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Neuroscience > neuron excitation > Flashcards

neuron excitation Flashcards

1
Q

what are action potentials?

A

transient reversals in this membrane potential that are actively propagated over the cell surface.

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2
Q

what are excitable cells

A

Excitable cells include neurons, skeletal, cardiac, and smooth muscle cells, and some endocrine cells.

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3
Q

what is the membrane potential fo an unstimulated excitable cell called?

A

resting potential

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4
Q

how does a resting potential arise?

A

A resting potential ( Vm) arises because there is a difference in the concentrations of ions between the inside and outside of the cell and because the cell membrane has different permeabilities for these ions.

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5
Q

what makes up the intracellular fluid of an excitable cell?

A

the intracellular fluid is an aqueous solution of potassium
ions balanced by a variety of anions—including organic acids, sulfates, phosphates, some
amino acids, and some proteins—

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6
Q

how is a diffusional force for potassium ions formed across cell membranes?

A

Cell membrane is permeable to potassium and because there is a concentration gradient for K+ across the membrane there is a diffusional force acting to drive the K+ from the inside to the outside of the cell

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7
Q

what balances out the diffusional force?

A

the electrostatic force. as potassium diffuses out due to the diffusional force, a potential difference forms across the membrane because of the excess of intracellular anions. an electrostatic force is the generated to prevent potassium ions diffusing out.

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8
Q

when the diffusional force is balanced out by the electrostatic force, what is the small potential difference called?

A

equilibrium potential/ potassium equilibrium potential

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9
Q

what is the usual potassium equilibrium potential of nerve cells?

A
  • 90 mV
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10
Q

the potential difference exists only at the plasma membrane, which by storing charge acts as a _____

A

capacitor

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11
Q

how can equilibrium potentials be calculated?

A

using the Nernst equation: E = (RT/zF) ln Ce/Ci

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12
Q

what are neuron resting potentials?

A
  • 60 –> -90 mV
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13
Q

what is the reason for the small discrepancy between potassium equilibrium potential and resting potential?

A

The discrepancy between EK and Vm arises because ions other than potassium also make a contribution by virtue of their equilibrium potentials. The most important is sodium (ENa = +55 mV).

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14
Q

what is the ionic driving force and what is it a measure of?

A

it is the difference between the resting potential and equilibrium potential for any ion, it is a measure of the electrochemical force tending to move the ion across the cell membrane

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15
Q

at rest the driving force for potassium is low, but that of sodium is high, why does sodium not flow into the cells?

A

the permeability of sodium compared to potassium is very low

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16
Q

in most excitable cells, why is the ionic driving force for chloride ions zero?

A

This is because Cl- ions are passively distributed across the membrane according
to the resting potential set up by the combined effects of EK and ENa.

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17
Q

what actively maintains the concentration gradients of sodium and potassium?

A

Na/K ATPase (cation pump)

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18
Q

the permeability of cell membranes to ion sis conferred by protein ion channels termed _____

A

leak channels

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19
Q

how many potassium leak channels have been identified?

A

15

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20
Q

how are neurons excited?

A

Neurons are naturally excited either by the cascade of synaptic inputs onto their dendrites and cell body from other neurons or by receptor potentials generated by sensory
organs

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21
Q

what is depolarisation?

A

a drop in membrane potential, i.e for the membrane potential to become less negative

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22
Q

what constitutes the spike of the action potential

A

the membrane potential rapidly depolarizes to zero, overshoots to about +30 mV then repolarizes
back towards Vm all in less than 1 ms

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23
Q

What is hyper polarisation?

A

Immediately after the spike the neuron membrane potential becomes larger (more inside
negative) than the normal resting potential

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24
Q

how long does it take for the after-hyperpolarization following an action potential spike to decay?

A

it decays over a few milliseconds, and the potential returns to its resting value.

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25
Q

what is a threshold stimulus?

A

A threshold stimulus is defined as the current that will cause a neuron to fire on 50% of occasions, and its amplitude depends on the size of the neuron because this
affects the electrical resistance of the cell

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26
Q

where are action potentials triggered?

A

They are triggered at the axon hillock, this region has the lowest threshold.

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27
Q

what is the latentcy or latent period?

A

There is a short delay between the onset of the stimulus and the start of the action potential. The latency gets shorter as the strength of the stimulus increases.

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28
Q

what is the absolute refractory period?

