L8-13: Excitable Cells Flashcards

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1
Q

What charge is the inside of the axon membrane, relative to the outside?

A

negative

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2
Q

How is the negative charge of the membrane maintained?

A

high permeability of K+
Active transport of Na+

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3
Q

How does the Na+ cause a slight charge on the outside?

A

Because it is electrogenic

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4
Q

What gradient do the ions move down?

A

Electrochemical

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5
Q

How is equilibrium potential determined?

A

Nernst equation

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6
Q

What are the 2 different types of refractory periods?

A

Absolute and relative

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7
Q

What happens during the absolute refractory period?

A

The membrane cant generate another action potential (AP) no matter how big the stimulus

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8
Q

Why cant another AP be stimulated during the absolute refractory period

A

Because the Na+ channels are inactivated

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9
Q

What happens during the relative refractory period?

A

Membrane can generate another AP but only if the stimulus is bigger than normal

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10
Q

How can another AP be stimulated during relative refractory period?

A

some K+ channels are still open and some Na+ are recovered

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11
Q

When does the relative refractory period occur?

A

From deploarisation to hyper-polarisation

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12
Q

Why is the refractory period useful?

A

Because it stops action potentials going backwards

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13
Q

What are the 5 stages of transmission of an action potential?

A

1) Resting state
2) Slow rising phase
3) Rapid rising phase
4) Early repolarisation
5) Hyperpolarisation

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14
Q

What factor makes the inactivation gate close?

A

Time

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15
Q

What factors makes the activation gates close?

A

Voltage and time

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16
Q

What is the approximate mV for threshold?

A

-55mV

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17
Q

What are the stages the Na+ gates go through?

A

Open, Inactivated and closed

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18
Q

What are myelin sheath made of?

A

Schwann cells

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19
Q

What is the term used when depolarisation jumps from node to node?

A

Saltatory conduction

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20
Q

What structural changes can be made to make depolarisation faster?

A

Increase diameter of axon and increase the membrane resistance (using myelin sheath)

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21
Q

What is a key feature of the nodes of ranvier?

A

There are a high density of Na+ channels

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22
Q

What are the 2 types of axons?

A

Myelinated and Unmyelinated

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23
Q

What happens when an AP invades a terminal?

A

Membrane is depolarised and Voltage Gated (VG) Ca2+ channels open

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24
Q

When Ca2+ channels are open where does Ca2+ diffuse?

A

Into the axon terminal

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25
Q

How is neurotransmitter (NT) released into the synaptic cleft?

A

Via exocytosis once vesicles fuse with the presynaptic membrane

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26
Q

What happens once the NT binds to the postsynaptic membrane?

A

Causes ligand-gated Na+ channels to open and Na+ diffuses into muscle endplate (at NMJ!)

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27
Q

How is End Plate Potential calculated?

A

(ENa+EK)/2

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28
Q

When do mini-EPPs occur?

A

When nerve muscles are at rest

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29
Q

What is the approximate amount of vesicles released in response to an AP and why?

A

~200-300 and the extra margin is a safety factor

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30
Q

What are the 5 zones, lines and bands of the sarcomere and what do they consist of?

A

M line - middle of myosin
Z line - End of actin
A band - actin and myosin
I band - actin only
H zone - myosin only

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31
Q

What happens to each zone, line and band during muscle contraction?

A

M line - stays same
Z line - distance decreases
A band - length stays the same
I band - length decreases
H zone - length decreases

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32
Q

What are thin filaments made up of?

A

Actin, tropomyosin and troponin

33
Q

What molecules form F-actin strands?

A

G-actin molecules

34
Q

What is the structure of the F-actin strands?

A

They are wrapped in a double helix

35
Q

How are tropomyosin filaments arranged?

A

They are wound around the F-actin double helix

36
Q

What are the 3 subunits of troponin?

A

T, I and C

37
Q

Which subunits are bound to troponin and actin, blocking the myosin binding site?

A

T and I

38
Q

How does the AP get into other parts of the muscle?

A

T-tubules

39
Q

What is the structure of the T-tubule?

A

There are invaginations of the muscle membrane (sarcolemma) that penetrates deep into muscle fibre

40
Q

What is the structure of the sarcoplasmic reticulum?

A

It is a tubular structure surrounding myofibrils that enlarges into terminal cisternae

41
Q

How does muscle relaxation occur?

A

Removal of Ca2+ by SR so ATP stays bound to myosin so myosin remains bound therefore preventing muscle contraction

42
Q

When does myosin bind to the binding site?

A

When myosin is in its high energy state (ATP is hydrolysed to ADP + Pi)

43
Q

How does the power stroke take place?

