Action potential - Part II Flashcards

(88 cards)

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
What are gap junctions?
between axon terminals and post-synaptic membrase - fast - uncommon in CNS
26
Where are gap junctions mainly located?
in the inferior olivary nucleus, where we learn new skills = need fast reactions!
27
What is the MOST common communicating unit?
Chemical synapse
28
What is a presynaptic axon terminal?
vesicles with neurotransmitters
29
What is the postsynaptic membrane receptors?
- ligand-gated ion channels - G-protein coupled receptors
30
What is a synaptic cleft?
- the gap between the presynaptic membrane and the postsynaptic membrane
31
What is a synaptic vesicle?
contains neurotransmitters - diffuse through synaptic cleft to perform effects on postsynaptic membrane
32
What are receptor potentials?
- receptor potential: around sensory neurons, detect stimuli and stimulants on the receptive area
33
What are synaptic potentials?
soma, induced through synapses
34
What is intentsity of synaptic potentials represented by?
amplitude, below threshold
35
What are action potentials?
above threshold, sum, short duration
36
What is the intensity of action potentials represented by?
frequency
37
What is the first step in transformation of electrochemical signals?
- Arrival of AP at axon terminal, changes membrane potential (inside should be neg)
38
What happens second in transformation of electrochemical signals?
the opening of voltage-gated calcium channels - allows Ca+ ions to flow in, helps synaptic vesicle fuse to presynaptic membrane
39
What happens third in transformation of electrochemical signals?
Docking and fusion of vesicles - Ca2+ binds to docking protein
40
What happens 4th in transformation of electrochemical signals?
release to neurotransmitters - they fuse to synaptic cleft
41
What happens 5th in transformation of electrochemical signals?
Diffusion of neurotransmitters - across the synaptic cleft released from high to low concentration - bind to the receptors on the post synaptic membrane
42
What happens last in transformation of electrochemical signals?
Binding Ligand-Gated ion Channels - bind to receptors, changes the activity of their target cell
43
What are the two type sof vesicles for electrochemical transformation?
small and big
44
What do small vesicles have for electrochemical transformation?
different neurotransmitters - dont need high/strong stimuli - fuse with presynaptic membrane to release neurotransmitters
45
Where are ionotropic receptors located?
on post-synaptic membrane
46
What are ionotropic receptors?
- Ligand-gated ion channels - FAST: point-to-point and SPECIFIC
47
What happens with depolarization or hyperpolarization of Ionotropic receptors?
* depolarization: excitatory postsynaptic potential (EPSP) (i.e. Glutamate) * hyperpolarization: Inhibitory postsynaptic potential (IPSP) (i.e. GABA)
48
How many AP is enough for an electrochemical transformation?
1! Only takes one single presunaptic AP to induce process
49
How can chloride ions hyper polarize cells
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
How do large vesicles transform neurotransmitters?
neurotransmitters through exocytosis - wont only affect target bc of diffusion - active process, axon terminal "spits out"
51
How do small vesicles transform neurotransmitters?
neurotransmitters to synaptic gap
52
What are metabotropic receptors?
- GPCR (G protein coupled receptor), 2nd messenger system - SLOW!, nonspecific, have broad and diffuse functions, point-to-area
53
What happens with depolarization or hyperpolarizaiton of metabotropic receptors?
- Depolarization: excitatory postsynaptic potential (EPSP) - Hyperpolarizatoin: inhibitory post synaptic potential (IPSP)
54
How many AP are needed for metabotropic receptors?
Multiple presynaptic action potentials
55
What are the two types of summation of synaptic potentials?
- spatial summation - temporal summation
56
What is spatial summation?
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
What is temporal summation?
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
What is depolatization between?
rest potential and threshold - above rest potential starts AP if big enough
59
When does an AP happen?
above the threshold
60
What is hyperpolarization?
below the threshold, more negative inside
61
What is the presynaptic membrane of the neuromuscular junction (NMJ)?
LMN axonal terminal
62
What are synapses shaped like?
buttons
63
What is the postsynaptic membrane of the NMJ?
skeletal muscle membrane
64
What are the conduction speed of an AP dependent on?
- myelin sheath - diameter
65
What is the neurotransmitter in the neuromuscular junction?
acetylcholine
66
What is a nicotinic receptor?
ligand-gated sodium channel, EPSP - always excitatory - Ach released, binds, Na+ ions flow into muscle cells, depolarize muscle cell membrane potential
67
What is Lambert Eaton syndrome?
Blocked Ca2+ channel = weakness, faccidity - blocked by self immune response - cannot initiate muscle contraction
68
What happens when Ca+ flows into a cell pre-synaptically?
- 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
What is Isaacs' Syndrome?
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
What is the most common NMJ pathology?
Myasthenia Gravis
71
What does Myasthenia gravis cause?
weakness, eye muscles the worst
72
What causes Myasthenia Gravis?
- Blocked Ach receptor - Compromised AchR localization
73
What is the treatment for Myasthenia Gravis?
Block Acetylocholinesterase
74
What happens to the neurotransmitter?
- reuptake - degradation - diffusion away - endocytosis
75
What part of neurotransmitter process to NMJ problems prevent?
reuptake and degradation
76
What does endocytosis need?
energy! - swallows neurotransmitters, how large neurotransmitters get out
77
What does a small molecular neurotransmitter need to be synthesized and transported?
- need enzymes synthesized in the soma - transports to terminals through antigrade-transportation (kinesin) - Synthesizing neurotransmitters in the terminals (uses substrates)
78
How does a peptide neurotransmitter synthesize and transport?
- prepeptide/ enzymes from the nucleus - transported to the terminals - digested to form active neurotransmitter
79
What are pharmaceuticals targeting neurotransmitters that increase neurotransmitter release?
- L-dopa - ampheatmine
80
What are pharmaceuticals targeting neurotransmitters that are agonists?
- Barbiturate - Morphine
81
What are pharmaceuticals targeting neurotransmitters that prevent reuptake?
- Fluoxetine (prozac/ SSRI) :)
82
What are pharmaceuticals targeting neurotransmitters that block degradation?
Pyridostigmine
83
What are pharmaceuticals targeting neurotransmitters that perform disinhibition?
- caffeine
84
What are pharmaceuticals targeting neurotransmitters that decrease neurotransmitter release?
- Vesamicol and resepine - Botox
85
What are pharmaceuticals targeting neurotransmitters that are antagonists?
- strychnine - Haloperidol - atropine
86
Which types of summation are available for a neuron to integrate all the receptor or synaptic potentials?
- temporal: same location, different times - spatial: same time, different locations
87
What are the presynaptic channelopathies?
- Ca2+ blocked: no muscle contraction, flaccid - K+ channel blocked: no repolarization, spasm
88
What are the postsynaptic channeopathies?
- Ach receptor or fixing molecules compromised