Section 6 - Unit 15: Nervous coordination and muscles Flashcards
Describe the roles of calcium ions and ATP in the contraction of a myofibril (5 marks
- Calcium ions diffuse into myofibrils from (sarcoplasmic) reticulum
- The ions cause the movement of tropomyosin (on actin)
- This movement causes the exposure of the binding sites on the actin
- Myosin heads attach to binding sites on actin
- Hydrolysis of ATP (on myosin heads) causes myosin heads to bend
- Pulling the actin molecules
- Attachment of a new ATP molecule to each myosin head causes myosin heads to detach (from actin sites)
Multiple sclerosis is a disease in which parts of the myelin sheaths surrounding neurones are destroyed. Explain how this results in slower responses to stimuli (2 marks)
- Less saltatory conduction / action potential / impulse unable to ‘jump’ from
node to node - More depolarisation over the area of membranes
Suggest one reason why damage to the myelin sheaths of neurones can lead to problems controlling the contraction of muscles (2 marks)
- Action potentials travel more slowly
- So delay in muscle contraction
OR - Action potentials / depolarisation ‘leaks’ to adjacent neurones
- So wrong muscle (fibres) contract
Cannabinoid receptors are found in the pre-synaptic membrane of neuromuscular junctions. When a cannabinoid binds to its receptor, it closes calcium ion channels. Suggest how cannabinoids could prevent muscle contraction (4 marks)
- Prevents influx of calcium ions (into pre-synaptic membrane)
- Synaptic vesicles don’t fuse with membrane / vesicles don’t release neurotransmitter
- Neurotransmitter does not diffuse across synapse / does not bind to receptors
- No action potential / depolarisation / sodium (ion)
channels do not open / prevents influx of sodium ions
A myelinated axon conducts impulses faster than a non-myelinated axon. Explain this difference (3 marks)
In myelinated axon:
- Action potential / depolarisation only at the node
- Nerve impulse jumps from node to node / saltatory
- Action potential does not travel along the whole length
Serotonin diffuses across the synaptic gap and binds to a receptor on the post synaptic membrane. Describe how this causes depolarisation of the post-synaptic membrane
- Causes sodium ion channels to open
- Sodium ions enter (cell and cause depolarisation)
After exercise, some ATP is used to re-establish the resting potential in axons. Explain how the resting potential is re-established (2 marks)
- Pump / active transport / against concentration gradient
- Of sodium from axon / sodium out / of potassium in
Describe the sequence of events leading to the release of acetylcholine and its binding to the postsynaptic membrane (4 marks)
- Action potential arrives / depolarisation occurs
- Calcium ions enter synaptic knob
- Vesicles fuse with membrane
- Acetylcholine diffuses (across synaptic cleft)
- And binds to receptors
The binding of GABA to receptors on postsynaptic membranes causes negatively charged chloride ions to enter postsynaptic neurones. Explain how this will inhibit transmission of nerve impulses by postsynaptic neurones (3 marks)
- Inside becomes more negatively charged / hyperpolarised
- Stimulation does not reach threshold level / action potential not produced
- Depolarisation does not occur / reduces effect of sodium ions entering
Describe the sequence of events which allows information to pass from one neurone to the next neurone across a cholinergic synapse (6 marks)
- (impulse causes) calcium ions / Ca2+ to enter axon
- Vesicles move to / fuse with (presynaptic) membrane
- Acetylcholine (released)
- Acetylcholine) diffuses across synaptic cleft / synapse
- Binds with receptors on (postsynaptic) membrane
- Sodium ions / Na+ enter (postsynaptic) neurone
- Depolarisation of (postsynaptic) membrane
- If above threshold nerve impulse / action potential produced
Explain how a resting potential is maintained in a neurone (4 marks)
- Membrane relatively impermeable / less permeable to sodium ions / gated channels are
closed / fewer channels - Sodium ions pumped / actively transported out
- By sodium ion carrier / intrinsic proteins
- Inside negative compared to outside / 3 sodium ions out for two potassium ions in
Explain why it is important that a neurotransmitter such as serotonin is transported back out of synapses (2 marks)
- (If not removed) keeps binding (to receptors)
- Keeps causing action potentials / depolarisation (in post-synaptic membrane)
Synapses are unidirectional. Explain how acetylcholine contributes to a synapse being
unidirectional (2 marks)
- Acetylcholine released from presynaptic side
