How nerves work 4 + 5 Flashcards

1
Q

how are action potentials produced?

A

they are evoked by voltage gated sodium channels opening which causes a massive depolarisation that brings the cell to threshold.

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2
Q

what is the common threshold potential value?

A

about -55 mV

so if a graded potential reaches this an action potential will be released

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3
Q

what happens once the threshold is reached?

A

sodium channels open
sodium rushes into the cell depolarising it
it goes all the way to about +40 mV
to repolarise- potassium channels open up letting potassium move out of the cell in attempt to balance out charge
this all happens very quickly

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4
Q

why would there be a delayed effect if you poisoned the Na+/K+ pump?

A

it takes time for gradients to run down

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5
Q

why is cell excitability low when Na+ channels are open?

A

it’s in refractory period- the cell cannot respond to another depolarisation- voltage gated Na+ channels are tired and need to rest before working again.

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6
Q

What are properties of an action potential?

A

self probagating- ie self spreading/transmission
need G.P to reach threshold for A.P to exist
refractory period
a bigger G.P doesn’t do anything different as A.P is just produced once target threshold is reached and because so much Na+ flows in the threshold is always reached therefore it’s ALL OR NONE

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7
Q

why is refractory period so important?

A

by not responding it makes sure an action potential can only travel in one direction (not backwards)
current flow can move backwards but it does NOT produce a new A.P that way as they are in refractory state

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8
Q

how does a bigger graded potential lead to more action potentials being produced?

A

it stays above threshold for longer

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9
Q

why are there no Na+ channels within myelinated parts of axons?

A

if depolarisation is evoked from Na+ channels at one end then the myelination helps to insulate the neuron and the depolarisation spreads passively quickly along to the next node. Decay is slow at node however it still reaches threshold

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10
Q

what is saltatory conduction?

A

Saltatory conduction is the propagation of action potentials along myelinated axons from one node of Ranvier to the next node, increasing the conduction velocity of action potentials.

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11
Q

de-myelination and multiple sclerosis

A

an auto-immune, neurological disease which occurs from damage to the myelin sheathes. When one end depolarises the transmission is not good as it decays quickly and is not big enough at next node to reach threshold. Channels therefore never get activated and there is failure of transmission more and more as the disease progresses/gets worse

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12
Q

Why are some nerves unmyelinated?

A

myelination has a huge metabolic cost so they’re only myelinated if there is an advantage to their potentials being transmitted faster
ie Neurons which pass information about temperature change and prolonged ache don’t need to be fast- these are called C fibres + aren’t myelinated!
However, neurons which have to pass information about sudden pain (touching a burning hot pan) need to be myelinated to protect the body

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13
Q

recording conduction velocity process

A

stimulating the nerve trunk at one end will cause lots of axons to depolarise at the same time and all fire an A.P at the same time which causes a big wave of depolarisation. They’re all effected at different rates and you can record the velocity of each

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14
Q

what is compound action potential

A

a series of waves

- The measure of the activity of an individual nerve cell by how frequently it fires A.P

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15
Q

fastest wave

A

Aalpha - big myelinated

proprioception (detecting a stretch in a muscle)

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16
Q

slowest wave

A

C- unmyelinated, just fibres- pain from heat

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17
Q

B wave

A

smallest myelinated- really slow conductions

18
Q

A gamma

A

myelinated- muscle spindles

19
Q

A delta

A

fairly small, even slower conduction (touch, cold)

20
Q

A beta

A

Sensory neurons

21
Q

what happens at the NMJ

A
  • At N.M.J the A.P comes down and activates voltage gated Ca2+ channels there to open, releasing calcium into own cytoplasm.
  • The flow of Ca2+ ions causes synaptic vesicles to fuse with cell membrane and release ACh.
  • ACh then diffuses across the synaptic cleft and binds to nicotinic receptors (ionotropic) on post-synaptic membrane. Depending on which neurotransmitter binds different channels open but here Na+ and K+ channels open which causes depolarisation and here we call this specific potential the end plate potential- it always reaches threshold- muscle always acted on
22
Q

what is acetylcholine removed by after it has diffused across synaptic cleft and bound to receptors? and why?

A

acetylcholinesterase

To stop any spasms occuring as many action potentials are fired

23
Q

What is the neuromuscular junction?

A

a synapse between motor neuron and skeletal muscle in the PNS

24
Q

what is the sarcolemma?

A

cell membrane of a striated muscle fiber cell

this membrane has junctional folds with ACh receptors leading deeper into the muscle to allow for a deeper contraction

25
Q

Tetrodotoxin (T.T.X)

A

blocks Na+ channels and stops action potential from flowing through channel and so A.P (end plate potential) can’t be produced- would affect all neurons so very bad

26
Q

joro spider toxin

A

blocks calcium channels and so stops the neurotransmitter from being released

27
Q

synapses in the CNS are more difficult than in the PNS for what 5 reasons?

A
range of neurotransmitters
range of receptors
range of different post- synaptic potentials
arrangement of synapses 
synaptic connectivity
28
Q

range of neurotransmitters in CNS

A

ACh is sometimes used in CNS but can also use inhibitory= GABA, serotonin
excitatory= glutamate, noradrenaline, dopamine, adrenaline, histamine

29
Q

what does glycine do?

A

all the fast inhibitory transmission in the spinal cord

30
Q

range of receptors in CNS

A

all the neurotransmitters used in CNS act on different receptors and are able to gate different ion channels

31
Q

range of different post- synaptic potentials

A
fast EPSPs 
slow EPSPs
fast IPSPs 
slow IPSPs
CNS has all of these
32
Q

arrangement of synapses

A

synpasing onto soma of cell- axo-somatic
synapsing onto dendrites- further from axon hillock so less of an effect- axodendritic
synapsing onto axon terminals- axo-axonal- can usually inhibit neurotransmitters from here

33
Q

synpaptic connectivity CNS

A

convergence

divergence

34
Q

convergence meaning

A

lots of cells synapsing onto one cell- look at all inputs and decide whether AP can be fired

35
Q

divergence meaning

A

one cell synapsing onto lots of others

36
Q

where is the only source of divergence in synapse activity in PNS

A

At the NMJ when one cell serves lots of muscle fibres

37
Q

nerve fibre types

A

A B and C
A and B are myelinated
C is not myelinated- things like body temp not needing a quick response to
A- quick response- preventing your body from harm/danger

38
Q

what do somatic nerves supply

A

the skeletal muscles of the body

39
Q

Guillain- Barre syndrome

A

myelin may only be under attack for a few hours before symptoms occur

40
Q

demyelinating diseases- what are they and examples

A

damage to the myelin sheath that surrounds nerve fibers in your brain, optic nerves and spinal cord.
Multiple Sclerosis (MS)
Guillain- Barre syndrome

41
Q

symptoms of demyelinating diseases

A

numbness
pain
mobility problems
progressively worse as you get older

42
Q

Which form of synaptic anatomical arrangement in the CNS usually produces the largest response?

A

Axo somatic (onto the soma)