How nerves work 4 + 5 Flashcards
how are action potentials produced?
they are evoked by voltage gated sodium channels opening which causes a massive depolarisation that brings the cell to threshold.
what is the common threshold potential value?
about -55 mV
so if a graded potential reaches this an action potential will be released
what happens once the threshold is reached?
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
why would there be a delayed effect if you poisoned the Na+/K+ pump?
it takes time for gradients to run down
why is cell excitability low when Na+ channels are open?
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.
What are properties of an action potential?
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
why is refractory period so important?
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
how does a bigger graded potential lead to more action potentials being produced?
it stays above threshold for longer
why are there no Na+ channels within myelinated parts of axons?
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
what is saltatory conduction?
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.
de-myelination and multiple sclerosis
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
Why are some nerves unmyelinated?
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
recording conduction velocity process
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
what is compound action potential
a series of waves
- The measure of the activity of an individual nerve cell by how frequently it fires A.P
fastest wave
Aalpha - big myelinated
proprioception (detecting a stretch in a muscle)
slowest wave
C- unmyelinated, just fibres- pain from heat
B wave
smallest myelinated- really slow conductions
A gamma
myelinated- muscle spindles
A delta
fairly small, even slower conduction (touch, cold)
A beta
Sensory neurons
what happens at the NMJ
- 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
what is acetylcholine removed by after it has diffused across synaptic cleft and bound to receptors? and why?
acetylcholinesterase
To stop any spasms occuring as many action potentials are fired
What is the neuromuscular junction?
a synapse between motor neuron and skeletal muscle in the PNS
what is the sarcolemma?
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
Tetrodotoxin (T.T.X)
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
joro spider toxin
blocks calcium channels and so stops the neurotransmitter from being released
synapses in the CNS are more difficult than in the PNS for what 5 reasons?
range of neurotransmitters range of receptors range of different post- synaptic potentials arrangement of synapses synaptic connectivity
range of neurotransmitters in CNS
ACh is sometimes used in CNS but can also use inhibitory= GABA, serotonin
excitatory= glutamate, noradrenaline, dopamine, adrenaline, histamine
what does glycine do?
all the fast inhibitory transmission in the spinal cord
range of receptors in CNS
all the neurotransmitters used in CNS act on different receptors and are able to gate different ion channels
range of different post- synaptic potentials
fast EPSPs slow EPSPs fast IPSPs slow IPSPs CNS has all of these
arrangement of synapses
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
synpaptic connectivity CNS
convergence
divergence
convergence meaning
lots of cells synapsing onto one cell- look at all inputs and decide whether AP can be fired
divergence meaning
one cell synapsing onto lots of others
where is the only source of divergence in synapse activity in PNS
At the NMJ when one cell serves lots of muscle fibres
nerve fibre types
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
what do somatic nerves supply
the skeletal muscles of the body
Guillain- Barre syndrome
myelin may only be under attack for a few hours before symptoms occur
demyelinating diseases- what are they and examples
damage to the myelin sheath that surrounds nerve fibers in your brain, optic nerves and spinal cord.
Multiple Sclerosis (MS)
Guillain- Barre syndrome
symptoms of demyelinating diseases
numbness
pain
mobility problems
progressively worse as you get older
Which form of synaptic anatomical arrangement in the CNS usually produces the largest response?
Axo somatic (onto the soma)
