axon, from triggering another action potential, in opposite direction. Thus, hyperpolarization ensures that the signal proceeds unidirectionally.

3.

When the Dendron of the neurons receive signal/stimulus, Na+ channels open. This causes enough Na+ to enter into the cell and change the interior potential from -70 mV to -50 mV. This potential is called action threshold. Once action threshold is reached, more Na+ channels open to facilitate the influx of more Na= into the cell, till the potential reaches + 30 - +50 mV (depending on the organism). This process of influx of Na+ ions into the cell is called depolarization. The process of depolarization does not occur across the entire membrane, it actually occurs at structures called Nodes of Ranvier.

4.

Anesthetics block nerve conduction by reducing the influx of sodium ions into the cytoplasm of a neuron. They bind directly to the intracellular voltage-dependent sodium channels in the membrane of neuron. This binding of the anesthetic alters the structure of the channels, closes the “trap door” that allows sodium to flow into the cell. Once influx of sodium ions is blocked, efflux of potassium ions too is blocked, thus inhibiting the depolarization of the membrane (of neuron). If sufficient Ranvier nodes are inhibited, the nerve impulses generated downstream cannot propagate into the ganglion.

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