L3 - Graded Potentials and APs (Chapter 5) Flashcards

1
Q

What was the basic idea of Galvani’s experiment?

A

Galvani did experiment where he hooked a frog up to a lightning rod, and when lightning would strike, the frog would move (muscles were contracting)

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2
Q

Who were Luigi Galvani and Alessandro Volta?

A
  • Galvani had a rivalry with Volta (invented the battery to create a set of data in order to compete with Galvani) as to whether or not animals had an innate ability to intrinsically produce electrical activity (animal electricity)
  • Galvani was proved correct
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3
Q

Who was involved in the discovery of APs in 1865?

A
  • Emil du Bois-Reymond developed the galvanometer
  • Julius Bernstein developed the differential rheotome
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4
Q

Who was involved in the first intracellular recording in 1939?

A
  • Alan Hodgkin and Andrew Huxley
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5
Q

Who was involved in the first voltage clamp recording in 1947?

A

Kenneth Cole and George Mormont

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6
Q

Who was involved in the discovery of the ionic basis of APs in 1949?

A

Alan Hodgkin and Bernard Katz

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7
Q

Who was involved in the first patch clamp recording in the 1970s?

A

Erwin Neher and Bert Sakmann

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8
Q

Depolarization

A
  • membrane potential becomes less negative/more positive
  • excitatory effect
  • 1st arrow in picture
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9
Q

Repolarization

A
  • membrane potential becomes more negative/less positive
  • 2nd arrow in picture
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10
Q

Hyperpolarization

A
  • membrane potential goes more negative than resting membrane potential
  • inhibitory effect
  • 3rd arrow in picture
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11
Q

What are graded potentials?

A
  • variable/graded in amplitude
  • amplitude is proportional to the amplitude of the stimulus
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12
Q

How are APs different from graded potentials?

A

APs are all or none, and once threshold is reached, the same amplitude will be generated every time

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13
Q

How do AP’s and GP’s propagate differently?

A
  • APs are unidirectional, and propagate away from the soma because the membrane behind the AP enters a refractory period
  • Graded are bidirectional, depolarization occurs in both directions
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14
Q

Which type is regenerative (AP or graded)? Which type is decremental? What do these terms mean?

A
  • Graded are decremental, meaning that the voltage change does not get regenerated and continues to diminish
  • APs are regenerative, there is a mechanism that actively regenerates the voltage change through positive feedback
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15
Q

Which can summate and which cannot (APs or graded)? Why or why not?

A
  • Graded summate - have a slower response than APs, which allows for the amplitude to be summated, creating an AP
  • APs do not summate because they follow the all or none principle - meaning that they must reach a specific voltage in order to be generated
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16
Q

Where can AP’s be generated vs GP’s? What determines the parts of the cell where AP’s are generated?

A
  • APs are generated in the axon/axon hillock - require specific membrane proteins in order to be propagated across long distances
  • Graded are generated in the soma or dendrite
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17
Q

What name does your Guyton and Hall textbook use to refer to graded potentials? What does this name mean? What properties does it refer to?

A
  • acute local potential
  • short lived and short distance
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18
Q

What is the time constant?

A
  • The time it takes for the membrane potential to change by 63% of the total change
  • How much time it takes the membrane to change/depolarize based on the stimulus
  • measured in seconds or milliseconds
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19
Q

How is the time constant calculated? Can you draw this graph?

A

= to membrane resistance x membrane capacitance (T = Rm x Cm)

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20
Q

What biophysical properties of cells affects their time constant?

A
  • Membrane capacitance and membrane resistance
  • Rm can be altered by number of channels and whether or not they are open – more channels = less resistance
  • Cm can be altered by the thickness of the membrane (depends on myelination) - increased myelination will decrease capacitance
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21
Q

How can the time constant affect signaling in excitable cells?

A
  • the larger the time constant of a cell, the longer it takes to respond to a stimulus
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22
Q

In the picture, which cell has the larger time constant? Cell A or B?

A
  • A has the larger time constant bc it’s taking longer to reach max potential
  • B has the smaller time constant bc it has more channels, meaning that the membrane resistance is smaller than that of A
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23
Q

What is the length/space constant?

