Propagation And Tranimssion Of Action Potentials Flashcards

1
Q

What happens to depolarization as distance from stimulus increases?

A

Decay rapidly

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2
Q

Distance between axon hillock and synapse

A

Long

  • can be meters long
  • AP has to maintain strength to elicit response
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3
Q

Single APs

A

Usually not sufficient to carry info along a neuron

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4
Q

What kind of feed back is AP propagation?

A

Positive

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5
Q

AP propagation

A

Initial AP begets new APs in adjacent membrane

-bi direction if able, physiologically in one direction

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6
Q

Each new AP in propagation

A

Is full strength and follows the same steps and propagates itself

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7
Q

What allows for full strength APs to travel along length of neuron?

A

Each new AP is full strength and follows the same steps and propagates itself

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8
Q

Speed at which APs are conducted away from initiation site

A

Conduction velocity

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9
Q

What is conduction velocity dependent upon

A

Time and length constants

-how quickly you change charge across membrane

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10
Q

How fast membrane can depolarize to 63% of max AP voltage

A

How far depolarization travels before falling below 63% of max

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11
Q

Smaller time constant (t)

A

Faster depolarization, faster conduction

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12
Q

What does the time constant depend on (Rm)

A

Number of open channels (resistance)

-more open channels, lower resistance, more ion flow, faster depolarization

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13
Q

What is the second thing that the time constant depends on? (Cm)

A

How well the membrane holds charge (capacitance)

-less charge in membrane, more is transferred inside, faster depolarization

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14
Q

What allows depolarization to travel further?

A

High resistance, less open channels fewer ions leaking out, depolarization can travel further

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15
Q

How easy current can flow inside the cell

A

Internal resistance (Ri)

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16
Q

What is a better conductor than the membrane?

A

Cytoplasm

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17
Q

_____ nerves have more cytoplasm than thinner nerves (better conduction)

A

Thicker

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18
Q

Increasing diameter does what to Ri

A

Lowers by increasing area of cytoplasm to membrane

-higher length constant means further/faster conduction

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19
Q

____ nerves conduct impulses faster than smaller nerves

A

Thick

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20
Q

What limits the size of nerves?

A

Anatomical constraints

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21
Q

Which of the following set of conditions would give you the most rapid conduction?

A
  • low time constant

- high length constant

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22
Q

Layers of glial cells wrapped around axon

A

Myelination

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23
Q

What are the cells that myelinated in the CNS

A

Oligodendrocytes

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24
Q

What are the cells that myelinated in the PNS

A

Schwann

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25
Q

Myelin distribution in axons

A

Evenly distributed along axon with small spaces between

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26
Q

What are the small spaces between the myelination

A

Node of ranvier

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27
Q

What does myelin do for the axons?

A

Insulates the axon to make AP ‘jump’ between nodes

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28
Q

What is it called when the AC jumps between the nodes of ranvier

A

Saltatory conduction

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29
Q

Myelin wraps around axon and doesn’t allow any ______ in the area it surrounds

A

Ion flux

30
Q

What does myelin do the Rm (membrane resistance) under the sheath?

A

Increases it to increase the length constant

31
Q

Rm (membrane resistance at the nodes

A

Allows for ion channels to be enriched, so decreases Rm at node to decrease time constant

32
Q

Myelin essential does what to the nerve

A

Shortens it

33
Q

Which nerve is likely the most heavily myelinated?

A

Motor neuron because its long distance and needs to be quick (reflexes)

34
Q

What are some examples of demyelination diseases?

A
  • MS (central)
  • Guilin-Barre syndrome (peripheral)
  • Diabetic Neuropathy (peripheral)

Usually autoimmune

35
Q

Because myelin makes nerves fast, they control __________- receptors

A

Skeletal muscle and pain/touch receptors

36
Q

Los of myelin decreases ____ to a point where APs might not be propagated

A

Length constant

-low number of ion channels under sheath. When destroyed are unable to depolarize

37
Q

What does loss of myelin cause?

