Lecture 3- Neuron physiology Flashcards

1
Q

What is a cell body?

A

input zone, organelles and nucleus inside

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2
Q

What are dendrites?

A

input zone, plasma membrane contains receptors binding to chemical messengers

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3
Q

Describe an axon.

A

-one of the longest cells in the body -still cellular size, not that thick -conducting zone

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4
Q

What is the axon hillcock?

A

-trigger zone -particularly sensitive, where graded potentials trigger AP - at the beginning of the axon

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5
Q

What are the axon terminals?

A

-output zone

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6
Q

What is the difference between a nerve and a fibre tract?

A

nerve= bundle of axons outside the CNS fibre tract= bundle of axons inside the CNS

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7
Q

What do voltage-gated ion channels do?

A

open or close in response to changes in membrane potential, crucial to action potentials

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8
Q

What do chemically-gated channels do?

A
  • (ligand gated) change conformation allosterically (= binding of a regulatory molecule to the allosteric site=binding site) in response to the binding of chemical messenger with a membrane receptor associated with the channel
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9
Q

What do mechanically gated channels do?

A

respond to stretching or other mechanical deformation such as touch, important in sensory transduction

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10
Q

What do thermally gated channels do?

A

respond to local changes in temperature, important in sensory transduction

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11
Q

What makes the channels open?

A

Channel opening results from graded potentials (more primitive) or action potentials.

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12
Q

What are graded potentials?

A

-local changes in membrane potential -the stronger the triggering event the stronger the graded potential, since more gated channels open -trigger event causes gated ion channels to open -the ions flow in, depolarizing or hyperpolarizing the small region of the plasma membrane (usually K+ so it depolarizes the axon)

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13
Q

Does spread of graded potential happen locally or does it affect the rest of the membrane?

A

-graded potential happens locally, the rest of the membrane remains at resting potential

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14
Q

What is the temporarily depolarised region in graded potential called?

A

-active area

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15
Q

How is the graded potential spread?

A

-there is a constant current flow – ions in the depolarized area will spread to the neighbouring inactive areas along the membrane this causes the potential in the other areas to change -results from the imbalance of ion pumps

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16
Q

Which direction does graded potential spread to and how far-reaching is its influence?

A

-the potential spreads in both directions from the initial area but the ions spread out and the potential weakens evens with short distance (a few millimeters) then dies out due to the dilution and movement through open channels= this type of spread of potential is called passive

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17
Q

Why is graded potential termed graded?

A

-graded= depends on how much stimulation there is

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18
Q

How long does graded potential last?

A

-variable duration

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19
Q

What two factors can affect graded potential?

A

-electrical field change- can also change the potential -chemical messengers too

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20
Q

What values of membrane potential are there during an action potential?

A

-70mV resting up to +20/+30 (depolarisation) down to -80mV (hyperpolarisation)

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21
Q

What is the spread of AP called?

A

-spread unlike graded is nondecremental (no diminishment in strength during propagation) that’s why they’re good for long distance signals

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22
Q

How much of the membrane is excited when an AP takes place?

A

-like graded, small portion of membrane excited

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23
Q

What property must portion of a membrane have to be able to generate AP?

A
  • can only be generated in portions of the membrane with abundance of Na+ channels, graded potential brings these more sensitive areas to threshold
  • brief, rapid, large changes in the membrane potential when the inside becomes more positive than the outside
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24
Q

What triggers an AP?

A

-if graded potential is of sufficient magnitude it can initiate AP before dying off (normally the membrane bit that was in graded potential doesn’t experience AP- the adjacent regions do)

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25
Q

What is an action potential (AP)?

A

-action potential is the entire rapid change from threshold to peak back to resting

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26
Q

How long does an action potential last?

A

-duration is mostly fixed= 1msec (0.001sec) (bit longer in muscle)

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27
Q

Will stronger stimulus generate largere APs?

A

No.

-the strength of a stimulus is coded by the frequency of AP, stronger stimulus will trigger more APs not bigger APs

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28
Q

What must be achieved to have an AP?

A
  • must reach threshold, all or nothing event
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29
Q

Which ion is the plasma membrane more permeable to K+ or Na+?

A
  • plasma membrane much more permeable to K+ than Na+ so K+ contributes most to establishing resting potential
  • many leaky K+ channels so membrane more permeable to it than Na+ (20 to 30 times more)
30
Q

What effect does an AP have on the permeability of the plasma membrane?

A

-during AP changes to permeability of K+ and Na+ because of voltage gated channels (Na+ and K+ ones) opening and allowing ions in (positive feedback- the ions carry the current responsible for the voltage gated channels opening, reinforcing the effect)= some Na+ open further depolarizing the membrane which leads to more channels opening etc…

31
Q

What do voltage channels consist of and how is that affected by the membrane potential?