A
  • How far the potential will travel before the amplitude of the membrane diminishes to 37% of the maximum value
  • Measured in units of distance (meters or millimeters), and is indicated by lambda
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24
Q

How is the length constant calculated? Can you draw this graph?

A

= Square root of membrane resistance/axial resistance

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25
Q

What biophysical properties of cells affects their length constant?

A
  • Rm and Ra
  • Rm is altered by number of ions channels - would need to increase in order for signal to go further
  • Ra is altered by the size of the membrane - would need to decrease in order for the signal to go further
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26
Q

Spatial summation

A
  • summation over space, the combination of amplitudes to create a larger one
  • in the picture, spatial summation is shown by 1+3 and 2+3
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27
Q

Do graded potentials or APs participate in spatial summation?

A

graded potentials

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28
Q

What is a receptor potential?

A

type of graded potential that is generated by activation of sensory receptors

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29
Q

What are some different types of sensory receptors we discussed?

A
  • mechanoreceptors transduce mechanical force into electrical changes (mechanically gated ion channels open, allowing for APs to be created)
  • thermoreceptors, chemoreceptors, baroreceptors, photoreceptors
30
Q

What is a PSP?

A
  • post synaptic potential, the potential that occurs in the postsynaptic cell, receptors that respond to neurotransmitters create a voltage change, which is a PSP
  • EPSPs – excitatory, depolarization
  • IPSPs – inhibitory, hyperpolarization
  • type of graded potential
31
Q

What is an EPP?

A
  • end plate potential, only found in skeletal muscle in the NM junctions
  • large, have ligand gated ion channels (ACh binds to these) that create PSPs
  • type of graded potential
32
Q

What is AP threshold? What is the typical value of threshold?

A
  • high enough depolarization that allows the cell to create an action potential
  • 10-20mV depolarization from resting membrane potential
33
Q

What is the mechanism of threshold?

A
  • All or nothing response is a positive feedback loop – carries the cell away from homeostasis quickly
34
Q

Who is credited with discovery of the action potential?

A

Emil du Bois-Reymond

35
Q

Be able to draw/label/identify graphs displaying changes in conductance or current that occurs during each phase of the AP.

A
36
Q

Did Hodgkin and Katz demonstrate a dose-dependent effect of diminishing [Na+]e? Why is this important?

A
  • Yes, when extracellular Na was reduced, the amplitudes of the AP got smaller
  • cannot do this with K bc you’ll be interrupting the cell’s membrane, which will make the cell sick and alter results
37
Q

How were Hodgkin and Katz able to rescue the AP after abolishing it?

A
  • By adding choline
  • By adding sodium back into the seawater/extracellular Na
  • Did this in order to prove that the effects of diminished Na were reversible, and that they weren’t killing the cells
38
Q

Be able to compare and contrast v-gated Na+ and K+ channels.

A
  • K channels
    • do not have an inactivation mechanism
    • have a lower activation rate
    • activation occurs at peak of AP
  • Na channels
    • more complex than K channels
    • have two gates
    • faster activation, slow inactivation
39
Q

How does the kinetics of activation/inactivation compare between Na+ and K+ channels?

A
  • Na channels are fast channels, but do have a slow inactivation
  • K channels are slow channels
40
Q

What are some ways in which AP waveforms can be changed?

A
  • Phosphorylation of channels, or binding of hormones or NTs
  • Extracellular concentration of ions can also alter channel gating
41
Q

What are some potential consequences for changing AP shape?

A
42
Q

Absolute refractory period

A
  • period in which no matter how much stimulus is given, absolutely no AP can be generated
  • excitability is nil, and threshold can be equated to infinity
43
Q

Relative refractory period

A
  • period of time following generation of an AP where the cell membrane becomes insensitive to further stimulation
  • requires a larger stimulus to create another AP
44
Q

Which is longer? Relative or absolute refractory period?

A

relative refractory periods are longer

45
Q

What is the mechanism of relative refractory periods?

A
  • due to leakiness of membrane to potassium
  • once K channels are repolarized or hyperpolarized back to resting membrane potential, Na channels are reset, in which an AP can be generated
46
Q

What is the mechanism of absolute refractory periods?

A
  • due to the inactivation of Na channels
47
Q

AP firing frequency

A

the rate at which APs are being generated

48
Q

What determines the maximum AP firing frequency?