A

Myosin heads rotate to the centre of the sarcomere

44
Q

How does the actin-myosin cross-bridge break?

A

When ATP binds to myosin

45
Q

Describe the structure of a myelinated motor neurone

A

Dendrites, cell body, myelinated axon, axon and axon terminal

46
Q

What is the difference between bipolar and pseudo-polar neurones?

A

Pseudo-polar has myelinated axons but bipolar does not

47
Q

What are the 2 different types of electrical impulses?

A

Action potential and graded potential

48
Q

What is the main principle of an action potential?

A

All or nothing

49
Q

Describe the action of a graded potential

A

It has variable strength, travels short distances and loses strength

50
Q

Where do graded potentials take place?

A

In the dendrites, cell bodies and axon terminals

51
Q

How do graded potentials have a variable strength during depolarisation?

A

Na+ diffuses through the membrane so concentration decreases causing depolarisation to get weaker

52
Q

What is a depolarising graded potential known as?

A

An excitatory postsynaptic potential (EPSP)

53
Q

What is a hyperpolarising graded potential?

A

An Inhibitory postsynaptic potential (IPSP)

54
Q

Where in the neurone does the graded potential have to reach in order to stimulate an AP?

A

Axon Hillock

55
Q

What is it known as if the threshold is not reached at the axon hillock?

A

Sub-threshold EPSP

56
Q

What is it know as if the threshold is reached at the axon hillock?

A

Supra-threshold EPSP

57
Q

What are the characteristics of the intracellular make-up? (Hint: there’s 6)

A

-Synaptic vesicle recycling
-Retrograde fast axonal transport
-Old membrane components digested in lysosomes
-peptides synthesised and packed by golgi
-fast axonal transport along microtubule network
-vesicle contents released by exocytosis

58
Q

What changes when the strength of a stimulus is very big?

A

Frequency (stimulus intensity is frequency encoded)

59
Q

Why do neurones require an abundant amount of glucose and oxygen?

A

As they have a high metabolic rate

60
Q

When multiple pre-neurones connect to a singular post-neurone what is this known as?

A

Spatial summation (different points in space)

61
Q

How is summation caused by 1:1 neurones?

A

From graded potentials, by them being close enough together to stimulate an AP

62
Q

How can 2 EPSPs be diminished by summation? and what is this known as?

A

By an IPSP, postsynaptic inhibition

63
Q

What is it called when graded potentials overlap in time?

A

Temporal summation

64
Q

What is it called when the summation of graded potentials are demonstrated?

A

Postsynaptic modulation/integration

65
Q

What happens during presynaptic modulation?

A

An inhibitory or excitatory neurone is found near the axon terminal causing either a release of NT or no release of NT

66
Q

What are the presynaptic similarities?

A

During an action potential Ca2+ channels open, the increase causes exocytosis of NT that diffuses across the synaptic cleft

67
Q

What are the postsynaptic differences?

A

NT identity differs and receptor identity differs (as they work differently)

68
Q

What are the different types of NT? (Hint: there’s 6)

A

-Acetylcholine
-Amines
-Polypeptides
-Purines
-Gases

69
Q

What are the main IPSP and EPSP NTs?

A

GABA (Gamma-aminobutyric acid)-IPSP
Glycine-IPSP
Glutamate-EPSP

70
Q

What are the 2 different types of receptors?

A

Ligand-gated ion channels (ionotropic)
G-protein coupled receptors (metabotropic)

71
Q

What are the main functions of the 2 receptors?

A

Ionotropic - fast synaptic potentials
Metabotropic - slow synaptic potentials

72
Q

What are the NTs associated with ionotropic receptors?

A

Acetylcholine
Glutamate
GABA

73
Q

What are the NTs associated with metabotropic receptors?

A

Adrenaline (both hormone and NT)
Histamine
Cholecystokinin
ATP
Acetylcholine (used in both receptors)

74
Q

How do G-protein coupled receptors work?

A

2nd messenger pathway, modifys proteins and regulates synthesis of new proteins which coordinates an intracellular response

75
Q

What is variation in electrical activity called?

A

Synaptic plasticity

76
Q

How does synaptic plasticity work?

A

neuronal synapses change in response to past activity which causes variation in the electrical impulse

77
Q

What is the process of long-term potentiation (LTP)

A

Repetitive stimulation at a synapse which increases the efficacy of transmission

78
Q

How does LTP work?

A

Glutamate is released, binds to 2 ionotropic receptors, AMPA receptor is Na+ channel so EPSP (may or may not trigger AP), NMDA blocked by Mg2+, due to repetitive stimulation there’s greater depolarisation so Mg2+ is ejected, Ca2+ flows through NMDA receptor, makes post-neurone more sensitive to glutamate so more glutamate released