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15. Nervous Coordination and Muscles

Terms in this set (49)

Neurones are adapted to carry electrochemical charges called ( 1 ). Each neurone comprises a cell body that contains a ( 2 ) and large amounts of ( 3 ), which is used in the production of proteins and neurotransmitters. Extending from the cell body is a single long fibre called an axon and smaller branched fibres called ( 4 ).
( 1 ) Impulses / action potentials
( 2 ) Nucleus
( 3 ) Rough endoplasmic reticulum
( 4 ) Dendrites
Axons are surrounded by ( 5 ) cells, which protect and provide ( 6 ) because their membranes are rich in a lipids known as ( 7 ). There are three main types of neurone. Those that carry nerve impulses to an effector are called ( 8 ) neurons. Those that carry nerve impulses from a receptor are called ( 9 ) neurons and those that link the other two types are called ( 10 ) neurons.
( 5 ) Schwann cells
( 6 ) Insulation
( 7 ) Myelin
( 8 ) Motor
( 9 ) Sensory
( 10 ) Intermediate
List three ways in which a response to a hormone differs from a response to a nerve impulse.
1. Hormone response is slow, widespread and long-lasting.
2. Nervous response is rapid, localised and short-lived.
(Ageing neurones) Describe changes in the neurons that take place when healthy humans age.
Dendrites become longer with age.
(Ageing neurones) Comment on the appearance of the neurone from the 70 year old who has Alzheimer's disease.
Dendrites are fewer, are much shorter and are less branched.
(Ageing neurones) After the age of 50 years, humans lose 5% of the neurones in this region of the brain every 10 years. Calculate how many neurones will be left at the age of 70 years from each 2000 neurones present at the age of 50 years.
After 10 years (age 60) there will be:
2000 - (0.05 x 2000) = 1900 neurones remaining.
After further 10 years (age 70) there will be:
1900 - (0.05 x 1900) = 1805 neurones remaining.
Describe how the movement of ions establishes the resting potential in an axon.
1. Active transport of sodium ions out of the axon by sodium-potassium pumps is faster than active transport of potassium ions into the axon.
2. Potassium ions diffuse out of the axon but very few sodium ions diffuse into the axon because the sodium 'gates' are closed.
3. Overall, there are more positive ions outside than inside and so the outside is positive relative to the inside.
(Refer to measuring action potentials pg.353) Between 0.5 and 2.0 ms there is a considerable change in membrane potential. Explain how this change is brought about.
1. At resting potential (0.5 ms) there is a positive charge on the outside of the membrane and a negative charge inside - due to the high concentration of sodium ions outside the membrane.
2. The energy of the stimulus causes the sodium voltage-gated channels in the axon membrane to open and sodium ions diffuse in through the channels, along their electrochemical gradient.
3. Being positively charged, they begin a reversal in the potential difference across the membrane.
4. Sodium ions enter and more sodium ion channels open, causing an even greater influx of sodium ions and an even greater reversal of potential difference: from -70 mV up to +40 mV at 2.0 ms.
In a myelinated axon, sodium and potassium ions can only be exchanged at certain points along it:
(a) State the name given to these points.
(b) Explain why ions can only be exchanged at these points.
(c) Describe the effect this has on the way an action potential is conducted along the axon.
(d) State the name that is given to this type of conduction.
(e) Describe how it affects the speed with which the action potential is transmitted compared to an unmyelinated axon.
(a) Node of Ranvier.
(b) The remainder of the axon is covered by a myelin sheath that prevents ions being exchanged / prevents a potential difference being set up.
(c) It moves along in a series of jumps from one node of Ranvier to the next.
(d) Saltatory conduction.
(e) It is faster than in an unmyelinated axon.
Describe what happens to the size of an action potential as it moves along an axon.
It remains the same.
Explain how the refractory period ensures that nerve impulses are kept separate from one another.
During the refractory period, the sodium voltage-gated channels are closed so no sodium ions can move inwards and no action potential is possible. This means there must be an interval between one impulse and the next.
State the all-or-nothing principle.
