Chapter 15 - Nervous Coordination and Muscles Flashcards
what is an action potential
when the neuron’s voltage increase beyond a set point from the resting potential which generates a nervous impulse
draw and label the motor neurone structure
- cell body - where organelles are found and where protein and neurotransmitters are made
- dendrites - carry action potentials
- axon - carries nerve impulse
- Schwann cells - wraps around the axon to form the myelin sheath to prevent charged ions from passing through it
- node of Ranvier - gaps between myelin sheath
what is the resting potential
the difference in electrical charge between inside and outside of the neurone when it is not conducting an impulse
process on how resting potential is maintained
1) The sodium potassium pump actively transports 2 potassium ions into the axon and 3 sodium ions out of the axon
2) this creates an electrochemical gradient
3) this results in potassium ions diffusing out via facilitated diffusion through the potassium ion channels and sodium ions diffusing in via facilitated diffusion through the sodium ion channels
why is the concentration of sodium ions and potassium ions not the same on each side of the membrane
As the membrane is more permeable to the potassium ions because:
- since there are more potassium ion protein channels than sodium ion protein channels
- sodium ion channels only open when you reach a high enough voltage
draw and label the graph that represents the generation of an action potential
labels
- resting potential
- depolarisation
- action potential
- replorization
- hyperpolrisation
- refractory period
What happens to the neurone when an action potential is triggered
1) Resting potential - The membrane is at rest and polarised at around -70 mV.
2) Stimulus - When a stimulus is generated Voltage-gated Na+ channels open, so more Na+ flows into the axon making the inside less negative.
3) Depolarisation - If the threshold potential of -55 mV is reached, more voltage gated Na+ channels open causing an influx of Na+.
4) Repolarisation - At around +30 mV, Na+ channels close and K+ channels open, so K+ flows out of the axon and the membrane starts repolarising and become more negative.
5) Hyperpolarisation - An excess of K+ leaves the axon, dropping the potential below the -70 mV resting level.
6) Refractory period - Various ion pumps and channels work together to restore the membrane back to the resting potential.
why is there a peak in action potential at 40mv
As once 40mv is reached inside the axon the voltage gated sodium ion channels will close, so the voltage cannot increase any further
what is the all or nothing principle
- if depolarisation does not exceed -55mv then action potential and the impulse is not produced
- any stimulus that does trigger depolarisation at -55mv will always peak at the same maximum voltage (40mv)
- bigger stimuli increases the frequency of action potential rather than the size of the peak
what is the importance of the refractory period
- it ensures that discrete impulses are produced, so that action potentials cannot be generated immediately after another one
- it ensures that impulses can only travel in one direction
- limits the frequency at which impulses are transmitted which prevents over reaction to a stimulus, overwhelming the senses
How does a nerve impulse travel along an axon in one direction?
1) The opening of Na+ channels results in local depolarisation, allowing positive ions to spread sideways.
2) Adjacent voltage-gated Na+ channels open in response to this change.
3) This action leads to the depolarisation of nearby membrane
4) As each membrane activates the next, an advancing wave is formed.
5) Areas of the membrane that have just been depolarisation are in the refractory period and remain unresponsive while they repolarise (K+ exits the axon and Na+ channels are closed).
6) This ensures that the wave moves in one direction, preventing the backward flow of the nerve impulse.
What are the three key factors that affect the speed of conductance in an axon?
- Myelination (Saltatory conduction)
- Axon diameter
- Temperature
How does myelination affect the speed of conductance?
Myelination increases speed by saltatory conduction, where the action potential jumps between nodes of Ranvier, this means that action potentials only have to be generated at the nodes of Ranvier
Why is conduction slower in unmyelinated axons?
In unmyelinated axons, the action potential must be generated along the entire length of the axon, rather than jumping between nodes, making conduction slower.
How does axon diameter affect the speed of conductance?
A wider axon increases speed because:
* A larger axon diameter means there is less resistance to ion flow, so the wave of depolarisation travels faster along the axon.
Therefore, broader axons transmit impulses faster.
How does temperature affect the speed of conductance?
A higher temperature increases speed by:
1. faster diffusion of ions via facciliated diffusion, leading to faster depolarisation and faster impulse transmission.
2. Increased ATP production for active transport (Na+/K+ pump) due to faster respiration
What happens to the speed of conduction if the temperature gets too high?
Enzymes involved in respiration and active transport denature, reducing ATP production and slowing conduction
What is a synapse
the gaps between the end of the axon and the dendrite of another one
Describe the process of cholinergic synapses
1) an action potential arrives at the synaptic knob
2) depolarisation of the synaptic knob leads to the opening of calcium ion channels, causing calcium to diffuse into the synaptic knob
3) vesicles containing acetylcholine will move towards and fuse with the presynaptic membrane, causing the acetylcholine to be released into the synaptic cleft
4) acetylcholine diffuses down the concentration gradient across synaptic cleft to post synaptic membrane
5) the acetylcholine bind to complementary receptors on the surface of the postsynaptic membrane
6) this binding will cause the sodium ion channels on post synaptic membrane to open causing an influx of sodium ions depolarising the post synaptic membrane, if enough sodium ions diffuse in it generates an action potential
7) the acetylcholine is broken down by acetylcholinesterase into acetyl and choline and released from the receptor to be recycled back to the presynaptic neurone and reformed using the mitochondria in the presynaptic neurone
8) this causes the sodium ion channels to close and the post synaptic neurone can go back to resting potential
what is summation
the rapid build up neurotransmitter in the synapse to help generate an action potential
two types of summation
- spatial summation
- temporal summation
why is summation important
as it is needed to add up sufficient concentrations of neurotransmitters to open up sufficient numbers of sodium ion channels to trigger an action potential
what is spatial summation
when there is multiple presynaptic neutrons attached to one synapse and one post synaptic neuron
how does spatial summation works
each presynaptic neurone will release neurotransmitters these neurotransmitters will combine so threshold can be reached
what is temporal summation
this is where one neurone releases neurotransmitters repeatably over a short period of time until threshold is reached
how does inhibitory synapses work
1) Inhibitory neurotransmitters are released into the synaptic cleft.
