Action Potentials 1-3 Flashcards
Understand how the passive electrical properties of axons render them poor conductors of electrical signals over distances greater than a few millimeters.
Without the sodium channels, electrical signals can’t spread more than a few millimeters from the site of the stimulus. The take-home message here is simply that the ‘passive’ electrical properties of axons. That is, their properties without the special sodium channels are pathetically, laughably inadequate to do the job.
Describe the analogy between an electrical ‘booster station’ and an action potential.
You simply can not rely on the passive electrical properties of a wire; one has to construct booster stations at proper + regular intervals along a wire. Each booster station would do two things. First, of course, it would provide an energy boost to the decaying signal. Second, it would have to know when to apply the boost; that is, it would need to detect the incoming signal. The action potential mechanism in axons is analogous to the engineer’s booster station; the energy source is the sodium ‘battery’, and the detector is a voltage- sensing gate in the sodium channel.
Know how changes in membrane resistance, membrane capacitance, and internal (axial) resistance affect the passive spread of voltage along an axon.
↑ capacitance = ↓ voltage spread↑ internal resistance = ↓ voltage spread↑ membrane resistance = ↑ voltage spread
Describe the positions of the activation and inactivation gates in sodium channels during an action potential.
At rest, the activation gate (m) is shut and the inactivation gate (h) is open. Upon depolarization, the activation gate opens and fora brief instant both gates are open and sodium can then rush into the cell. A short time laterthe inactivation gate closes.
Understand that intracellular concentrations of sodium and potassium do not change much after a single action potential.
Ok. The movement of a few ions can produce large electrical forces but the cellular concentration of such ions barely changes.
Understand the role of the sodium/potassium pump during the action potential.
Ultimately the Na+/K+ pump must be called upon to restore proper ion balances. While the Na+/K+ pump is necessary over the long run, most axons can give long bursts of AP’s without requiring pump activity. It’s an elegant system: a large reserve of stored energy (the Na+ and K+ ‘batteries’) can be tapped rapidly and repeatedly, and restored leisurely at a later time.
Describe the mechanisms underlying the refractory period of the action potential.
After producing an action potential, an axon cannot generate another one for a few milliseconds. This is called the refractory period. It can be subdivided into an absolute refractory period, during which time no stimulus, no matter how strong, can evoke another AP, followed by a relative refractory period, during which time a stronger-than-normal stimulus is required to evoke another AP. The refractory period results primarily from the fact that the sodium channel inactivation (h) gates require time to reopen after repolarization. If a stimulus is applied when some h gates are still closed, the sodium channel activation (m) gates may swing open, but no Na+ can flow owing to the closed inactivation gates. Whenever any channel is blocked by a closed inactivation gate, we say that the channel is inactivated. The K+ channels also contribute to the refractory period. After the axon repolarizes, it takes time (several msec) for the K+ channel gates to close again. The higher K+ conductance makes it harder for a stimulus to depolarize the axon.
What is accommodation of an action potential?
Accommodation concerns a nerve cell’s loss of excitability to a stimulus that is applied slowly, rather than quickly. If an axon is depolarized quickly, as occurs normally, an action potential is generated at the usual threshold voltage. However, if the depolarization is applied slowly, many neurons do not generate an action potential as effectively (some fail entirely); this is called accommodation of the action potential.
What are two possible mechanisms for accommodation in action potentials?
Normally, physiological stimuli evoke fast membrane depolarization. A slow depolarization, however, provides time for the inactivation gates to close first, so that, when activation gates do open, any channel in which the inactivation gate has already closed is useless; it cannot conduct sodium ions. Susceptibility to accommodation varies widely among different neurons. Some fail to give an action potential when depolarized slowly, while others are barely affected. Accommodation also manifests itself during hyperkalemia. ↑ ECF [K+] causes steady membrane depolarization which causes some inactivation gates to close. Consequently, when a physiological stimulus arrives, producing a rapid depolarization, inactivated channels are incapable of contributing to the action potential. This is the mechanism that underlies the generation of cardiac arrthymias.
Define threshold for an action potential.
It’s the point at which sodium and potassium currents are exactly equal and opposite.
Understand the explosive positive-feedback nature of the rising phase of the action potential.
If the inward Na+ current momentarily exceeds the outward K+ current, it will produce a little bit more depolarization, which will open more Na+ channels and the Na+ entry process will become ‘explosive’, producing an AP. Once threshold is exceeded, a miniature ‘explosion’ occurs. Remember, at threshold, not all sodium channels are conducting yet. But the sodium entering the channels that are conducting will depolarize the membrane further, and that depolarization will cause more sodium channels to start conducting, which will cause more sodium entry, which will cause more channels to open…. This is called ‘positive feedback.’ In a few tens of microseconds, the sodium channels are all open, and Vm is well on its way to ENa.
Know why action potential propagation is much slower than the velocity of light
Because channels along the whole length of the axon need to open one after another as a result of serial chemical reactions; it is not a “bump your neighbor” type of situation as in light transmission.
Know what myelination does to axonal membrane resistance and membrane capacitance and why these changes increase conduction velocity.
Membrane capacitance (Cm) between the nodes is reduced by the myelin and membrane resistance (Rm) is increased, so that little current is lost between the nodes and the next node is depolarized to threshold very quickly. Because of this elegant specialization, the action potential jumps” from node to node; this is called saltatory conduction (L. saltare to jump). Myelination greatly increases conduction velocity.”
Describe refractoriness and explain how it prevents an action potential from reversing its direction of propagation.
An AP doesn’t reverse direction because, looking backwards (like riding in the last car on a train and looking back), all one sees is refractory axon – the sodium channels are incapable of firing an AP immediately after the active zone passes because their inactivation gates are closed.
Understand why demyelination can slow or block action potential conduction.
Demyelination causes ↑ capacitance and ↓ membrane resistance. Thus, axons would be leakier (↓Rm) and hold more charge (↑Cm) making it less likely for the signal to reach the next node to set off another AP.