There is a particular level of stimulus that triggers an action potential. At any level above this threshold, a stimulus will trigger an action potential that is the same regardless of the size of the stimulus (the 'all' part). Below the threshold, no action potential is triggered (the 'nothing' part).
Earthworms have unmyelinated axons and so to increase the speed of conduction of action potentials these are relatively large in diameter. Suggest two reasons why mammals do not require large diameter axons to achieve rapid transmission of action potentials.
1. Mammals have myelinated neurones and so have saltatory conduction.
2. Mammals are endothermic and their constant (usually higher) body temperature increases the rate of diffusion of ions across the axon membrane and hence the speed of conduction of the action potential.
Explain why a myelinated axon conducts an action potential faster than an unmyelinated axon.
In myelinated axons, the myelin acts as an electrical insulator. Action potentials can only form where there is no myelin (at nodes of Ranvier). The action potential therefore jumps from node to node (saltatory conduction) which makes its conductance faster.
Name the cells whose membranes make up the myelin sheath around some types of axon.
Schwann cells.
Squids are ectothermic animals. This means that its body temperature fluctuates with the temperature of the water in which it lives. Suggest how this might affect the speed at which action potentials are conducted along a squid axon.
1. Temperature affects the speed of conductance of action potentials.
2. The higher the temperature, the faster the conductance.
3. The conductance of action potentials in the squid will change as the environmental temperature changes.
4. It will react more slowly at lower temperatures.
Explain how a presynaptic neurone is adapted for the manufacture of neurotransmitter.
It possess many mitochondria and large amounts of endoplasmic reticulum.
Explain how the postsynaptic neurone is adapted to receive the neurotransmitter.
It has receptor molecules for neurotransmitters (like acetylcholine) on its membrane.
Outline the events in the transmission of information from one neurone to another across a synapse.
Neurotransmitter is released from vesicles in the presynaptic neurone into the synaptic cleft when an action potential reaches the synaptic knob.
The neurotransmitter diffuses across the synapse to receptor molecules on the postsynaptic neurone to which it binds, thereby setting up a new action potential.
If a neurone is stimulated in the middle of its axon, an action potential will pass both ways along it to the synapses at each end of the neurone. However, the action potential will only pass across the synapse at one end. Explain why.
Only one end can produce neurotransmitters and so this end alone can create a new action potential in the neurone on the opposite side of the synapse.
At the other end there is no neurotransmitter that can be released to pass across the synapse and so no new action potential can be set up.
When walking along a street we barely notice the background noise of traffic. However, we often respond to louder traffic noises, such as the sound of a horn.
(a) From your knowledge of summation, explain this difference.
1. The relatively quiet background noise of traffic produces a low-level frequency of action potentials in the sensory neurones from the ear.
2. The amount of neurotransmitter released into the synapse is insufficient to exceed the threshold in the postsynaptic neurone and to trigger an action potential and so the noise is 'filtered out' / ignored.
3. Louder noises create a higher frequency and the amount of neurotransmitter released is sufficient to trigger an action potential in the postsynaptic neurone and so there is a response.
4. This is an example of temporal summation.
1. OR temperal summation: Many sound receptors with a range of thresholds.
2. More receptors respond to the louder noise.
3. More neurotransmitter.
4. Response is carried out.
When walking along a street we barely notice the background noise of traffic. However, we often respond to louder traffic noises, such as the sound of a horn.
(b) Suggest an advantage in responding to high-level stimuli but not to low-level ones.
1. Reacting to low-level stimuli (background traffic noise) that present little danger can overload the central nervous system.
2. This means that organisms may fail to respond to more important stimuli.
3. High-level stimuli (sound of a horn) need a response because they are more likely to represent a danger.
Explain why hyperpolarisation reduces the likelihood of a new action potential being created.
1. As the inside of the membrane is more negative than the outside at resting potential, more sodium ions must enter in order to reach the potential difference of an action potential.
2. It is more difficult for depolarisation to occur.
3. Stimulation is less likely to reach the threshold level needed for a new action potential.
Explain why the neural pathways of reflex arcs have very few synapses.
