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Foundations of Biomedical Sciences 1 > PPP: Electrical Properties of Cells > Flashcards

PPP: Electrical Properties of Cells Flashcards

1
Q

What are the 3 main methods to measure electrical events in cells?

A

1) intracellular - place an electrode near/inside a cell to record electrical changes in that cell e.g. glass micropipette inside the cell
2) extracellular - electrode outside the cell
3) patch clamping - electrode is sealed to the cell surface ∴ just on the CSM

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2
Q

What are the 3 ways that electrochemical gradients are established?

A

1) Na+/K+ ATPase pump moves ions against their conc gradients, providing energy for other processes
2) restricted ion movement through channels - ∴ there is electrical communication between the inside and outside of cells but the gradients do not run down quickly
3) the membrane stores ionic charges on its outer and inner surfaces of the membrane - ‘out of solution’ (capacitance)

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3
Q

What is capacitance?

A

The ability of a membrane to hold electrical charge

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4
Q

Describe how a shell of charge is created at a cell membrane using K+ and Cl- ions

A

1) the inside and outside of the cell are both respectively neutral when [K+]=[Cl-]
2) when only the K+ channel is open, K+ ions diffuse down their conc gradient out the cell passively
3) they then roll around the mouth of the channel and sit on the outside of the membrane
4) bc they are positively charged, K+ ions attract Cl- ions on the inside of the membrane which in turn prevent the K+ ions from leaving the outer surface of the membrane
5) these two ions stuck to either surface of the membrane causes the intracellular potential to decrease
- the ions are ∴ moved from the inside of the cell to be arranged in pairs across the membrane
6) ∴ the membrane is coated with charges creating two smears of charge on the inside/outside of the membrane and ∴ a shell of charge across the membrane (inside of cell becomes relatively negative)

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5
Q

Why does the concentration of ions not really change when K+ and Cl- ions create a shell of charge at the membrane?

A
  • The ions in the shell of charge stuck to the membrane can be regarded as effectively out of solution
  • However, the number of ions that actually stick onto the membrane is minute compared with the total number of ions inside/outside ∴ the concentration of ions inside/outside the cell remains effectively the same
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6
Q

How is energy needed to separate charges across the membrane?

A
  • Ions in solution have a net distance apart from each other as like charges attract and opposite charges repel
  • ∴ when oppositely charged ions are lined across the inside/outside of the cell membrane, the ions are separated by a bigger distance then they would be if they were free in solution - this further separation of attracted ions required energy from the pump
  • The work done to separate the charges across the membrane is the membrane voltage (as the electrostatic attraction works through the membrane)
  • ∴ the potential energy in terms of the gradient is transferred to a store of potential energy by separating charges across the membrane
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7
Q

What does the separation of charge across the membrane lead to?

A

It gives rise to the electrical activity of the cell

- e.g. “RMP of 70mV” = 70mV if work has been done to separate the charge across the membrane

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8
Q

How is voltage a measurement of work done?

A
  • 1 volt = 1 joule per coulomb
  • ∴ if you expend 1 joule of energy moving 1 coulomb of charge, you have done 1 volt of work
  • ∴ voltage = a measurement of work done
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9
Q

How is electrical drag-back created by concentration gradients?

A
  • K+ ions are pumped out to create a concentration gradient and Cl- ions are drawn up by electrostatic attraction
  • However, the two ions attract so that the Cl- ions try and stop the K+ ions from leaving
  • ∴ this create an electrical drag-back in the opposite direction ∴ electrical and concentration gradients often oppose each other
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10
Q

What evolutionary features allow concentration gradients and electrical gradients come to a point of equilibrium?

A

1) the thickness of the membrane (7nm)
2) the properties and numbers of the channels
3) the way that the pump works
4) the ‘just right’ concentration gradients
∴ there are points across membranes where the electrical work done and work done by the concentration gradient in the opposite direction can be equal

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11
Q

What is the equilibrium potential?

