Action potential - Part II Flashcards

1
Q

Which of the following axons can conduct the AP the fastest?
a. 4µm diameter, myelinated
b. 4µm diameter, unmyelinated
c. 8µm diameter, myelinated
d. 8µm diameter, unmyelinated

A

c - 8 µm diameter and myelinated

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2
Q

What are two important factors that define the speed the axon can conduct the AP?

A
  • diameter of the axon (bigger = faster)
  • myelination or not (myelinated = faster)
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3
Q

When do we have bidirectional AP conduction?

A

experimentally

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4
Q

When do we have unilateral conduction of the AP?

A

physiologically

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5
Q

What does multiple AP along one axon determine?

A

intensity

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6
Q

What is the myelin sheath?

A

layers of lipids, for insulation

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7
Q

What are nodes of ranvier?

A

small gaps in the myelin sheath that contain voltage-gated sodium channels

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8
Q

What do nodes of ranvier do?

A

regenerate 1 AP in the nodes

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9
Q

What is saltatory conduction?

A

jumping among nodes

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10
Q

With axon size the _______ the faster

A

thicker

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11
Q

What should we know about the squid giant axon?

A
  • nonmyelinated, 200~800µm diameter
  • 100~400 folds of 1 myelinated vertebrate axon
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12
Q

What nervous system has oligodendrocytes?

A

CNS

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13
Q

How many axons do oligodendrocytes have?

A

multiple

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14
Q

What surrounds nonmyelinated axons in the CNS?

A

astrocytes

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15
Q

What is multiple sclerosis?

A

destroy the own body, CNS disorder, degrades the myelin sheath
- self immune response, abnormal!

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16
Q

What can sporadic MS lesion cause?

A

various signs/symptoms based on location

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17
Q

What CN can be compromosed with MS?

A

CN II
- MS patients can lose smell, vision
- Cauda Equina impacted also

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18
Q

What are the PNS myelin sheath cells?

A

schwann cells

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19
Q

What do schwann cells do?

A

provides 1 axon a myelin sheath

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20
Q

What surrounds nonmyelinated axons in the PNS?

A

a single schwann cell

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21
Q

What is Guillain Barre Syndrome?

A

whole body compromosed, all myelinated axons in PNS compromosed
- general function loss

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22
Q

What does an electric synapse do?

A
  • connection of cells
  • Gap junctions, AP bidirectional Conduction
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23
Q

What are electric synapses for?

A

neurons cross-talking to targets

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24
Q

What are the two types of synapse?

A
  • electric
  • chemical
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25
Q

What are gap junctions?

A

between axon terminals and post-synaptic membrase
- fast
- uncommon in CNS

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26
Q

Where are gap junctions mainly located?

A

in the inferior olivary nucleus, where we learn new skills
= need fast reactions!

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27
Q

What is the MOST common communicating unit?

A

Chemical synapse

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28
Q

What is a presynaptic axon terminal?

A

vesicles with neurotransmitters

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29
Q

What is the postsynaptic membrane receptors?

A
  • ligand-gated ion channels
  • G-protein coupled receptors
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30
Q

What is a synaptic cleft?

A
  • the gap between the presynaptic membrane and the postsynaptic membrane
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31
Q

What is a synaptic vesicle?

A

contains neurotransmitters
- diffuse through synaptic cleft to perform effects on postsynaptic membrane

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32
Q

What are receptor potentials?

A
  • receptor potential: around sensory neurons, detect stimuli and stimulants on the receptive area
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33
Q

What are synaptic potentials?

A

soma, induced through synapses

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34
Q

What is intentsity of synaptic potentials represented by?

A

amplitude, below threshold

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35
Q

What are action potentials?

A

above threshold, sum, short duration

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36
Q

What is the intensity of action potentials represented by?

37
Q

What is the first step in transformation of electrochemical signals?

A
  • Arrival of AP at axon terminal, changes membrane potential (inside should be neg)
38
Q

What happens second in transformation of electrochemical signals?

A

the opening of voltage-gated calcium channels
- allows Ca+ ions to flow in, helps synaptic vesicle fuse to presynaptic membrane

39
Q

What happens third in transformation of electrochemical signals?

A

Docking and fusion of vesicles
- Ca2+ binds to docking protein

40
Q

What happens 4th in transformation of electrochemical signals?

A

release to neurotransmitters
- they fuse to synaptic cleft

41
Q

What happens 5th in transformation of electrochemical signals?

A

Diffusion of neurotransmitters
- across the synaptic cleft released from high to low concentration
- bind to the receptors on the post synaptic membrane

42
Q

What happens last in transformation of electrochemical signals?

A

Binding Ligand-Gated ion Channels
- bind to receptors, changes the activity of their target cell

43
Q

What are the two type sof vesicles for electrochemical transformation?

A

small and big

44
Q

What do small vesicles have for electrochemical transformation?

A

different neurotransmitters
- dont need high/strong stimuli
- fuse with presynaptic membrane to release neurotransmitters

45
Q

Where are ionotropic receptors located?

A

on post-synaptic membrane

46
Q

What are ionotropic receptors?

A
  • Ligand-gated ion channels
  • FAST: point-to-point and SPECIFIC
47
Q

What happens with depolarization or hyperpolarization of Ionotropic receptors?

A
  • depolarization: excitatory postsynaptic potential (EPSP) (i.e. Glutamate)
  • hyperpolarization: Inhibitory postsynaptic potential (IPSP) (i.e. GABA)
48
Q

How many AP is enough for an electrochemical transformation?