1. Reflex arcs allow rapid responses to potentially harmful situations.
2. Information passes across synapses relatively slowly compared to the speed it passes along an axon.
3. The fewer synapses there are, the shorter the overall time taken to respond to a stimulus - an advantage where a rapid response is required.
State the name of the substance described:
They diffuse into the postsynaptic neurone where they generate an action potential.
Sodium ions
State the name of the substance described:
A neurotransmitter found in a cholinergic synapse.
Acetylcholine
State the name of the substance described:
It is released by mitochondria to enable the neurotransmitter to be reformed.
ATP
State the name of the substance described:
Their influx into the presynaptic neurone causes synaptic vesicles to release their neurotransmitter.
Calcium ions
State why it is necessary or acetycholine to be hydrolysed by acetylcholinesterase.
To recycle the choline and ethanoic acid; to prevent acetylcholine from continuously generating a new action potential in the postsynaptic neurone.
(Effects of drugs on synapses) Suggest and explain the likely effect of drugs like morphine and codeine on the body.
They will reduce pain.
They act like endorphins by binding to the receptors and therefore preventing action potentials being created in the neurones of the pain pathways.
(Effects of drugs on synapses) Suggest a way that the drug Prozac might affect serotonin within synaptic clefts. Explain how this effect makes Prozac an effective antidepressant.
Prozac might prevent the elimination of serotonin from the synaptic cleft.
Prozac increases the concentration of serotonin in the synaptic cleft. Its activity is increased, reducing depression, which is caused by reduced serotonin activity.
(Effects of drugs on synapses) Suggest and explain the likely effect of Valium
It will reduce muscle contractions (cause muscles to relax).
Valium increases the inhibitory effects of GABA so there are fewer action potentials on the nerve pathways that cause muscles to contract.
(Effects of drugs on synapses) Epilepsy can be the result of an increase in the activity of neurones in the brain due to insufficient GABA. An enzyme breaks down GABA on the postsynaptic membrane. A drug called Vigabatrin has a molecular structure similar to GABA and is used to treat epilepsy. Suggest a way in which Vigabatrin might be effective in treating epilepsy.
1. The molecular structure of Vigabatrin is similar to GABA so it may be a competitive inhibitor for the active site of the enzyme that breaks down GABA.
2. As less GABA is broken down by the enzyme, more of it is available to inhibit neurone activity.
3. Or Vigabatrin might bind to GABA receptors on the neurone membrane and mimic its action, thereby inhibiting neuronal activity.
Suggest a reason why there are numerous mitochondria in the sarcoplasm.
Muscles require lots of energy for contraction. Most of this energy is released during the Krebs cycle and electron transport chain in respiration. Both of these take place in the mitochondria.
If we cut across a myofibril at certain points, we see only thick myosin filaments. Cut at a different point we see only thin actin filaments. Yet at other points we see both types of filament. Explain why.
The actin and myosin filaments lie side by side in a myofibril and overlap at the edges where they meet. If cut where they overlap, both filaments can be seen. If cut where they do not overlap, we see one or the other filament only.
Explain how slow-twitch fibres differ from fast-twitch fibres in the way they function.
Slow-twitch fibres contract more slowly and provide less powerful contractions over a longer period.
Fast-twitch fibres contract more rapidly and produce powerful contractions but only for a short duration.
Describe how each type of fibre (slow-twitch and fast-twitch) is adapted to its functions.
Slow-twitch fibres have: myoglobin to store oxygen.
Lots of glycogen to provide a source of metabolic energy.
A rich supply of blood vessels to deliver glucose and oxygen. Numerous mitochondria to produce ATP.
Fast-twitch fibres have thicker and more numerous myosin filaments. A high concentration of enzymes involved in anaerobic respiration.
A store of phosphocreatine to rapidly generate ATP from ADP in anaerobic conditions.
Explain how the shape of the myosin molecule is adapted to its role in muscle contraction.
Myosin is made of two proteins.
The fibrous protein is long and thin in shape, which enables it to combine with others to form a long thick filament along which the actin filament can move.