A

The point where there is no net movement of ions and the electrical force exactly balances the concentration (osmotic) force (the force of the concentration gradient pushing the ion out of the cell is exactly matched by the electrical force pulling the ion back in)
- i.e. the voltage to stop an ion being pushed in one direction by its concentration gradient

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12
Q

What is the name of the equation that can be used to determine the equilibrium potential (if the concentration gradient is known)?

A

The Nernst Equation

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13
Q

What is the Nernst equation?

A

E = RT/zF x ln([ion]out/[ion]in)

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14
Q

From what equation is the Nernst equation derived?

A
  • Electric work = osmotic work at equilibrium

- EzF = RT x ln([ion]out/[ion]in)

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15
Q

What do the different parts of the Nernst equation stand for?

A

1) z = valency (atomic number)
2) F = Faraday’s constant
- a mole of monovalent ions will contain zF coulombs of charge (takes charge into account)
3) E = equilibrium potential
4) R = universal gas constant
5) T = temperature (kelvin)
6) ln([ion]out/[ion]in) = ln(concentration gradient)

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16
Q

What are the only two things that need to be experimentally measured to work out the equilibrium potential using the Nernst equation?

A

Concentration gradient and temperature

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17
Q

How do you simplify the Nernst equation?

A

1) RT/zF has units J/C ∴ has units V
2) convert ln to log10
3) assume temperature is room temperature (25 degrees)
4) ∴ as R and F are constants, then for monovalent ions:
E = 58mV x ln([ion]out/[ion]in)

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18
Q

What is the equilibrium potential for an ion?

A

The membrane voltage that a cell needs to be at to prevent movement of that ion down/by its concentration gradient

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19
Q

What two things does the equilibrium potential of a cell need to accomplish to maintain [K+] and [Na+]?

A

1) K+ - high [K+] inside the cell ∴ want to make the inside of the cell negatively charge to restrict K+ moving out down its concentration gradient
2) Na+ - high [Na+] outside the cell ∴ want to make the inside of the cell positive so that it prevents entry of Na+, by repulsion, down its concentration gradient

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20
Q

What are the equilibrium potentials of K+ and Na+ (from Nernst equation) at physiological conditions?

A

1) Ek = -90mV

2) ENa = +60mV

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21
Q

Why is the resting membrane potential (Vm) -70mV?

A
  • To stop Na+ entering the cell and K+ from leaving the cell (balance between Ek and ENa)
  • ∴ at constant Vm, there is no net flow of ions bc the passive leak of K+ is matched by the leak of Na+ in
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22
Q

Why is Vm much closer to Ek than to ENa?

A

Bc the membrane is 50x more permeable to K+ than Na+ as there are more open K+ channels ∴ Ek dominates Vm

  • if a cell becomes permeable to an ion by opening channels for that ion, then that ion will drive Vm towards the equilibrium potential for that ion
  • ∴ as the membrane is more permeable to K+, K+ drives Vm towards Ek
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23
Q

What happens during APs (in terms of equilibrium potentials)?

A
  • If you open lots of Na+ channels, Na+ enters and drives Vm to ENa ∴ making the cell very positive
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24
Q

What is the equation for a driving force on an ion?

A

Driving force = Vm - Eion

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25
Q

Describe the driving force for K+

A
  • Driving force = -70mv - (-90mV) = +20mV
  • ∴ at rest, there is a force which is tending to drive K+ out (bc driving force is positive) ∴ it is not negative enough to attract all the K+ at the membrane
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26
Q

Describe the driving force for Na+

A
  • Driving force = -70mv - 50mV = -120mv

- ∴ at rest, there is a large force which is trying to force Na+ in

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27
Q

What is conductance?

A

The amount of current that actually flows across the membrane

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28
Q

What is permeability?

A

The ease with which an ion can get across (set by the number of open ion channels)

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29
Q

Why is there no net flow of ions?

A

Even though the membrane is much more permeable to K+, the driving force pushing K+ out is much weaker than the driving force pushing Na+ in
- ∴ the same number of K+ and Na+ leave/enter

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30
Q

What is altered in cells to change flow of ions?