A

During the spike, the neuron becomes completely inexcitable. a nerve cell will not fire again, no matter how high the stimulus.

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29
Q

what is the relative refractory period?

A

After the spike, while the neuron remains hyperpolarized, the neuron can be excited only by suprathreshold stimuli

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30
Q

what are the two consequences of the temporary refractive periods of neurons?

A
  • Upper limit on firing frequency
  • Action potentials are propagated in one direction
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31
Q

What are two properties of voltage dependant ion channels (transmembrane proteins?

A

Ion selectivity
Voltage selectivity

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32
Q

Voltage dependant ion channels are multi-subunit complexes. What are these subunits?

A

The alpha subunit(s) are accompanied by a variety of beta subunits which modify the channel properties

33
Q

What two interchangable states can voltage-dependant ion channels exist in and what does this depend on?

A

they can be open (activated) or closed. This depends on the voltage across them

34
Q

How many voltage dependant sodium channels alpha subunits have been identified

A

9

35
Q

What happens when NavS region of membrane is depolarized to the threshold voltage or beyond?

A

They change shape, so the channels open, permitting NA ions to flow down their electrochemical gradient into the neuron (up tp 6000 ions)

36
Q

How fast is NAvS activation

A

Approx 10 us

37
Q

How long will a sodium channel remain open during an action potential

A

0.5-1 ms

38
Q

What is the consequence of the influx of sodium ions via NAvS

A
  • produces the upstroke of the spike that is the depolarizing phase of the AP
  • drives other channels to open; driving a positive feedback explosive rise in Na permeability
39
Q

At the top of the spike of an AP, why is the self-regenerative rise in sodium permeability halted?

A
  • All available NAvS have been opened
    -Ionic driving force for sodium gets less as membrane depolarizes towards sodium equilibrium potential
    -NAvS flip into an inactivated state
40
Q

What is the difference between an inactivated vs closed state of NAvS?

A

Inactivated state- NAvS CANNOT be made to open. This state is responsible for curtailing the spike and for the absolute refractory period. Inactivation wears off after a few milliseconds as the channel relaxes into a closed state

41
Q

What is the function of the delayed outward rectifier Kv?

A

-Involved in repolarization phase (downstroke) of the action potential. Opened by depolarization, allow potassium ions to flow down their electrochemical gradient out of the cell.

42
Q

What is responsible for the after-hyperpolarization phase of the spike?

A

At the bottom of the downstroke, most of the NAvS are inactivated but the delayed outward rectifying Kv remain activated or are slow to inactivate. Therefore after the spike, K ions continue to leave the cell and make the membrane potential more negative than Vm. This accounts for relative refractory period of the cell

43
Q

How does the membrane return to resting potential

A

As the potassium channels flip into their closed or inactivated state in a time-dependent fashion

44
Q

What is the size of the after-hyper polarization determined by?

A

Potassium equilibrium potential (when the membrane potential reaches Ek, ionic driving force for K will be zero)

45
Q

depolarisation causes opening of K and NA channels. How does an AP result from this?

A

Sodium channels respond to depolarisation earlier than potassium channels.

46
Q

Which three techniques have been used to deduce the structures for voltage-dependant ion channels?

A

Hydropathicity plots, Site-directed mutagenesis, x-ray crystallography.

47
Q

What is the common structure for sodium channels and several potassium channels?

A

The basic subunit has 6 highly hydrophobic segements (s1-s6), thought to be alpha-helices spanning the membrane.

48
Q

What is the structure of the potassium channels subunits?

A

Each subunit is a separate molecule and the functioning channel is a tetrameric homo-oligomer (4 similar subunits around a central pore)

49
Q

How are the subunits arranged in sodium channels?

A

4 subunits are linked by cytoplasmic loops to form a single huge molecule, tertiary structure resembles a potassium molecule.

50
Q

What contributes to the pore of the ion channels?

A

Segments 5 and 6 and the H5 loop between them

51
Q

Why is the H5 loop thought to line the channel pore?

A

It contains amino acids that are crucial for conferring ion selectivity. The extracellular throat is line with oxygen atoms that are crucial for ion permeation.

52
Q

What does the s4 segment of a ion channel subunit usually have at its N-terminal

A

Several positively charged lysine or arginine residues.

53
Q

What function does the s4 segment serve?