A

1! Only takes one single presunaptic AP to induce process

49
Q

How can chloride ions hyper polarize cells

A

Chloride ions carry a 1- negative charge, if we have more chloride ions flow into cells when the channels open, more negative goes in which results in hyperpolarization which will INHIBIT

50
Q

How do large vesicles transform neurotransmitters?

A

neurotransmitters through exocytosis
- wont only affect target bc of diffusion
- active process, axon terminal “spits out”

51
Q

How do small vesicles transform neurotransmitters?

A

neurotransmitters to synaptic gap

52
Q

What are metabotropic receptors?

A
  • GPCR (G protein coupled receptor), 2nd messenger system
  • SLOW!, nonspecific, have broad and diffuse functions, point-to-area
53
Q

What happens with depolarization or hyperpolarizaiton of metabotropic receptors?

A
  • Depolarization: excitatory postsynaptic potential (EPSP)
  • Hyperpolarizatoin: inhibitory post synaptic potential (IPSP)
54
Q

How many AP are needed for metabotropic receptors?

A

Multiple presynaptic action potentials

55
Q

What are the two types of summation of synaptic potentials?

A
  • spatial summation
  • temporal summation
56
Q

What is spatial summation?

A

E1 (neuron cell body) and E2 (dendrite) locations
- stimuli from different locations simoultaneously, many arrive and add together
- Arrive at same time different spots and add together

57
Q

What is temporal summation?

A

E1 (neuron cell body) timeframe
- same location or locations with different timeframe
- different time points, same location, if strong enough can create an AP

58
Q

What is depolatization between?

A

rest potential and threshold
- above rest potential starts AP if big enough

59
Q

When does an AP happen?

A

above the threshold

60
Q

What is hyperpolarization?

A

below the threshold, more negative inside

61
Q

What is the presynaptic membrane of the neuromuscular junction (NMJ)?

A

LMN axonal terminal

62
Q

What are synapses shaped like?

63
Q

What is the postsynaptic membrane of the NMJ?

A

skeletal muscle membrane

64
Q

What are the conduction speed of an AP dependent on?

A
  • myelin sheath
  • diameter
65
Q

What is the neurotransmitter in the neuromuscular junction?

A

acetylcholine

66
Q

What is a nicotinic receptor?

A

ligand-gated sodium channel, EPSP
- always excitatory
- Ach released, binds, Na+ ions flow into muscle cells, depolarize muscle cell membrane potential

67
Q

What is Lambert Eaton syndrome?

A

Blocked Ca2+ channel = weakness, faccidity
- blocked by self immune response
- cannot initiate muscle contraction

68
Q

What happens when Ca+ flows into a cell pre-synaptically?

A
  • when Ca+ flows in, helps synaptic vesicle containing Ach to fuse with the presynaptic membrane then releases Ach, Ach interacts with its receptor on muscle cells = nicotic receptor
69
Q

What is Isaacs’ Syndrome?

A

Blocked K+ channel: impaired reporlarization; continuously release Ach- CAUSES SPASMS
- muscles always contracting
- not able to re-initiate polarization inside always +, Ca+ always coming in

70
Q

What is the most common NMJ pathology?

A

Myasthenia Gravis

71
Q

What does Myasthenia gravis cause?

A

weakness, eye muscles the worst

72
Q

What causes Myasthenia Gravis?

A
  • Blocked Ach receptor
  • Compromised AchR localization
73
Q

What is the treatment for Myasthenia Gravis?

A

Block Acetylocholinesterase

74
Q

What happens to the neurotransmitter?

A
  • reuptake
  • degradation
  • diffusion away
  • endocytosis
75
Q

What part of neurotransmitter process to NMJ problems prevent?

A

reuptake and degradation

76
Q

What does endocytosis need?

A

energy!
- swallows neurotransmitters, how large neurotransmitters get out

77
Q

What does a small molecular neurotransmitter need to be synthesized and transported?

A
  • need enzymes synthesized in the soma
  • transports to terminals through antigrade-transportation (kinesin)
  • Synthesizing neurotransmitters in the terminals (uses substrates)
78
Q

How does a peptide neurotransmitter synthesize and transport?

A
  • prepeptide/ enzymes from the nucleus
  • transported to the terminals
  • digested to form active neurotransmitter
79
Q

What are pharmaceuticals targeting neurotransmitters that increase neurotransmitter release?

A
  • L-dopa
  • ampheatmine
80
Q

What are pharmaceuticals targeting neurotransmitters that are agonists?

A
  • Barbiturate
  • Morphine
81
Q

What are pharmaceuticals targeting neurotransmitters that prevent reuptake?

A
  • Fluoxetine (prozac/ SSRI) :)
82
Q

What are pharmaceuticals targeting neurotransmitters that block degradation?

A

Pyridostigmine

83
Q

What are pharmaceuticals targeting neurotransmitters that perform disinhibition?

84
Q

What are pharmaceuticals targeting neurotransmitters that decrease neurotransmitter release?

A
  • Vesamicol and resepine
  • Botox
85
Q

What are pharmaceuticals targeting neurotransmitters that are antagonists?

A
  • strychnine
  • Haloperidol
  • atropine
86
Q

Which types of summation are available for a neuron to integrate all the receptor or synaptic potentials?

A
  • temporal: same location, different times
  • spatial: same time, different locations
87
Q

What are the presynaptic channelopathies?

A
  • Ca2+ blocked: no muscle contraction, flaccid
  • K+ channel blocked: no repolarization, spasm
88
Q

What are the postsynaptic channeopathies?

A
  • Ach receptor or fixing molecules compromised