A
  • For the same concentration gradient, the membrane permeability can halve ∴ halving the conductance
  • Concentration gradients are fixed but ion channels open and close, altering conductance
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31
Q

What does the Goldman Hodgkin Katz (GHK) equation consider?

A

The relative permeabilities of monovalent ions (modified Nernst)

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32
Q

What is the GHK equation?

A

Vm = 58mV x

log (Pk[K+]out + PNa[Na+]out)/(Pk[K+]in + PNa[Na+]in)

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33
Q

What does P stand for in the GHK equation?

A

The relative permeability of the membrane to the ion (can be experimentally determined
- units of P are the same for K+ and Na+ ∴ the ratio of the two permeabilities will be be a whole number

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34
Q

Why is the GHK equation important?

A
  • If you don’t take permeability into account, using the resting [K+] and [Na+], Vm = -1.0mV
  • If you do take relative permeability into account (Pk=50, PNa=1), Vm = -76mV (sensible value)
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35
Q

What are the 4 parts of an action potential?

A

1) Rest
2) Depolarisation
3) Repolarisation
4) Hyperpolarisation

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36
Q

What two parts can hyperpolarisation be split into?

A

1) Absolute refractory period - period where you can’t get another AP to occur
2) Relative refractory period - where the nerve is slightly less hyperpolarised and you can get some conduction of APs (intermittent)

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37
Q

What are the 6 key properties of an action potential?

A

1) triggered by depolarisation
2) a threshold of depolarisation is required for an AP
3) all or none
4) propagates without decrement - i.e. it stays the same amplitude as it goes along the axon/muscle fibre (doesn’t diminish)
5) at the peak, Vm approaches ENa (at trough, Vm approaches Ek)
6) after the AP, the membrane is inexcitable during the refractory period - this limits the frequency with which a nerve can conduct impulses

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38
Q

What determines information flow in the nervous system?

A

Frequency of AP firing, not the amplitude

39
Q

What is the probability of ion channels opening and closing determines by?

A

The voltage across the ion channels

40
Q

How does an ion channel open?

A
  • In an ion channel, either side of the central pore, is the molecular machinery with lots of scattered charges
  • When an electric field is applied across the channel, it is due to the scattered charges that they open
41
Q

What happens when an ion channel opens?

A
  • If a cell becomes permeable to an ion by opening ion channels, that ion will move down its electrochemical gradient and drive Vm towards its equilibrium potential
42
Q

What happens during an AP in terms of equilibrium potentials?

A
  • Na+ channels open, ∴ Na+ ions drive Vm towards ENa

- Then K+ channels open, driving Vm towards Ek

43
Q

Describe the depolarisation stage of the action potential (Vm to ENa)

A

1) depolarisation causes Na+ channels to open fast ∴ there is an influx of Na+
2) this influx then causes more opening of Na+ channels (positive feedback)
3) when this cycle starts, it abruptly finishes with a process called sodium inactivation which stops Na+ from entering (peak of AP)

44
Q

What is sodium inactivation?

A
  • Prolonged depolarisation (few ms) means the channels open, start opening even faster and then all of a sudden, the depolarisation causes them all to shut
  • It is a spontaneous property of the channels
45
Q

Describe the repolarisation stage of the action potential (Vm to Ek)

A

1) depolarisation causes K+ channels to open slowly

2) ∴ there is a K+ (positive charge) efflux (repolarisation)

46
Q

What are the two currents underlying the AP and how do they change during the AP?

A
  • gNa and gK (sodium/potassium conductance)
    1) initially, gNa increases
    2) then repolarisation occurs due to gK increase
47
Q

Describe the relationship between the flow of ionic current through the membrane and the change in voltage across it during an AP

A

1) voltage starts to change before the ionic currents start to increase
2) the peak of gNa comes just underneath the peak of the voltage change in the AP (sodium inactivation)
3) K+ channels (with a slight delay) begin to open and reach a peak of opening halfway down the falling phase of the AP
4) the AP hyperpolarises and then returns

48
Q

Why is a threshold potential necessary to the functioning of the AP?

