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Flashcards in 1: Action Potentials Deck (26)
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1
Q

Define capacitance. What do capacitors do? How does capacitance affect speed of membrane potential changes along an axon?

A

Capacitance: occurs whenever conducting materials are separated by insulating material (thinner insulator = more capacitance)

Capacitors store charges of opposite sign on opposing surfaces

Membrane capacitance slows time course of voltage changes
-Results in gradual, rather than sharp, change in ionic current/membrane potential

2
Q

How does myelination affect membrane capacitance and length constant?

A

Myelination DECREASES membrane capacitance and therefore INCREASES speed and INCREASES length constant

3
Q

Name several of the most widely known reagents that block the activity of voltage-gated ion channels. (5)

A

Tetrodotoxin (from pufferfish) and saxitoxin (from red algae): blocks Na channels

Conus toxins (from fish-eating snails): blocks Ca channels

Tetraethylammonium (TEA): blocks K channels

Lidocaine: blocks Na channels

4
Q

Illustrate the 4 different phases of action potentials and correlate them with the types of ion channels that are active during them.

A
  1. Depolarizing/rising phase: MP approaches equilibrium for Na ions
    - Voltage-gated Na channels are open
  2. Overshoot: MP may become positive
    - Voltage-gated Na channels still open
  3. Repolarizing phase: MP rapidly becomes more negative
    - Na channels are closed and inactive, “delayed rectifier” K channels are open
  4. Hyperpolarizing phase: MP becomes more negative than it was originally
    - “Delayed rectifier” K channels are open, then close
5
Q

Explain how HCN channels and A current K channels can influence the frequency of firing in rhythmically active cells.

A

HCN channels: hyperpolarization, cyclic nucleotide-gated channels

  • Open upon strong hyperpolarization
  • Cation-selective: Na ions go in
  • Drive membrane potential to threshold
  • Important in rhythmically active, pacemaking cells

“A current” K channels prolong interspike interval between APs

  • Open upon depolarization -> counteract depolarization
  • Rapid inactivation
  • Only a few, so don’t prevent AP, but do DELAY reaching threshold
6
Q

Illustrate how action potentials propagate along an axon.

A

Involves both active and passive spread

Active depolarization -> passive spread to next channel -> active depolarization and so on

7
Q

Describe how myelination occurs in the CNS and PNS, including the cell types thought to play important roles.

A

CNS: individual oligodendrocytes form myelin sheaths around multiple axons
-Myelin genes unaffected by axon presence or absence

PNS: individual Schwann cells form myelin sheaths around one axon (myelinated), or loose wraps around multiple axons (unmyelinated)
-Myelin gene expression depends upon axonal contact

8
Q

Illustrate how saltatory conduction occurs and why it is advantageous (2).

A

Nodes of Ranvier: uncovered regions of the axon membrane between myelin sheath
-Have high concentration of Na channels

APs only regenerated at nodes of Ranvier, spreads passively in between nodes
-“Jumps” from node to node rather than regenerating at all points along the axon

  1. Increased velocity
  2. Metabolically more efficient: less ATPase activity needed because ion flow is only at nodes
9
Q

Explain how demyelinating diseases can slow and even prevent the propagation of action potentials along an axon. (3)

A

Demyelinating diseases: segments of myelin absent

  • Slow/prevent propagation by increasing capacitance (decrease rate of depolarization) and decreasing membrane resistance (shorter length constant)
  • —May result in failure of AP to be propagated if depolarization at next excitable region doesn’t reach AP threshold
  1. Guillain-Barre syndrome: loss of PNS myelin due to immune response
  2. Multiple sclerosis: loss of CNS myelin, involves autoimmune response
    - Get formation of astrocyte scars/plaques
    - No treatment available, use immunosuppressives
  3. Charcot-Marie-Tooth syndrome: myelin loss from mutation in gap junctions connecting the cytoplasm of the different layers of myelin
10
Q

Define membrane time constant. How does it relate to the concept of temporal summation?

