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KNES259 > Membrane Potential and Action Potential > Flashcards

Membrane Potential and Action Potential Flashcards

1
Q

How do cells communicate (two ways)?

A

-Endocrine (hormones)
-Nervous system (cells/tissues/organs/systems)

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2
Q

Function of axon hillock

A

-Region that decides whether to send action potential or not
-Right at the beginning of the axon

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3
Q

Where are synapses formed?

A

Between the axon terminals of the pre-synaptic cell and dendrites of the post-synaptic cell

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4
Q

3 different types of neurons and their general structure

A

Bipolar: dendrites converge to form one structure which leads to the cell body

Pseudo-unipolar: cell body has a peripheral axon coming from dendrites and a central axon leaving to axon terminals

Multipolar: cell body in the middle of all the dendrites

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5
Q

Function of cell body

A

Houses nucleus and organelles

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6
Q

Function of dendrites

A

Increases surface area for receiving signals and send signal to cell body

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7
Q

Function of axon

A

-Nerve fibre
-Conducts impulses away from cell body

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8
Q

Where do chemical messengers release from?

A

Axon terminals

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9
Q

Kinesins

A

-Carry nutrients enzymes organelles away from cell body
-Ride the railway of micotubules

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10
Q

Dyneins

A

-Carries recycled vesicles, chemical messengers back towards cell body

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11
Q

At rest, where is most of the Na+ found?

A

Extracellular fluid (outside cell)

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12
Q

At rest, where is most of the K+ found?

A

Intracellular fluid (inside cell)

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13
Q

What is the resting membrane potential?

A

-70 mV

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14
Q

What are the two competing gradients in the nerve cell? Which one wins?

A

There is a concentration gradient (of K+ wanting to leave the cell) and an electrical gradient (the inside being more negative wants more positive charge inside). The concentration gradient is stronger and ultimately K+ will leave the cell.

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15
Q

What is the Nernst potential for Na+?

A

+60 mV

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16
Q

What is the Nernst potential for K+?

A

-89 mV

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17
Q

What does Nernst potential mean? How do Na+ and K+ differ?

A

-It’s the point at which equilibrium would be reached if ions were allowed to move
-When they are allowed to move, they’ll try really hard to reach that potential
-Because K+ wants to leave the cell to beat the concentration gradient, the inside of the cell would get much more negative until -89 mV
-Because Na+ wants to enter the cell to beat the concentration gradient AND electrical gradient, the inside of the cell would get more positive until +60 mV

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18
Q

At resting membrane potential, what gates are open/closed, and which pumps are working?

A

-Na+ and K+ gates are closed
-There is some K+ leakage
-Na+/K+ pump is working to maintain the -70 mV membrane potential

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19
Q

Which 4 mechanisms maintain membrane potential?

A

-Impermeable membrane that does not allow ions to move across
-Na+/K+ ATPase pump is working to make outside more positive
-Increased permeability to K+ results in K+ leakage, making the inside more negative
-Large anions inside the membrane cannot leave, making the inside more negative

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20
Q

What are the 4 different membrane states?

A
  1. Polarization: state when membrane potential is other than 0 mV (basically net neutral)
  2. Depolarization: membrane becomes more positive
  3. Repolarization: membrane returns to resting potential after a depolarization by becoming more negative
  4. Hyperpolarization: membrane becomes more negative than at rest
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21
Q

What distance do graded potentials cover?

A

Short distance

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22
Q

What initiates graded potentials?

A

-Mechanical stimulus (pushing on skin)
-Chemical stimulus (sending NT to open a gate)
-Electrical stimulus

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23
Q

Where are graded potentials initiated?

A

Dendrites

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24
Q

The amplitude of a GP depends on __________

A

Stimulus strength

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25
Q

How do graded potentials become action potentials?

A

They can summate, which might get the membrane potential to the threshold, which triggers an action potential

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26
Q

What are the 3 phases of action potentials?

A
  1. Depolarization
  2. Repolarization
  3. Hyperpolarization
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27
Q

Examples of graded potentials

A

-Postsynaptic potentials: decide whether to continue the message
-Receptor potentials: have to be big enough to send to brain to do an AP
-End-plate potentials: muscle
-Pacemaker potentials: heart
-Slow-wave potentials: smooth muscle in gut

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28
Q

What is the threshold for an action potential to occur?

A

-55 mV

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29
Q

Do Na+ and K+ gates get involved in graded potentials?

A

No

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30
Q

Do action potentials decrease in size as they travel down the axon?

A

No

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31
Q

During depolarization, what ion moves and in what direction?