A
  • At rest, Pk is much larger then PNa ∴ if just let Na+ trickle into the cell slowly, then as fast as Na+ would come in, K+ would leave and this would lead to no change in membrane potential
  • ∴ there has to be a short, sharp shock into the nerve to make it open the Na+ channels
  • This threshold allows a net flow of Na+ in before K+ has a chance to just flow out
  • ∴ need to get enough Na+ into the cell to kickstart the opening of Na+ channels
49
Q

What are the units of charge storage?

A

Farads (F) - ∴ the ability of a membrane to store charge can be measured

50
Q

What is the charge storage for 1cm^2 of membrane?

A

1 μF

51
Q

What is the equation relating charge, capacitance and voltage?

A

Charge = capacitance x voltage

52
Q

How many moles of ions are separated across 1 cm^2 of membrane if you do 100mv of work on it and what does this mean?

A

1 picomole (10^-12)

  • this is extremely small compared to the [Na+] and [K+] on either side of the cell
  • ∴ the cell has huge reservoirs of ions and the number of ions involved in these big electrical changes in cells are extremely small
  • ∴ the concentration gradients are not affected each time an AP occurs
  • ∴ there are also no osmotic changes so the cell stays the same shape and size
53
Q

What is orthodromic conduction?

A

Travelling in a normal direction in a nerve fibre

54
Q

How is orthodromic conduction ensured?

A
  • The receptors (in skin and joints etc) are in the right places
  • The signal is initiated here by depolarising the tip of the receptor that sends an AP the right way to the CNS
55
Q

What happens when you hit your elbow?

A
  • It causes depolarisation to spontaneously occur in the radial and ulna nerves
  • This sends APs in both directions down to the hand, activating all the sensory receptors there which then send the signal all the way back
  • The signal is reflected back to the CNS ∴ the nervous system gets confused, causing a painful sensation
56
Q

What happens to subthreshold current flowing inside an axon?

A
  • It meets an axoplasmic resistance ∴ most of it flows out closest to the spot where it is put in
  • What’s left then moves on a bit further but then flows out again etc
  • ∴ the current seeps out of the cell exponentially in relation to distance (like ripples in pond)
57
Q

What are the two resistances to current flowing in an axon?

A

1) RL = resistance along the axoplasm (longitudinal)

2) RM = resistance across the membrane

58
Q

What is resistance across the membrane due to?

A

The resistance of the ion channels

59
Q

What is axoplasmic resistance caused by and what does this mean?

A
  • Organelles and other cell features
  • This is why thick axons conduct faster than thin axons bc there is less cross-sectional resistance to the flow of current
60
Q

How does conduction occur in axons?

A

The ions hit each other (like newton’s balls) at 100,000s mph

61
Q

Describe the path of local current flow around an axonal membrane which occurs in all axons

A

1) depolarisation occurs and Na+ channels open so that Na+ flows in
2) the current flows in both directions up inside the axon against RL
3) then the current flows out, across the membrane and against RM, then around and back to the source point
4) ∴ the current flows around in a local circuit (all currents have to flow around in circuits)

62
Q

What are the two ways that transmembrane current can be?

A

1) resistive - ions flow through channels

2) capacitative - when an ion approaches one surface of the membrane, another is expelled from the other side

63
Q

Describe capacitative transmembrane current

A
  • If you have a positive ion (Na+) coming into the cell, this will neutralise negative charges close to where Na+ enters
  • This then releases positive charge (K+) from the other side of the membrane
64
Q

Explain the delay between the AP and the opening of Na+ channels

A
  • During an AP, the flow of current from entry of Na+ along the membrane stimulates the opening of Na+ channels further along (initiating gNa)
  • ∴ the reason that gNa starts later than the AP is due to a small depolarisation beginning due to current which has flowed up the axon from open Na+ channels further back
  • When the small depolarisation gets to a critical level, it opens all the Na+ channels
65
Q

Why does the AP propagate without decrement all the way along up the axon?

A
  • When the small depolarisation gets to a critical level, it opens all the Na+ channels
    (Negative charge density is less where the AP propagates than in an unexcited part of the axon)
66
Q

Why do faster axons have more myelin around them?