A

Part of the voltage sensor for activation. In response to depolarisation , s4 acts like a paddle swinging through the membrane towards the extracellular side (+ charges repelled by the voltage change), this pulls an s4-s5 linker region, opening the intracellular throat of the pore

54
Q

What is N-inactivation by the ball and chain mechanism that causes closure of potassim channels?

A

A cluster of amino acids swing up to block the internal mouth of the channel by interacting with an amino acid at the internal tip of the H5 loop

55
Q

How do local anaesthetics block conduction of APs?

A

They enter open sodium channels and stabilise them in the inactivated state. It can take up to 1000 times longer for inactivation to wear off.

56
Q

What is the structure of most local anaesthetics?

A

Consist of a lipophilic group linked via an ester or amide to an ionizable amine. They are weak bases with a pKa around 8-9 (at Ph 6.8-7.4 the protonated form predominates)

57
Q

Why do local anaesthetics demonstrate use-dependant blockade?

A

-unable to penetrate the hydrophobic walls of the channel, access to site of action is denied until channel is open.
-Open and inactivated states of sodium channel have a greater affinity for local anaesthetics than the closed state.

58
Q

How are the linkages of local anaesthetics metabolised?

A

The ester and amide linkages are hydrolyzed by plasma cholinesterases or liver P450 respectively

59
Q

why are small diameter nociceptor afferents are more susceptible to LA than large diameter afferents?

A
  • Distance that local circuit currents passively spread to propagate an AP is shorter
  • Smaller diameter fibres fire at higher frequencies and have longer AP –> use-dependant blockade
60
Q

Why are myelinated fibers more sensitive to LAs than non-myelinated fibers of the same diameter?

A

Nodes of Ranvier have fewer barriers to drug access

61
Q

Where is an AP initiated and why?

A

In the axon hillock, this region has the greatest density of NAvs and therefore, the lowest threshold

62
Q

What is an alternative name for the axon hillock

A

Spike initiation zone

63
Q

What is the region of an axon invaded by AP called?

A

Active Zone- it is a few cm long

64
Q

How do local circuit currents flow passively between the axon segments of unmyelinated neurons?

A

Part of the active zone occupied by the overshoot of the spike will be inside positive, far away from this, the inside potential will be negative. A potential difference exists between the two segments. (read pg 37)

65
Q

What is the conduction velocity in unmyelinated axons?

A

0.5- 2 m.s; depending on the diameter of the axon.

66
Q

what is the relationship between axon diameter and conduction velocity in unmyelinated axons?

A

Small axons have a higher resistance to currents flowing through their core, so local currents spread less well, and have a slower speed. Velocity=k x diameter/2

67
Q

In the PNS, Schwann cells line up along the axon surrounding it in what structure?

A

the mesaxon- a pseudopodium-like structure

68
Q

How to the schwann cells complete the process of myelination after formation of the mesaxon?

A

Mesaxon spirals around the axon 8-12 times ensheating it with a series of concentric double layers of plasma membrane, the cytoplasm gets left behind

69
Q

How much of the axon does a single schwann cell myelinate?

A

between 0.15- 1.5 mm of an axon

70
Q

How large is a node of ranvier?

A

0.5 um

71
Q

What is the range of myelinated nerve fiber diameters?

A

3- 15 um. the diameter contributed by the myelin sheath is constant across this range

72
Q

what is the main difference between myelination in the CNS and PNS?

A

Each oligodendrocyte extends several processes so that it can contribute to the myelination of several adjacent axons. Fewer glial cells are needed, saving space.

73
Q

What gives the myelin sheat a high electrical resistance ?

A

The sheath consists largely of plasma membrane, which has a large phospholipid content.

74
Q

Where are local circuits established between in myelinated axons and what is the name for this type of conduction?

A

Between adjacent nodes of ranvier. AP jump from node to node, this is called saltatory conduction.

75
Q

What reduces the risk of nodes not firing in response to weakened local currents?

A

The density of NAvS is 100 times greater in the nodes than unmyelinated axon membranes, making the node threshold much lower

76
Q

Why is the conduction velocity faster in myelinated axons?

A

-Myelination reduces membrane capacitance, increasing the speed of AP propagation
-In myelinated axons, only the nodes have to be excited, instead of every region of the plasma membrane

77
Q

what is the range of conduction velocities for myelinated axons?

A

7- 100 m.s

78
Q

what is the relationship between conduction velocity and the diameter of an unmyelinated axon

A

velocity= K x diameter

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