A
  • voltage channels consist of proteins with number of charged groups, the electric field (potential) surrounding the channels can distort the channel structure (some bits attracted or repelled by charges in the surrounding fluid)
  • voltage channels are very sensitive to changes in membrane potential
  • faster reacting animals have faster opening ion channels
32
Q

What are the two gates of the Na+ channel?

A

activation gate: guards channel by opening and closing like a hinged door
inactivation gate: consists of ball and chain like sequence of amino acids at the channel opening facing the ICF, open when the ball is dangling free, closed when ball binds to its receptor at the channel opening= blocking the channel

33
Q

What allows Na+ to pass through the Na+ channel?

A
  • both gates must be open to permit Na+ through, closure of either prevents it
  • put electrical charge= causes distortion= arm opens
34
Q

What are the three possible confirmations of a Na+ channel?

A

1) closed but capable of opening (activation g. closed, inactivation g. open)
2) open or activated (both open)
3) closed and not capable of opening (activation g. open, inactivation g. closed)

35
Q

Why does Na+ channel close?

A

-Na+ closes because when the activation gate opens it triggers the inactivation gate to start closing but it’s much slower so the Na+ enters the cell and after 0.5 msec delay the inactivation gate closes

36
Q

How does K+ channel compare to Na+ channel?

A
  • simpler
  • less sensitive
  • open slightly after Na+
37
Q

How many gates does K+ channel have?

A

-only one gate which can be open or closed

38
Q

When is K+ channel triggered to open?

A

-K+ is triggered to open at the same time as Na+ but there is a delay in how fast it opens

39
Q

Are K+ channels open most of the time?

A
  • no but K+ is always leaking out, so even if the gates unopened the membrane would reach resting potential but this way it’s much faster
40
Q

What type of channels are K+ and Na+ channels?

A

voltage gated

41
Q

Describe an action potential in steps:

A
  1. resting potential, all voltage channels closed
  2. graded potential gets the mombrane potential to threshold (-50mV) and here Na+ open (activation gate opens), now membrane more permeable to Na + than K+
  3. Na+ enters the cell, explosive depolarization to +30mV (since more negative inside, goes in)
  4. At peak Na+ inactivation gate closes and membrane potential falls at the same time K+ activation gate opens
  5. K+ leaves the cell (there is more negative outside now so it goes out) causing membrane potential to fall repolarisation!
  6. On return to resting potential Na+ activation gate closes and inactivation gate opens resetting the channel to be able to respond to another event
  7. Further movement of K+ out of the cell causes hyperpolarisation, the channels are slow to close so that’s why we get hyperpolarisation
  8. K+ activation gate closes and membrane returns to resting potential
42
Q

What happens at reaching threshold? (AP - in term sof ion movement)

A
  1. Rapid opening of Na+ activation gates
  2. Slow closing of Na+ inactivation gates
  3. Slow opening of K+ activation gates
43
Q

What does the Na+/K+ pump do at the end of AP?

A

At completion of action potential membrane potential has been restored but the ion distribution differs slightly- the Na+/K+ pump restores this. It is a channel requiring ATP.-prevents equilibrium to be reached at the inside/outside.

44
Q

What direction does the AP propagate in?

A

-from the axon hillcock to the axon terminals

45
Q

Is more than one triggering event needed for an AP to be propagated along the axon?

A

-once AP initiated no further triggering event needed it is automatically propagated along the membrane

46
Q

Is AP in the beginning different to the AP at the end?

A

-no, identical

47
Q

What is meant by contiguous conduction of AP?

A

(=touching or next in sequence) conduction: spread of AP along every patch of the membrane down the length of the axon about 0.7 m/sec
-current flow from the area undergoing AP to the neighbouring areas (both sides) brings it to threshold and AP generated and so on and on

48
Q

What is the refractory period and what is its function?

A
  • period just after AP completion in which new AP can’t be initiated
  • sets a limit on the frequency of AP
  • ensures unidirectional propagation of the action potential, when the active bit transfers AP onto neighbouring part the previously active bit goes through refractory period that is long enough so the newly active site won’t spread the AP back to it but will continue in the other direction, away from the original site
49
Q

What is absolute and relative refractory period?

A
  • when undergoing AP can’t initiate a new one=absolute refractory period
  • just after AP completion, can’t initiate a new one unless it’s huge triggering event since we have hyperpolaristion= relative refractory period
50
Q

What is the function of myelination?

A
  • increases speed of conduction of APs and conserves energy in the process
  • the APs leap over the myelin covered area= great increase in speed 120 m/s (opposed to 0.7 m/sec in contagious)
  • don’t have to use the Na+/K+ pump on myelinatde bits (requiring ATP) = conserves energy
51
Q

What is myelin?