A

Myelin acts as a very good insulator as it stops current from flowing out of the axon

67
Q

Does axon diameter include myelin?

A

No

68
Q

Describe saltatory conduction

A
  • Na+ channels are clustered at the nodes of Ranvier

- ∴ current enters at one nodes and flows very rapidly up to the next node as it can’t get through the myelin

69
Q

Why does a nerve conduct muss less rapidly than you might expect from instant depolarisation of the nodes?

A

Bc it takes time to get the conformational change in the big molecules to open up channels ∴ they are depolarised but slow to respond

70
Q

What are the consequences of demyelination?

A
  • The current flows in, dissipates and then flows out along the axon
  • This leads to intermittent axonal conduction
  • As current flow is also temperature dependent, if people with e.g. MS get cold, they have much more difficulty in movement
71
Q

How does myelination increase conduction velocity?

A

(As the axon diameter increases, RL decreases)

  • Myelination increases RM ∴ current is forced through the axoplasm to the next node
  • Myelination decreases membrane capacitance (CM) ∴ it reduces the ability of the membrane to store charge and ∴ charge is not stored at the membrane and current flows node to node all the way along the axon
72
Q

Describe slower conducting unmyelinated axons

A
  • They have thinner axons ∴ a higher RL
  • They have a lower RM ∴ current dissipates more quickly and voltage falls more rapidly
  • They have a high CM ∴ voltage changes more slowly bc charge is being stored at the membrane
73
Q

What is the difference in conducting speed between myelinated and unmyelinated axons?

A

100 m/s vs 1-2m/s

74
Q

Describe ephaptic conduction in the heart

A
  • Conduction is transmitted across intercalated discs from cell to cell (no synapes)
  • Electrical current flows between cells through small pores ∴ whatever happens in one cell will happen in the next cell
75
Q

What are the three types of synapse?

A

1) axo-dendritic
2) axo-somatic
3) axo-axonic - prevents interaction with the next neuron (pre-synaptic inhibition)

76
Q

What happens in ligand-gated transmission?

A

The NT (ligand) is transmitted across the synapse and activates by binding to specific receptor sites on the post synaptic membrane (like enzyme reaction)

77
Q

What happens in synaptic transmission?

A

1) the influx of Ca2+ triggered by an AP at the pre-synaptic membrane causes mobilisation of vesicles and their fusion with the pre-synaptic membrane
2) when ACh binds to ACh-gated cation channels, it allows Na+ into the post synaptic membrane and K+ out simultaneously
- there are also voltage-gated Na+/K+/Ca2+ channels

78
Q

What is an end-plate potential?

A

When current flows into the cell at an motor end plate as Na+ flows in and a little K+ flows out
- the cell gains some positive charge from Na+ and loses some from K+ (small potential)

79
Q

How to Na+ channels along a muscle fibre open?

A
  • If there is sufficient depolarisation at the ACh channels, current flows in here, up inside the muscle fibre, then out and around and back
  • This flow of current (like ripples) is what actually causes voltage-gated Na+ channels further down the muscle fibre to open up
  • ∴ the propagation of the AP through the muscle fibre is initiated by this active chemical transmission, causing small depolarisations at the synaptic site which are sufficient to inject enough current to activate voltage-gated Na+ channels
80
Q

What are the 7 events of propagation of an AP in synaptic transmission?

A

1) presynaptic AP
2) depolarisation of synaptic terminal
3) opening of voltage-gated Ca2+ channels
4) Ca2+ entry and fusion of vesicles with the pre-synaptic membrane
5) NT release (+ reuptake/degradation of NT)
6) ACh-receptor activated cation channels open, causing local depolarisation and local circuits of current flow
7) activation and opening of Na+ and K+ channels

81
Q

What drugs inhibit reuptake of NT into the presynaptic terminal? Give an example of one and how it works

A

SSRIs (selective serotonin reuptake inhibitors)

  • e.g. prozac prevents the reuptake of serotonin, a NT which is found in synaptic circuits that are through to be involved in anxiety levels
  • ∴ [serotonin] increases in the synaptic cleft as uptake is inhibited
82
Q

What substances cause reduced vesicle release at synapses?