A

absolute refractory periods

49
Q

What are the two different patterns of AP generation?

A
  • tonic firing pattern - cell will continue to fire APs at a specific frequency in response to a prolonged stimulus (neurons in brain stem that are responsible for breathing)
  • phasic firing pattern - cell will fire a burst or one AP in response to a prolonged stimulus (learning and memory)
50
Q

What is the mechanism of phasic AP generation?

A

accommodation - in response to a prolonged stimulus, the cell may fire a single or a burst of action potentials, and then become insensitive to more stimulation

51
Q

Why is the ability for some excitable cells to adapt physiologically (accommodation) important?

A
  • some sensory receptors only need to measure change, and some need to have the ability to measure constantly
  • the receptors that only need to measure change will have the accommodation response (EX: recording the change in body position)
52
Q

How can changing the intensity of a stimulus affect the frequency of AP’s in excitable cells?

A
  • once the AP fires, the cell is in its relative refractory period, and depending on the intensity of the stimulus, threshold will be reached faster or slower
  • higher intensity stimuli = threshold reached more quickly
  • lower intensity stimuli = threshold reached more slowly
53
Q

Why is AP propagation said to be a regenerative process?

A

positive feedback loop due to Hodgkin Cycle

54
Q

Hodgkin Cycle

A
  1. Stimuli
  2. membrane is depolarized
  3. opening of voltage gated Na channels
  4. influx of Na further depolarizes membrane
  5. membrane is depolarized to threshold, creating an AP
55
Q

Continuous conduction

A
  • propagation of APs in unmyelinated axons
  • slower AP velocity
56
Q

Saltatory conduction

A
  • propagation of APs in myelinated axons
  • faster AP velocity
  • requires more energy
  • EX: quick reaction needed when you touch a hot stove
57
Q

Nodes of Ranvier

A
  • gaps in myelin sheath that regenerate APs
  • without these, APs wouldn’t be able to be propagated
  • voltage gated sodium channels are here
58
Q

Internodes

A

myelinated regions of the axon

59
Q

Why don’t AP’s back-propagate once they begin to propagate in a given direction?

A
  • if in the SIZ - there are no Na channels in the cell body present to allow it
  • if further down the axon - the membrane behind the AP is in its refractory period
60
Q

In neurons, why do AP’s propagate away from the cell body toward the axon terminal?

A
  • because they are initiated in the Spike Initiation Zone, which is located at the axon hillock
  • there are no Na channels behind the axon hillock (in the cell body) that allow the AP to propagate backwards
61
Q

Experimentally, how can one cause AP’s to propagate in the opposite direction?

A
  • stimulation at a more distal site on the axon
  • like lighting a fuse in the middle
62
Q

What is the difference between antidromic and orthodromic propagation?

A
  • orthodromic - propagation of the AP in a single direction from the cell body to the axon terminal
  • antidromic - propagation of the AP towards the cell body AND towards the axon terminal
63
Q

How can conduction velocity be measured and calculated experimentally?

A
  • via a stimulator and recording electrode
  • measure the distance btwn the two, and measuring the time it takes for the stimulus to reach the recording electrode
  • distance/time
64
Q

How does myelin affect Rm? Cm? Ra?

A
  • increases Rm and Ra
  • decreases Cm (capacitors need a thin membrane to function well)
65
Q

How does Rm and Cm differ at internodal regions?

A
  • both are lower at internodal regions
  • signals travel faster because of this
66
Q

How does myelin affect conduction velocity?

A
  • increased myelin decreases Cm and increases Rm
  • decreases passive (electrotonic) conduction, and will increase the length constant
67
Q

How axon diameter affect conduction velocity?

A
  • the larger the diameter, the smaller the resistance (Ra), allowing for faster propagation & vice versa
  • increases passive (electrotonic) conduction, and will decrease the length constant
68
Q

What are the mechanisms for how each adaptation affects CV?

A
68
Q

How does the length constant affect CV and node spacing in myelinated axons?

A
  • the larger the length constant, the further the depolarization spreads, the faster the AP is propagated = faster CV
  • larger jumps btwn internodal areas = faster CV
68
Q

How does myelin affect the length constant?

A

increases it