2) Inhibitory neurotransmitters bind to chloride (Cl-) channels on the postsynaptic membrane.
3) The opening of these channels allows an influx of Cl- into the postsynaptic neurone via facilitated diffusion.
4) Potassium (K+) channels also open, and K+ leaves the postsynaptic neurone.
5) The combined effect of negative ions moving in and positive ions moving out make the membrane potential increase to -80mV which results in the hyperpolarisation of the postsynaptic membrane, preventing the generation of an action potential.
what is a neuromuscular junction
the synapse that occurs between a motor neurone and a muscle
difference between excitatory (E) and inhibitory (I) neurotransmitters
Effect on the postsynaptic membrane - E causes Depolarisation and I causes Hyperpolarisation
affect on action potential - E triggers an action potential if threshold is reached and I - Prevent action potentials
difference and similarities between neuromuscular junction and cholinergic synapses
sim
unidirectional due to receptors only being on the post synaptic membrane
difference
NJ - excitatory whilst CS- inhibitory or excitatory
NJ - connect motor neurone to muscle whilst CS- connects two neuron’s which could be sensory relay or motor
NJ - it is the end point for the action potential whilst CS- a new action potential is generated in the next neurone
NJ - acetylcholine binds to receptors on muscle fibre membranes whilst CS - acetylcholine binds to receptors on post synaptic membrane
labels in order muscle tissue, myofibrils, muscle fibre, sarcomere, myosin and actin
muscle tissue
muscle fibre
myofibril
sarcomere
myosin and actin
draw and label the sarcomere including the myosin protein and the bands
stages in neuromuscular transmission
1) The action potential arrives at the end of the neurone.
2)This triggers the opening of calcium ion (Ca2+) channels, and Ca2+ enters the neurone.
3) This causes acetylcholine vesicles to release their contents into the synaptic cleft.
4) Acetylcholine diffuses across the synaptic cleft.
5) Acetylcholine binds to receptors on the sarcolemma, leading to the opening of sodium ion channels.
6) This results in the depolarisation of the sarcolemma.
7) Depolarisation extends deep into the muscle fibre through T tubules as sodium ions diffuse into the t tubules
8) This triggers the release of calcium ions from the sarcoplasmic reticulum (SR).
process of sliding filament theory
1) when an action potential reaches a muscle it stimulates a response, causing the release of calcium ions from the sarcoplasmic reticulum
2) Calcium ions (Ca2+) enter and bind to troponin this causes tropomyosin to move away from actin’s binding sites, making them available for myosin.
3) Whilst ADP is attached to Myosin heads the myosin heads attach to these exposed actin binding sites, forming actin-myosin cross-bridges.
4) The angle created in the cross brige creates tension causing the myosin heads to execute a power stroke, pulling the actin filament along and releasing ADP and Pi.
5) An ATP molecule binds to the myosin head causing the head to change shape so no longer comp to actin binding site, leading to its detachment from actin.
6) Ca2+ activates myosin’s ATPase activity, breaking down ATP to ADP and phosphate, releasing energy.
7) This energy resets the myosin head to its original position and the process is repeated
different ways ATP can be generated for muscle contraction
- Aerobic respiration - This is suitable low-intensity exercise.
- Anaerobic respiration - This is used during short, high-intensity exercise.
- The phosphocreatine system - phosphocreatine which is stored in the muscle provides phosphate to regenerate ATP from ADP during anaerobic respiration. It is used for short bursts of vigorous exercise
What happens to the bands when the muscle contracts
Contract:
I band shortens
H zone shortens
A band stays the same
Z lines move closer together
what happens when the muscle relaxes
1) Ca2+ is actively transported back into the sarcoplasmic reticulum.
2) Tropomyosin repositions, blocking the actin-myosin binding sites.
3) Myosin heads detach from the actin filaments.
4) Without cross-bridge formation, sarcomeres revert to their relaxed length.
describe the structure of slow twitch muscles
contains a large store of myoglobin, a rich blood supply and lots of mitochondria
describe the structure of fast twitch muscles
thick and contain more myosin filaments, contains a large store of glycogen, a store of phosphocreatine for the production of ATP and a high concentration of enzymes for aneorobic respiration
location of slow twitch muscles
calf muscles
location of fast twitch muscles
biceps
describe properties of slow twitch muscles
contracts slower
respires aerobically for longer periods of time due to the the rich blood supply and myoglobin store
describe properties of fast twitch muscles
contracts faster to provide short powerful contraction
