Question #97 of GRE Sample Subject test (MolBio)
Propagation of a regenerative action potential
along an axon can be accelerated by which of the
following?
(A) A decrease in the transmembrane resistance
(B) A decrease in the axoplasmic resistance
(C) Reduced myelin wrapping
(D) Shortened internodal lengths
(E) Narrowing of the axon diameter
Show answer
Propagation of a regenerative action potential
along an axon can be accelerated by which of the
following?
(A) A decrease in the transmembrane resistance
(B) A decrease in the axoplasmic resistance
(C) Reduced myelin wrapping
(D) Shortened internodal lengths
(E) Narrowing of the axon diameter
Show answer
Answer:
(B)
First of all, what "regenerative" action potential means? Kandel's textbook defines just an action potential (AP) as a regenerative electrical signal.
Now we can unwrap answers and say what will happen in each case.
(A) A decrease in the transmembrane resistance = essentially that is increase in channels number. But not Hodgkin's channels, but so-called "leaky" channels that prevent absolute ion separation by Na/K-ATPase. If leaky channels were more abundant (or more active, you can imagine some drug that does that) it would be more difficult for membrane to stay polarized.
(C) Reduced myelin wrapping = As we all know, myelin facilitates rapid AP propagation by essentially increasing membrane resistance. Thinning of myelin will slow down impulse propagation.
(D) Shortened internodal lengths = shortening of distance between ranvier nodes. This will also slow down signal propagation. There are two ways for AP to travel along axon: as it happens in umyelinated axons and "jumping" from one node to another (saltatory conduction). In latter case, because of myelin isolation (high resistance of membrane), depolarization at one node is enough to trigger channels' opening in nearby nodes (on distance ~200-2000 um). "Inside" nodes signal is propagated in general fashion: channels opens one by one in orderly manner and go through open-closed/inactivate-close/active cycle.
Shortening of internodal length will slow down signal. However, increase in distance between nodes might decrease sensitivity of axon to signal propagation. That is, not every single AP or not every packets of APs will propagate from one node to distal one, because depolarization will essentially be lost on the road due to diffusion of ions.
(E) Narrowing of the axon diameter = Seemingly useful change for rapid ion diffusion, that will not speed up signals. Axon diameter is very important for AP since it is resistance that prevent signal from travelling. Lower resistance can be achieved by increasing diameter or ions concentration. However, I suppose, that ion concentration change will affect channels activity and other physiological properties before change in conductivity. Ions here act like free electrons in semiconductors.
(B) A decrease in the axoplasmic resistance. Now, that is one correct answer. As discussed on (E) resistance of cytoplasm in axon (axoplasm, duh) plays important role in AP propagation.
Now, what is bad with answer (A)? Honestly, it was on my correct-answers-list for that question. if you think about it, axon consists of two parts: conductivity and depolarization mechanisms. Cytoplasm resistance contribute to conductivity, however leaky channels and voltage-dependent channels influence depolarization and AP generation. AP propagation does not really change with membrane resistance, but rather act as filter for action potentials that are too low. Or other wise, permit easily AP generation by keeping cell membrane closer to threshold (you know what that is, right?)
(B)
First of all, what "regenerative" action potential means? Kandel's textbook defines just an action potential (AP) as a regenerative electrical signal.
Now we can unwrap answers and say what will happen in each case.
(A) A decrease in the transmembrane resistance = essentially that is increase in channels number. But not Hodgkin's channels, but so-called "leaky" channels that prevent absolute ion separation by Na/K-ATPase. If leaky channels were more abundant (or more active, you can imagine some drug that does that) it would be more difficult for membrane to stay polarized.
(C) Reduced myelin wrapping = As we all know, myelin facilitates rapid AP propagation by essentially increasing membrane resistance. Thinning of myelin will slow down impulse propagation.
(D) Shortened internodal lengths = shortening of distance between ranvier nodes. This will also slow down signal propagation. There are two ways for AP to travel along axon: as it happens in umyelinated axons and "jumping" from one node to another (saltatory conduction). In latter case, because of myelin isolation (high resistance of membrane), depolarization at one node is enough to trigger channels' opening in nearby nodes (on distance ~200-2000 um). "Inside" nodes signal is propagated in general fashion: channels opens one by one in orderly manner and go through open-closed/inactivate-close/active cycle.
Shortening of internodal length will slow down signal. However, increase in distance between nodes might decrease sensitivity of axon to signal propagation. That is, not every single AP or not every packets of APs will propagate from one node to distal one, because depolarization will essentially be lost on the road due to diffusion of ions.
(E) Narrowing of the axon diameter = Seemingly useful change for rapid ion diffusion, that will not speed up signals. Axon diameter is very important for AP since it is resistance that prevent signal from travelling. Lower resistance can be achieved by increasing diameter or ions concentration. However, I suppose, that ion concentration change will affect channels activity and other physiological properties before change in conductivity. Ions here act like free electrons in semiconductors.
(B) A decrease in the axoplasmic resistance. Now, that is one correct answer. As discussed on (E) resistance of cytoplasm in axon (axoplasm, duh) plays important role in AP propagation.
Now, what is bad with answer (A)? Honestly, it was on my correct-answers-list for that question. if you think about it, axon consists of two parts: conductivity and depolarization mechanisms. Cytoplasm resistance contribute to conductivity, however leaky channels and voltage-dependent channels influence depolarization and AP generation. AP propagation does not really change with membrane resistance, but rather act as filter for action potentials that are too low. Or other wise, permit easily AP generation by keeping cell membrane closer to threshold (you know what that is, right?)