A

-Na+ gates open and Na+ rushes into the cell
-When the membrane potential reaches +30 mV, the gates close and are unable to open again until they reset

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32
Q

During repolarization, what ion moves and in what direction?

A

-K+ gates open at the +30 mV mark
-K+ wants to leave the cell due to the positive charge inside the cell and the concentration gradient of K+ outside cell

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33
Q

Why does hyperpolarization occur?

A

-K+ gates are very slow to close to we overshoot the mark and end up with a more negative inside of the cell

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34
Q

What is the membrane potential during hyperpolarization?

A

-80 mV

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35
Q

How do we restore the cell from hyperpolarization back to resting membrane potential?

A

-The Na+/K+ pump gradually restores the concentration gradients
-Sodium is pumped outside the cell
-Potassium is pumped inside the cell

36
Q

When is the absolute refractory period?

A

-From the time that Na+ gates open until they close
-No second AP is possible even with large stimulus

37
Q

When is the relative refractory period?

A

-As the cell repolarizes and becomes hyperpolarized
-A second AP is possible with a bigger stimulus

38
Q

How do neurons self-propagate?

A

-An impulse in one region is enough of a disturbance to cause the neighbouring regions to reach threshold and trigger an AP

39
Q

Why are action potentials uni-directional?

A

-Once they move down the axon, the impulse cannot trigger an action potential in the previous regions because they are still in their refractory periods

40
Q

Comparison of GPs to APs characteristics:

A

Graded Potentials:
-Can summate
-No refractory period
-Can vary in size
-Can be excitatory or inhibitory

Action Potentials:
-Cannot summate
-Refractory period
-All or nothing –> does not vary in size
-Only excitatory

41
Q

How do we get an action potential to inhibit something?

A

-We excite neuron to release an inhibitory NT

42
Q

Is Na+ still inside the cell during repolarization?

A

Yes

43
Q

Is K+ still inside the cell during depolarization?

A

Yes

44
Q

Contiguous conduction

A

-Conduction in unmyelinated fibres
-Moves down axon
-Action potential spread along every portion of the membrane

45
Q

Saltatory conduction

A

-Rapid conduction in myelinated fibres
-Impulse jumps over sections of the fibre covered with insulating myelin (bare region to bare region)
-Much quicker

46
Q

Myelin

A

-Fatty insulator
-Leaves nodes of ranvier exposed where neuron transmits impulse

47
Q

Where is myelin made?

A

In CNS: ogligodendrocytes
In PNS: schwann cells

48
Q

Does the membrane underneath the Myelin get depolarized?

A

No, only the nodes of ranvier

49
Q

Multiple Sclerosis

A

-Loss of myelin
-Decreased speed of impulses
-Loss of coordination in muscles and nerves

50
Q

Factors influencing nerve conduction

A

-Neuron diameter (bigger = faster)
-Myelination (myelinated = faster)
-Temperature (higher = faster)

51
Q

A-delta fibres vs C fibres

A

A-delta are big myelinated fibres for pain and muscle whereas C fibres are non-myelinated

52
Q

Which nerve fibres can regenerate vs cannot? Which cells help/do not help?

A

PNS fibres: schwann cells guide the regeneration of cut axons
CNS fibres: oligodendrocytes inhibit regeneration of cut axons

53
Q

Convergence of neurons

A

-Many neurons input onto one neuron
-Many axon terminals onto one cells dendrites

54
Q

Divergence of neurons

A

-One neuron’s axon terminals synapses with many other neurons

55
Q

Synaptic knob

A

Contains synaptic vesicles

56
Q

Synaptic vesicles

A

Stores neurotransmitters (carries signal across a synapse)

57
Q

Synaptic cleft

A

Space between the presynaptic and postsynaptic neurons

58
Q

What is the function of calcium in synaptic nerve transmission?

A

-Calcium gates are opened by AP
-Calcium moves into synaptic knob
-Calcium binds to synaptotagmin and stimulates SNARE proteins which ensnares the vesicles and releases the NT release into the cleft

59
Q

Steps of synaptic transmission

A
  1. AP arrives at terminal end
  2. Voltage-gated Ca+ open
  3. Ca+ moves into knob
  4. Triggers release of NT
  5. NT moves across synapse
  6. Binds to receptor site
  7. Opens ion gates
  8. Triggers graded potential in post-synaptic membrane (which may decide to pass along AP or not)
60
Q

How does an inhibitory NT work?

A

Neuron sends NT that binds to K+ gates so that K+ goes out and the cell is more negative (can’t trigger AP)

61
Q

EPSP: What does it stand for? What does it trigger? What happens to membrane potential?