A

Low Ca2+, high Mg2+ or curare (poison)

83
Q

What is the consequence of reduced vesicle release?

A
  • This could ensure that APs don’t occur when the pre-synaptic nerve is stimulated
  • ∴ would only see the sub-threshold response only as the Ca2+ was too low = end-plate potentials
84
Q

What happens in electrotonic conduction?

A

If you have a sub-threshold endplate potential. the further away from the site of origin, the smaller the potential becomes (it dissipates, like ripples)

85
Q

How do smaller potentials trigger action potentials?

A

Miniature end plate potentials (MEPPs) add up to form end-plate potentials which in turn add up to get threshold potentials which trigger the AP

86
Q

What are MEPPs?

A

Small responses that are spontaneous (not in response to a stimulus of small depolarisation) which vary in size and occur at random

87
Q

What distribution was shown when the height (mV) and timescale (ms) of the MEPP responses was measured and a histogram was plotted?

A
  • It gave a normal distribution (decreasing with increasing height) = poisson distribution?
  • ∴ vesicle release was occurring at random and the number of vesicles varied (single=1 vesicle released, double=two vesicles released etc)
  • ∴ random release of vesicles generates MEPPs
88
Q

When is it impossible to elicit a knee jerk reflex and why?

A

When you contract extensors and flexors at the same time

  • there is a system of alternating activity between muscle groups around joints (e.g. bicep/tricep contraction/relaxation) bc sensory input from stretch receptors in the extensor comes into the dorsal horn of the spinal cord and bifurcates/splits into two pathways
  • one causes contraction of the extensor and the other causes relaxation of the flexor on the other side
89
Q

How does the sensory path from the extensor cause contraction of the extensor?

A
  • One path goes directly onto the extensor motor neuron in the ventral horn of the spinal cord from the sensory neuron, causing the motor neuron to depolarise and then release ACh at neuromuscular junctions
  • NT = glutamate (excitatory)
90
Q

How is the flexor muscle actively inhibited by extensor sensory input?

A

1) glutamate is released from the other branch of the sensory neuron onto an interneuron
2) the interneuron releases glycine (inhibitory NT)
3) when glycine binds to the flexor motor neuron it causes hyperpolarisation

91
Q

What are excitatory/inhibitory post synaptic potentials (EPSPs/IPSPs)?

A
  • These are sub-threshold events, made up of MEPPs, which determine whether a neuron will reach threshold to fire an AP or not (they summate)
  • EPSPs add to generate depolarisation (e.g. at extensor) whereas IPSPs add to generate hyperpolarisation (e.g. at flexor)
  • EPSPs and IPSPs cancel each other out
  • IPSPs do not occur at neuromuscular junctions (only excitation
92
Q

Describe the process of temporal summation

A

1) if a burst of inhibition comes in (i.e. inhibitory neuron is stimulated), the neuron hyperpolarises (taken away from threshold) due to the release of glycine (inhibitory NT)
2) this hyperpolarisation is caused by the entry of Cl- ions into the cell - glycine opens chemically gated Cl- channels, increasing negative charge in the neuron
3) this leads to an IPSP
4) then, if excitation enters and lots of little EPSPs occur sitting on top of that inhibition, the cell gets more depolarised
5) if it is not sufficient to reach threshold there is no AP or contraction but if there has been sufficient excitation (EPSPs) in time to reach the threshold, AP and muscle contraction occurs

93
Q

Describe the process of spatial summation

A
  • Whether you reach threshold can also depend on where the synaptic circuits impinge upon the dendrites on a soma (cell body)
  • Further away, small depolarisations are not transmitted so faithfully to the soma
  • ∴ it is the sum total of inhibition and excitation which comes into the soma which determines if at the axon hillock, an AP will be generated
94
Q

What does inhibition through IPSPs disrupt?

A

The regular pattern of frequency coding of neuron signals

Foundations of Biomedical Sciences 1 (9 decks)

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