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KNES259 > Membrane Potential and Action Potential > Flashcards

Membrane Potential and Action Potential Flashcards

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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
How do graded potentials become action potentials?
They can summate, which might get the membrane potential to the threshold, which triggers an action potential
26
What are the 3 phases of action potentials?
1. Depolarization 2. Repolarization 3. Hyperpolarization
27
Examples of graded potentials
-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
28
What is the threshold for an action potential to occur?
-55 mV
29
Do Na+ and K+ gates get involved in graded potentials?
No
30
Do action potentials decrease in size as they travel down the axon?
No
31
During depolarization, what ion moves and in what direction?
-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
32
During repolarization, what ion moves and in what direction?
-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
33
Why does hyperpolarization occur?
-K+ gates are very slow to close to we overshoot the mark and end up with a more negative inside of the cell
34
What is the membrane potential during hyperpolarization?
-80 mV
35
How do we restore the cell from hyperpolarization back to resting membrane potential?
-The Na+/K+ pump gradually restores the concentration gradients -Sodium is pumped outside the cell -Potassium is pumped inside the cell
36
When is the absolute refractory period?
-From the time that Na+ gates open until they close -No second AP is possible even with large stimulus
37
When is the relative refractory period?
-As the cell repolarizes and becomes hyperpolarized -A second AP is possible with a bigger stimulus
38
How do neurons self-propagate?
-An impulse in one region is enough of a disturbance to cause the neighbouring regions to reach threshold and trigger an AP
39
Why are action potentials uni-directional?
-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
Comparison of GPs to APs characteristics:
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
How do we get an action potential to inhibit something?
-We excite neuron to release an inhibitory NT
42
Is Na+ still inside the cell during repolarization?
Yes
43
Is K+ still inside the cell during depolarization?
Yes
44
Contiguous conduction
-Conduction in unmyelinated fibres -Moves down axon -Action potential spread along every portion of the membrane
45
Saltatory conduction
-Rapid conduction in myelinated fibres -Impulse jumps over sections of the fibre covered with insulating myelin (bare region to bare region) -Much quicker
46
Myelin
-Fatty insulator -Leaves nodes of ranvier exposed where neuron transmits impulse
47
Where is myelin made?
In CNS: ogligodendrocytes In PNS: schwann cells
48
Does the membrane underneath the Myelin get depolarized?
No, only the nodes of ranvier
49
Multiple Sclerosis
-Loss of myelin -Decreased speed of impulses -Loss of coordination in muscles and nerves
50
Factors influencing nerve conduction
-Neuron diameter (bigger = faster) -Myelination (myelinated = faster) -Temperature (higher = faster)
51
A-delta fibres vs C fibres
A-delta are big myelinated fibres for pain and muscle whereas C fibres are non-myelinated
52
Which nerve fibres can regenerate vs cannot? Which cells help/do not help?
PNS fibres: schwann cells guide the regeneration of cut axons CNS fibres: oligodendrocytes inhibit regeneration of cut axons
53
Convergence of neurons
-Many neurons input onto one neuron -Many axon terminals onto one cells dendrites
54
Divergence of neurons
-One neuron's axon terminals synapses with many other neurons
55
Synaptic knob
Contains synaptic vesicles
56
Synaptic vesicles
Stores neurotransmitters (carries signal across a synapse)
57
Synaptic cleft
Space between the presynaptic and postsynaptic neurons
58
What is the function of calcium in synaptic nerve transmission?
-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
Steps of synaptic transmission
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
How does an inhibitory NT work?
Neuron sends NT that binds to K+ gates so that K+ goes out and the cell is more negative (can't trigger AP)
61
EPSP: What does it stand for? What does it trigger? What happens to membrane potential?
-Excitatory post-synaptic potential -Excites post-synaptic neuron -Binds to Na+ or ion gates -Membrane potential becomes more positive
62
IPSP: What does it stand for? What does it trigger? What happens to membrane potential?
-Inhibitory post-synaptic potential -Inhibits post-synaptic neuron -Binds to either K+ gates or Cl- gates -Membrane potential becomes more negative
63
Factors that affect size of post-synaptic potential
-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
Spatial summation
-Summation of many EPSPs at different locations on the pre-synaptic dendrites at the same time
65
Temporal summation
-Summation of many EPSPs occurring at the same location over a very short period of time
66
Example of pre-synaptic inhibition
Opiates are released by neuron A and can inhibit the release of pain NT by neuron B
67
If terminal B doesn't have receptors for signal released from terminal A in pre-synaptic inhibition, what happens?
They NT released by B doesn't get inhibited
68
How do neurotransmitters and neuropeptides differ?
-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
Examples of neurotransmitters
-Acetylcholine -Dopamine -Serotonin -Norepinephrine -Epinephrine -Histamine -Glutamate -GABA
70
Examples of neuropeptides
-Substance P (enhances pain) -Enkephalins/Endorphins (inhibit pain by blocking release of substance P) -Dynorphins
71
Which type of receptor is for Ach?
Cholinergic receptors
72
What does acetylcholine do? Bind to? Broken down by?
-Works in parasympathetic system and muscles -Binds to muscarinic and nicotinic receptors -Broken down by acetylcholinesterase and recycled
73
What does sarin gas do?
-Inhibits acetylcholinesterase to not reuptake the acetylcholine -Causes muscles contractions
74
Catecholamines
-Epinephrine/norepinephrine -Affect consciousness, mood, attention -BP and HR
75
Which receptors receive catecholamines and what enzyme breaks them down?
-Adrenergic/noradrenergic receptors -Broken down by MAO
76
Examples of anti-depressants
-MAO inhibitors (increase epi levels in synapse) -SSRI (seratonin reuptake inhibitors)
77
What does seratonin do?
-Excitatory on muscle control -Inhibitory on sensory mediation -Mood, anxiety, wakefulness
78
Parkinson's Disease
-Decrease release of dopamine from basal nucleii -Results in tremors and muscle rigidity
79
Agonists
-Mimic NT when they bind to receptors, activate receptor -Morphine (opiates)
80
Antagonists
-Bind but don't activate receptor (blocks site) -Atropine (Ach)
81
Cocaine
-Blocks reuptake of dopamine at pre-synaptic terminals
82
Black Mamba Toxin: Dendrotoxin K
-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
Curare
-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
Sevoflurane
-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
Lidocaine
-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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