A

-Excitatory post-synaptic potential
-Excites post-synaptic neuron
-Binds to Na+ or ion gates
-Membrane potential becomes more positive

62
Q

IPSP: What does it stand for? What does it trigger? What happens to membrane potential?

A

-Inhibitory post-synaptic potential
-Inhibits post-synaptic neuron
-Binds to either K+ gates or Cl- gates
-Membrane potential becomes more negative

63
Q

Factors that affect size of post-synaptic potential

A

-Calcium levels (fatigue)
-NT levels (not enough to trigger AP)
-Desensitization/hypersensitization
-Pre-synaptic inhibition or facilitation (when another neuron joins in and controls how much NT gets released)

64
Q

Spatial summation

A

-Summation of many EPSPs at different locations on the pre-synaptic dendrites at the same time

65
Q

Temporal summation

A

-Summation of many EPSPs occurring at the same location over a very short period of time

66
Q

Example of pre-synaptic inhibition

A

Opiates are released by neuron A and can inhibit the release of pain NT by neuron B

67
Q

If terminal B doesn’t have receptors for signal released from terminal A in pre-synaptic inhibition, what happens?

A

They NT released by B doesn’t get inhibited

68
Q

How do neurotransmitters and neuropeptides differ?

A

-Neuropeptides are generally bigger, consisting of 2-40 amino acids
-Neuropeptides have a bigger, longer, and slower response
-Neurotransmitters are formed at the axon terminals in knob while neuropeptides are formed in the neuronal cell body
-Neurotransmitters are quickly removed from synaptic cleft while neuropeptides slowly removed

69
Q

Examples of neurotransmitters

A

-Acetylcholine
-Dopamine
-Serotonin
-Norepinephrine
-Epinephrine
-Histamine
-Glutamate
-GABA

70
Q

Examples of neuropeptides

A

-Substance P (enhances pain)
-Enkephalins/Endorphins (inhibit pain by blocking release of substance P)
-Dynorphins

71
Q

Which type of receptor is for Ach?

A

Cholinergic receptors

72
Q

What does acetylcholine do? Bind to? Broken down by?

A

-Works in parasympathetic system and muscles
-Binds to muscarinic and nicotinic receptors
-Broken down by acetylcholinesterase and recycled

73
Q

What does sarin gas do?

A

-Inhibits acetylcholinesterase to not reuptake the acetylcholine
-Causes muscles contractions

74
Q

Catecholamines

A

-Epinephrine/norepinephrine
-Affect consciousness, mood, attention
-BP and HR

75
Q

Which receptors receive catecholamines and what enzyme breaks them down?

A

-Adrenergic/noradrenergic receptors
-Broken down by MAO

76
Q

Examples of anti-depressants

A

-MAO inhibitors (increase epi levels in synapse)
-SSRI (seratonin reuptake inhibitors)

77
Q

What does seratonin do?

A

-Excitatory on muscle control
-Inhibitory on sensory mediation
-Mood, anxiety, wakefulness

78
Q

Parkinson’s Disease

A

-Decrease release of dopamine from basal nucleii
-Results in tremors and muscle rigidity

79
Q

Agonists

A

-Mimic NT when they bind to receptors, activate receptor
-Morphine (opiates)

80
Q

Antagonists

A

-Bind but don’t activate receptor (blocks site)
-Atropine (Ach)

81
Q

Cocaine

A

-Blocks reuptake of dopamine at pre-synaptic terminals

82
Q

Black Mamba Toxin: Dendrotoxin K

A

-Inhibits K+ gates from opening
-Prevents AP repolarization
-Action potential is prolonged
-Neuron releases more NT
-Triggers muscle spasms, ataxia (can’t relax diaphragm)
-Suffer from convulsions and eventually die of respiratory failure or cardiac arrest

83
Q

Curare

A

-Paralyzing poison used on arrows
-Competes with Ach at nicotinic Ach receptors
-Ach can’t bind and trigger muscle contractions
-Causes muscle weakness and paralysis
-Eventual death by asphyxiation (paralysis of diaphragm)

84
Q

Sevoflurane

A

-General anesthetic
-Affects K+ leak channels that help maintain the resting membrane potential (-70 mV)
-This will hyperpolarize the membrane, making it harder to reach the threshold and you are less likely to send AP’s
-Inhaling keeps us unconscious and suppresses CNS so have to be careful that we don’t stop breathing

85
Q

Lidocaine

A

-Local anesthetic
-Blocks voltage-sensitive Na+ channels in sensory neurons (no depolarization)
-No APs
-Results in numbing
-Also blocks cardiac motor neurons, reducing arrythmias by making it harder to fire

KNES259 (11 decks)

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