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Exampro A-level Biology (2410)

BIOL 5.2

Name:

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Time: 186

Marks: 159

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Q1.  The diagram shows the change in the charge across the surface membrane of a non-myelinated axon when an action potential is produced. 

(a) Describe how the change shown in the diagram occurs when an action potential isproduced. 

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(b) Explain what causes the conduction of impulses along a non-myelinated axon to be slowerthan along a myelinated axon. 

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(Total 5 marks)

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Q2.  When a finger accidentally touches a hot object, a reflex action occurs. The biceps musclecontracts, causing the arm to be flexed and the finger is pulled away. The diagram shows thearrangement of the bones in the arm, the muscles used for flexing and straightening the arm andthe nervous pathways associated with the contraction of these muscles.

(a) Explain the importance of reflex actions. 

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(b) (i) Describe the sequence of events which allows information to pass from one neuroneto the next neurone across a cholinergic synapse. 

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(ii) Give two differences between a cholinergic synapse and a neuromuscular junction. 

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(Total 11 marks)

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Q3.  Acetylcholine is a neurotransmitter which binds to postsynaptic membranes and stimulatesthe production of nerve impulses. GABA is another neurotransmitter. It is produced by certainneurones in the brain and spinal cord. GABA binds to postsynaptic membranes and inhibits theproduction of nerve impulses. The diagram shows a synapse involving three neurones. 

(a) Describe the sequence of events leading to the release of acetylcholine and its binding to

the postsynaptic membrane. 

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(b) The binding of GABA to receptors on postsynaptic membranes causes negatively chargedchloride ions to enter postsynaptic neurones. Explain how this will inhibit transmission ofnerve impulses by postsynaptic neurones. 

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(c) Epilepsy may result when there is increased neuronal activity in the brain. 

(i) One form of epilepsy is due to insufficient GABA. GABA is broken down on thepostsynaptic membrane by the enzyme GABA transaminase. Vigabatrin is a newdrug being used to treat this form of epilepsy. The drug has a similar molecularstructure to GABA. Suggest how Vigabatrin may be effective in treating this form ofepilepsy. 

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(ii) A different form of epilepsy has been linked to an abnormality in GABA receptors.Suggest and explain how an abnormality in GABA receptors may result in epilepsy. 

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(Total 12 marks)

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Q5.  (a) Figure 1 shows part of a myofibril from skeletal muscle.

Figure 1 

(i) Describe two features, visible in the diagram, which show that the myofibril iscontracted.

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(ii) Explain the role of calcium ions and ATP in bringing about contraction of a musclefibre. 

Calcium ions ................................................................................……

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(b) Figure 2 shows the structure of a neuromuscular junction. The vesicles containacetylcholine. 

Figure 2 

(i) An action potential is generated at the cell body of the motor neurone. Explain how this action potential passes along the motor neurone to theneuromuscular junction.

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(ii) When the action potential arrives at the neuromuscular junction, it results in thesecretion of acetylcholine into the synaptic cleft. Explain how. 

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(c) Between the ages of 20 and 50, 10% of total muscle mass is lost. Between the ages of 50and 80, a further 40% of the original total muscle mass is lost. Most of the muscle lostconsists of fast fibres.

(i) Plot a graph on the grid below to show the percentage of muscle mass remainingbetween the ages of 20 and 80. Assume that the rate of muscle loss in each agerange is constant.

(3) 

(ii) Explain why explosive exercises, such as sprinting and weightlifting, will be moreaffected by this muscle loss than aerobic exercises, such as jogging.

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(Total 15 marks)

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Q6.  Secretion of neurotransmitters into a synaptic cleft may produce an action potential in apostsynaptic neurone. 

(i) Explain how the release of acetylcholine at an excitatory synapse reduces the membranepotential of the postsynaptic membrane. 

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(ii) Explain what causes transmission at a synapse to occur in only one direction. 

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(iii) GABA is a neurotransmitter which inhibits the production of action potentials. The diagram and the graph show how the release of GABA from a presynaptic membraneaffects the membrane potential of a postsynaptic membrane. 

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When the postsynaptic membrane is stimulated by acetylcholine, an action potential isless likely if GABA is released at the same time. Explain why. 

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(Total 8 marks)

Q7.  (a) The table shows the membrane potential of an axon at rest and during the differentphases of an action potential. Complete the table by writing in each box whether the

sodium ion (Na+) channels and potassium ion (K+) channels are open or closed. 

(2) 

Resting  Starting todepolarise 

Repolarising 

Membranepotential/mV 

 –70   –50   –20 

Na+ channels in 

axon membrane 

K+ channels in 

axon membrane 

(b) Describe how the resting potential is established in an axon by the movement of ionsacross the membrane.

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S  (c) Sodium and potassium ions can only cross the axon membrane through proteins.

Explain why. 

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(Total 6 marks)

Q8.  (a) Figure 1 shows the changes in membrane potential at one point on an axon when anaction potential is generated. 

Figure 1 

The changes shown in Figure 1 are due to the movement of ions across the axonmembrane. Complete the table by giving the letter (A to D) that shows where eachprocess is occurring most rapidly.