- Receptors in postsynaptic (side) / binds on postsynaptic (side)
Explain why during an action potential, the membrane potential rises to +40 mV and then falls (3 marks)
- Potassium channels open
- Potassium out
- Sodium channels close
Describe how the resting potential is established in an axon by the movement of ions across the membrane (2 marks)
- Active transport of Na+ out of axon
- Diffusion of K+ out of axon / little diffusion of Na+ into the axon
Explain how the release of acetylcholine at an excitatory synapse reduces the membrane potential of the postsynaptic membrane (2 marks)
- Binds to receptor / proteins
- And opens Na channels
- Na+ enter and make membrane potential less negative/depolarised
Explain what causes transmission at a synapse to occur in only one direction (2 marks)
- Neurotransmitter only in presynaptic membrane
- Receptor / proteins only in postsynaptic membrane
Describe how the release of acetylcholine into a neuromuscular junction causes the cell membrane of a muscle fibre to depolarise (3 marks)
- Movement by diffusion
- Binding to receptors on (post-synaptic) membrane
- Causing sodium channels to open / sodium ions to move in to muscle (cell)
Explain why when a neurone transmits a series of impulses, its rate of oxygen consumption increases (3 marks)
- More respiration
- More energy / ATP supplied
- For active transport of ions / pumping
out sodium ions
Describe how calcium ions are involved in synaptic transmission (2 marks)
- Nerve impulse causes Ca ions to enter presynaptic neurone/membrane
- Ca ions entry causes fusion of vesicles with presynaptic membrane
What is the role of ATP in myofibril contraction (2 marks)
- Reaction with ATP breaks/allows binding of myosin to actin
- Provides energy to move myosin head;
Explain why both slow and fast muscle fibres contain ATPase (2 marks)
- Breakdown of ATP
- Muscle contraction requires energy / ATP
- Use of ATP by myosin
Explain the importance of tropomyosin in myofibril contraction (2 marks)
- Moves out of the way when calcium ions bind
- Allowing myosin to bind to actin
Explain the importance of myosin in myofibril contraction (2 marks)
- Head (of myosin) binds to actin and slides actin past
- Myosin detaches from actin and moves further along actin
- This uses ATP
When the sarcomeres contract, what happens to the length of the I-band and why (2 mark)
- Decreases
- Thin filaments enter H zone / actin filaments slide in between myosin
When the sarcomeres contract, what happens to the length of the A-band (1 mark)
- Stays the same length
Explain what leads to the differences in appearance between the relaxed myofibril and the contracted myofibril (4 marks)
When contracted:
- Thick & thin filaments/myosin & actin overlap more
- Interaction between myosin heads & actin / cross-links form
- Movement of myosin head
- Thin filaments / actin moved along thick filaments / myosin
- Movement of thin filaments / actin pulls Z-lines closer together
- Displacement of tropomyosin to allow interaction
Explain the importance of ATP in myofibril contraction (2 marks)
- Releases myosin from actin
- Causes myosin head to move
- Used in active transport of Ca ions
Explain how muscles maintain posture (3 marks)
- Antagonistic muscles / opposing pairs of muscles
- Working across/at joints
- Both contract to keep joint/the body at certain angle / upright
- Isometric contraction
- Only a few fibres contract to avoid fatigue/slow muscle fibres used
Explain how a decrease in the concentration of calcium ions within muscle tissues could cause a decrease in the force of muscle contraction (3 marks)
- Less tropomyosin moved from binding site
- Less actinomyosin bridges formed
- Myosin does not pull actin (filaments)
OR
Myosin head does not move
OR
Less ATP hydrolase
Describe how muscle contraction occurs, explaining the roles of ADP and ATP in detail (7 marks)
- Calcium ions diffuse into myofibrils from (sarcoplasmic) reticulum
- The ions cause the movement of tropomyosin (on actin)
- This movement causes the exposure of the binding sites on the actin
- ADP molecules bound to the myosin heads means that they can bind to the actin filament and cause a cross bridge
- Once attached to actin, myosin head bend, pulling the actin filament as they do so and this releases ADP
- ATP then binds to a myosin head, causing it to become detached
- Calcium ions then activate ATPase which hydrolyses ATP to ADP – the energy released allows myosin heads to return to their original position
- As myosin now has ADP bound to it, it can form another cross bridge further along the actin filament