The globular protein forms two bulbous structures (the head) at the end of a filament (the tail). This shape allows it to exactly fit recesses in the actin molecule, to which it can become attached. Its shape also means it can be moved at an angle. This allows it to change its angle when attached to actin and so move it along, causing the muscle to contract.
Trained sprinters have high levels of phosphocreatine in the muscles. Explain the advantage of this.
1. Phosphocreatine stores the phosphate that is used to generate ATP from ADP in anaerobic conditions.
2. A sprinter's muscles often work so strenuously that the oxygen supply cannot meet the demand.
3. The supply of ATP from mitochondria during aerobic respiration therefore stops.
4. Sprinters with the most phosphocreatine have an advantage because ATP can be supplied to their muscles for longer, and so they perform better.
During the contraction of a muscle sarcomere, a single actin filament moves 0.8 micrometres. If the hydrolysis of a single ATP molecule provides enough energy to move an actin filament 40 nm, calculate how many ATP molecules are needed to move the actin filament 0.8 micrometres.
A single ATP molecule is enough to move an actin filament a distance of 40 nm.
Total distance moved by actin filament = 0.8 micrometres = 800 nm.
Number of ATP molecules required = 800 / 40 = 20.
Dead cells can no longer produce ATP. Soon after death, muscles contract, making the body stiff - a state known as rigor mortis. From your knowledge of muscle contraction, explain the reasons why rigor mortis occurs after death.
One role of ATP in muscle contraction is to attach to the myosin heads, causing them to detach from the actin filament and making the muscle relax. As no ATP is produced after death, there is none to attach to the myosin, which therefore remains attached to the actin, leaving the muscle in a contracted state, i.e. rigor mortis.
Explain what causes the change in potential difference during depolarisation.
1. A stimulus causes sodium ion channels in the neurone cell membrane to open.
2. Sodium ions diffuse into the cell, so the membrane becomes depolarised.
Suggest why a potential difference of -45 mV is significant for a postsynaptic membrane.
It is the threshold that needs to be reached for an action potential to fire.
Explain how an action potential is created via temporal summation in the graph (pg.141)
1. Before an action potential is fired, the potential difference across the membrane increases three times in quick succession.
2. Increases in potential difference are caused by nerve impulses arriving at the synapse and releasing neurotransmitters, which cause sodium ion channels to open on the postsynaptic membrane.
3. This allows an influx of sodium ions into the postsynaptic membrane, which increases the potential difference across the membrane.
4. It was not until the arrival of a third impulse that enough neurotransmitter acts on the membrane to allow the threshold level to be reached and the action potential to be fired.
Myasthenia gravis is a disease in which the body's immune system gradually destroys receptors at neuromuscular junctions. This leads to weaker muscular responses than normal. Explain why.
1. There will be fewer receptors for acetylcholine to bind to, so fewer sodium ion channels will open at neuromuscular junctions.
2. So less likely that action potentials will be generated in the muscle cells.
Galantamine is a drug that inhibits the enzyme acetylcholinesterase (AChE). Predict the effect of Galantamine at a neuromuscular junction and explain your answer.
1. Galantamine would stop acetylcholinesterase breaking down acetylcholine.
2. There would be more acetylcholine in the synaptic cleft and it would be there for longer.
3. This means more nicotinic cholinergic receptors would be stimulated.
Describe how the lengths of the different bands in a myofibril change during muscle contraction.
The A-bands stay the same length during contraction.
The I-bands get shorter.
Rigor mortis is the stiffening of muscles in the body after death. It happens when ATP reserves are exhausted. Explain why a lack of ATP leads to muscles being unable to relax.
1. Muscles need ATP to relax because ATP provides the energy to break the actin-myosin cross bridges.
2. If the cross bridges can't be broken, the myosin heads will remain attached to the actin filaments.
3. The actin filaments can't slide back to their relaxed position so the muscle stays contracted.
Bepridil is a drug that blocks calcium ion channels. Describe and explain the effect this drug will have on muscle contraction.
1. The muscles won't contract because calcium ions won't be released into the sarcoplasm.
2. Tropomyosin will continue to block the actin-myosin binding sites.
3. No actin-myosin cross bridges can be formed.
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