A
  • meylin= mainly lipid
  • secreted by oligodendrocytes
  • the ions Na+ K+ etc can’t get through the lipid barrier, the myelin acts as an insulator
  • only some axons have it

-myelin covers axons at regular intervals along the length of the axon

52
Q

What is saltatory conduction?

A
  • spread of conduction along myelinated fibres= SALTATORY CONDUCTION
  • saltere in latin= to leap
53
Q

oligodendrocytes

A

myelin forming cells in the CNS that wrap themselves around the axon in concentric rings

54
Q

Schwann cells?

A

myelin forming cells in the PNS

55
Q

Nodes of Ranvier

A

exposed, non-myelated regions of the axonal membrane and AP can only flow there and be generated there since ions can get across the membrane, Na+ channels concentrated here
-usually about 1 mm apart from each other

56
Q

What is demyelination: Canine distemper?

A
  • disease causing demyelination in the brain
  • very contagious (spreads to lions for example)
  • animal can’t co-ordinate movement
  • too slow AP propagation (only contiguous)
  • nerve stimulation too slow
  • non curable
57
Q

What is synaptic and postsynaptic neuron?

A

Singalling neuron= presynaptic target neuron= postsynaptic

58
Q

What types of transmission are there in synapses?

A

-transmissions: chemical, electrical

59
Q

Describe electrical transmission in synapse.

A
  • gap junctions connect presynaptic and postsynaptic neuro
  • AP essentially transmitted across, almost instantaneous
60
Q

Describe chemical synaptic transmission.

A
  • Chemical-
  • postsynaptic and presynaptic don’t make direct contact = synaptic cleft
  • synaptic cleft approx 20-40nm wide, too big for electrical transmission
  • neurotransmitters released from the presynaptic to the postsynaptic neuron
  • neurotransmitter binds with a receptor on the postsynaptic membrane
  • the receptor alters the activity of the target cell
  • slower than electrical, rely on diffusion
  • advantages: only one directional + allow for variety of signaling events not just AP transmission
61
Q

What happens in neuron to neuron synapses?

A
  1. AP reaches axon terminal of presynaptic neuront, triggering opening of Ca2+ channels
  2. Ca2+ enters synaptic knob (presynaptic terminal) (more of it in the ECF)
  3. Neurotransmitter is released by exocytosis of vesicles into synaptic cleft (induced by Ca2+)
  4. Neurotransmitter binds to receptors on postsynaptic membrane
  5. Binding of neurotransmitter to receptor opens specific channels, changing the permeability of the membrane - chemically gated channels

Synaptic delay: 0.5 to 1 msec increasing reaction time when lot of neurons involved

62
Q

What is the neurotrasmitter action ESPS?

A

excitatory postsynaptic potential

  • open Na+ K+ channels = bring membrane towards threshold
  • different channels than before the permeability to both can be increased at the same time
  • at resting: lot of Na+ will go in while only a few K+ will go out- depolarization
63
Q

What is the neurotransmitter action ISPS?

A

inhibitory postsynaptic potential

  • K+ or Cl- channels = brings membrane away from threshold
  • Bring about small hyperpolarisation, Cl moving in and K+ moving out
64
Q

How is neurotransmitter removed from the synaptic cleft?

A
  • diffusion away from the cleft
  • inactivation by a specific enzyme in postsynaptic membrane
  • transport back into the axon terminals= reuptake on the presynaptic membrane

also on slow synapses: some neurotrasmitters (serotonin) use activation of intracellular second messengers eg: camp

-slower responses, the camp can activate the receptor sites

65
Q

What determines the overall postsynaptic potential?

A
  • composite of all the ESPS and ISPS- may be thousands
  • ISPS and ESPS= graded potentials so depends how many how strong to elicit a response
  • excitatory/inhibitory cancel each other out
  • proximity to hillcock affects how much effect an event has
  • APs initiated on the hillcock because it has the lowest threshold
66
Q

What is meant by temporal summation in graded potentials?

A
  • if graded potentials close to each other, builds up and reaches threshold
67
Q

What is meant by spatial summation in graded potentials?

A
  • if more act together= spatial summation
68
Q

What is converegence and divergence in neural networking?

A

Convergence –the neurons synapsing with a neuron, thus one neuron influenced by thousands others
and divergence- branching of axon terminals, single cell influences many others

69
Q

Strychnine poisoning:

A
  • what happens when convergence divergence mechanisms stop working
  • strychnin binds on post synaptic sites pereventing glycine binding= glycine inhibition
  • gycine inhibitory neurotransmitter important for balance in animals
70
Q

Behavioural modification (neurotransmittal manipulation):

A
  • crib-biting horse= Prozac inhibits serotonin reuptake
  • only limited success but does have some effect
  • feather picking birds: haloperidol- dopamine antagonist