A

Muscle weakness, loss of coordination, loss of sensation, paralysis, death

38
Q

Site of communication fro one cell (usually a neuron) to another

A

Synapse

39
Q

Electrical synapse

A

Gap junctions (not that common)

40
Q

Chemical synapse

A

Most common

41
Q

Direct connections between cells which allows ions to flow between (easiest)

A

Electrical synapse

42
Q

What type of synapse creates a syncytium?

A

Electrical synapses

43
Q

What is the purpose of the gap junctions in electrical synapses?

A

Connexons make holes in neighboring membranes

44
Q

Examples of electrical synapses

A

Heart, smooth muscle, bladder, where coordinated contraction is required

45
Q

Is there integration in electrical synapse?

A

No

46
Q

Speed of electrical synapses

A

Fast

47
Q

Information is transported via chemicals across the synaptic cleft in a unidirectional flow

A

Chemical synapse

48
Q

What alters the membrane potential on the post synaptic cell

A

neurotransmitters released from presynaptic cell by the AP

49
Q

What do neurotransmitters do once released

A

Bind to receptors on post synapse

50
Q

Speed of chemical synapse

A

Slow

51
Q

Is there integration in a chemical synapse?

A

Yes

52
Q

Synaptic transmission

A
  • propagation of AP
  • release of neurotransmitter
  • binding of neurotransmitter to receptors
  • effect on post synaptic cell
53
Q

Propagation of AP

A

AP is propgated down the axon of the pre synaptic nerve

54
Q

Release of neurotransmitter

A
  • When AP reaches the terminal, voltage gated calcium channels *VGCC) open
  • Ca2+ enters, causes the release of NT into the synaptic cleft
55
Q

What happens when the AP reaches the terminal?

A

Voltage gated calcium channels (VGCC) open

56
Q

Binding of neurotransmitter to receptors

A
  • NT diffuse across the cleft from pre to post synaptic cell

- bind to receptors on post synaptic cell membrane

57
Q

Effect on post synaptic cell of NT

A
  • binding of NT to receptor alters membrane potential
  • depolarize - excitatory- more likely for AP to fire (Na+, Ca+)
  • hyperpolarize - inhibitory - less likely for AP to fire (K+, Cl)
58
Q

Predict the effect of calcium ionosphere on NT release

A

More NT is released because voltage gated calcium channels open in the terminal bouton

59
Q

Predict the effect of hypocalcemia on NT release

A

Less NT release

60
Q

Action of NT at the neuromuscular junction

A
  • AP travels down motor neuron, open VGCC, allow influx of Ca+
  • Ca2+ causes release of Ach
  • Ach binds to nicotinic receptors (nAchr) on post synaptic cell
  • nAchr are Na+ channels-leads to EPP(Na goes in, hypopolarization, AP)
  • if enough open, depolarization reaches threshold. New AP in the muscle causes contraction
61
Q

What is Ach broken down by?

A

Acetylcholine esterase (AchE)

62
Q

What does acetylcholine get broken down into?

A

Choline and acetate

63
Q

_____ is taken up by pre and used to regenerate Ach for next transmission

A

Choline

64
Q

Once Ach is no longer bound

A

EPPs stop, APs stop and contraction stops

65
Q

Altering the NMJ

A

Done therapeutically for anesthesia or treating diseases. Can be fatal

66
Q

Predict the mechanism of action of neostigmine

A

Inhibits acetylcholine esterase (allows Ach to accumulate in synapse)

67
Q

What are some chemicals that affect NMJ?

A
  • Botulinum toxin-Botox
  • Curare-arrow poison
  • Neostigmine -AchE inhibitor
  • hemicholinium-blocks choline reabsoroption - no Ach
68
Q

How does botulinum toxin (Botox) affect NMJ?

A

Blocks release of Ach- paralysis

  • locally, no wrinkles on your forehead.
  • systemically, paralyzed respiratory muscle, dead
69
Q

How does curare (poison arrow) affect NMJ?

A

Blocks Ach receptors-paralysis

-no medicinal use, paralyzed respiratory muscle, dead

70
Q

How does neostigmine affect NMJ?

A

AchE inhibitor-prolongs time Ach stays in cleft, increases contractions
-used in myasthenia gravis and to reverse paralytic anesthesia

71
Q

What are some uses of disruption of the NMJ?

A
  • potent chemical ware fare

- pesticides (organophosphates)