A

Time to reach 63% of total potential charge (rather, to decay to 37% of original potential change)

Important for temporal summation

  • Stimuli too small by themselves can add up if the stimulus interval is shorter than the time constant
  • Longer time constant = more potential for temporal summation
11
Q

What is the length constant? How does it relate to spatial summation?

A

The distance at which 37% of the original change in membrane potential still occurs

Receptor potentials will summate if they are within the length constant

12
Q

How do capacitance and axon diameter relate to speed of propagation?

A

Capacitance is INVERSELY proportional to speed of propagation (thinner membrane = higher capacitance = lower speed)

Axon diameter is DIRECTLY proportional to speed of propagation (larger diameter = higher speed)

13
Q

Define action potential.

A

A rapid depolarization and then repolarization of the membrane in response to a membrane depolarization of sufficient magnitude

14
Q

Define threshold potential. Why are APs “all or none”?

A

The membrane potential at which the inward current through the Na channels that are opening up is finally greater than the outward K current through other channels

All or none because reaching this threshold -> very rapid positive feedback cycle (more Na channels open)

15
Q

Define refractory period.

A

A period of time in which another AP cannot be generated or can only be generated with some difficulty

16
Q

What are the two refractory periods and what causes each?

A

Absolute refractory period: impossible to generate another AP
–Na channels are inactivated

Relative refractory period: AP can be elicited, but requires a stronger stimulus
–Residual K channel activity counteracts depolarization

17
Q

True/false: The activity of the Na/K ATPase plays an important role in the time course of an AP

A

FALSE!

Proportion of ions that move during an AP is very small

18
Q

Describe the structural features of voltage-gated ion channels that are responsible for their ion selectivity.

A

Ion selectivity: determined by pore loops (selectivity filter)

  • Select for size (hydrated radius) and hydration energy (more E required to strip water from small ion)
  • AAs on tips of pore loops are key
19
Q

Describe the structural features of voltage-gated ion channels that are responsible for their voltage-gated activation.

A

Activation: determined by S4 voltage sensors

  • Channels rapidly open, “all or none”
  • Charged residues (arg, lys) in S4 TM region -> “helical twist” outward when inside becomes positive
20
Q

Describe the structural features of voltage-gated ion channels that are responsible for their inactivation.

A

Inactivation: determined by intracellular loops and AA clusters

  • K has “Ball and chain”: (+) charge group of AA plugs channel like a bathtub stopper
  • Na and Ca channels have (+) charged AA cluster on loop that flips up and inactivates the channel
21
Q

What is a Ca shoulder?

A

A plateau in the repolarization phase of an AP

Results from a delayed rate of repolarization due to slowly inactivating Ca channels
—Ca influx keeps cell somewhat depolarized

Important in NT release

22
Q

Give two examples of the role of ion channels in disorders.

A

Neuromas (severed nerve -> tangle of axons) -> (phantom) pain through increased Na channel expression

Channelopathies -> epilepsies/seizures

23
Q

How is backpropagation prevented?

A

The part of the axon that was just traversed is in the refractory period and cannot initiate a regenerative response

24
Q

What is the AIS?

A

Axon initial segment, or axon hillock

Initial part of axon next to the cell body; site of AP generation

Separates axonal compartment of cell from somatodendritic compartment

25
Q

Describe 5 proteins thought to play important roles in myelination.

A
  1. Neuregulin (NRG): from axon; regulates number of layers of myelin sheath
    - More layers for larger axons
  2. Myelin associated protein (MAG): initial axon/glia recognition/adhesion
  3. Po: over 50% of protein in PNS myelin
    - Mediates myelin compaction
  4. Proteolipid protein (PLP): over 50% of protein in CNS myelin
    - Mediates myelin compaction
  5. Myelin basic protein (MBP): along inner surface of membrane
    - Mediates myelin compaction
26
Q

Briefly, describe the therapeutic use of oligodendrocyte transplantation.

A

Used to remyelinate CNS axons in experimental models

-Problem = thinner myelin than the original sheath