(2) 

Process  Letter 

Active transport of sodium and potassium ions 

Diffusion of sodium ions

Diffusion of potassium ions

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(b) Figure 2 shows the relationship between axon diameter, myelination and the rate ofconduction of the nerve impulse in a cat (a mammal) and a lizard (a reptile). 

Figure 2 

(i) Explain the effect of myelination on the rate of nerve impulse conduction. 

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S  (ii) For the same diameter of axon, the graph shows that the rate of conduction of thenerve impulse in myelinated neurones in the cat is faster than that in the lizard.Suggest an explanation for this. 

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Figure 3 shows how a stimulating electrode was used to change the potential difference acrossan axon membrane. Two other electrodes, P and Q, were used to record any potentialdifference produced after stimulation. The experiment was repeated six times, using a differentstimulus potential each time. In experiments 1 to 4, the stimulating voltage made the inside of theaxon less negative. In experiments 5 and 6, it made the inside of the axon more negative. 

Figure 3 

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(c) Explain the results of experiments 1 to 4. 

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(d) Figure 4 shows two neurones, X and Y, which each have a synapse with neurone Z. 

Figure 4 

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Neurone X releases acetylcholine from its presynaptic vesicles. Neurone Y releases a

different neurotransmitter substance which allows chloride ions (Cl-) to enter neurone Z .Use this information, and information from Figure 3, to explain how neurones X and Yhave an antagonistic effect on neurone Z. 

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(Total 15 marks)

Q9.  The graph shows the electrical changes measured across the plasma membrane of an axonduring the passage of a single action potential. 

(a) Explain the shape of the curve 

(i) over the range labelled A ; 

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(ii) over the range labelled B; 

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(b) Fewer action potentials occur along a myelinated axon than along an unmyelinated axon ofthe same length. Explain why. 

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(Total 5 marks)

Q10.  (a) Effectors bring about responses in the body. They are stimulated when neuronessecrete substances, called neurotransmitters, on to them.

(i) Name the type of neurone that stimulates muscles. 

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(ii) Other than muscle tissue, name one type of tissue that acts as an effector.

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(b) Substances, called hormones, can also stimulate effectors.Humans produce a large number of different hormones but only a small number ofdifferent neurotransmitters. Explain the significance of this difference. 

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(Total 5 marks)

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Q11.  During an action potential, the permeability of the cell-surface membrane of an axon

changes. The graph shows changes in permeability of the membrane to sodium ions (Na+) and

to potassium ions (K+) during a single action potential. 

(a) Explain the shape of the curve for sodium ions between 0.5 ms and 0.7ms. 

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(b) During an action potential, the membrane potential rises to +40 mV and then falls. Useinformation from the graph to explain the fall in membrane potential. 

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(c) After exercise, some ATP is used to re-establish the resting potential in axons. Explainhow the resting potential is re-established. 

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(Total 8 marks)

Q12. Essay 

You should write your essay in continuous prose. 

Your essay will be marked for its scientific accuracy.

It will also be marked for your selection of relevant material from different parts of thespecification and for the quality of your written communication. 

The maximum number of marks that can be awarded is

Write an essay on the following topic: 

A cycle is a biological pathway or process in which the end product of one cycle becomes thestarting point for the next cycle. Write an essay about cycles in biology. 

(Total 25 marks)

Scientific

Breadth of knowledge 

Relevance 

Quality of written communication 

16 

3 

3 

3 

Q13.  Different substances are involved in coordinating responses in animals. 

(a) Hormones are different from local chemical mediators such as histamine in the cells theyaffect. 

(i) Describe how hormones are different in the cells they affect. 

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(ii) Describe how hormones and local chemical mediators reach the cells they affect.

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(b) Synapses are unidirectional. Explain how acetylcholine contributes to a synapse beingunidirectional. 

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(c) Cells in the stomach wall release gastric juice after a meal. The graph shows how thevolumes of gastric juice produced by nervous stimulation and by hormonal stimulationchange after a meal. 

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(i) Describe the evidence from the graph that curve A  represents the volume of gastric juice produced by nervous stimulation. 

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(ii) Complete the table to show the percentage of gastric juice produced by nervousstimulation at the times shown.

(1) 

(Total 8 marks)

Time after meal / hours 

1  2  3 

Percentage of gastric juice produced by

nervous stimulation 

Q14.  The black mamba is a poisonous snake. Its poison contains a toxin. 

The table shows the base sequence of mRNA that codes for the first two amino acids of thistoxin. 

Complete the table to show 

(a) (i) the base sequence of the anticodon on the first tRNA molecule that would bind to this mRNA sequence

(1) 

Base sequence of anticodon on tRNA 

Base sequence of mRNA A   C  G  A   U  G 

Base sequence of DNA 

(ii) the base sequence of the DNA from which this mRNA was transcribed. (1) 

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(b) The length of the section of DNA that codes for the complete toxin is longer than themRNA used for translation. Explain why. 

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(c) A mutation in the base sequence of the DNA that codes for the toxin would change thebase sequence of the mRNA. 

Explain how a change in the base sequence of the mRNA could lead to a change in thetertiary structure of the toxin. 

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(d) The black mamba’s toxin kills prey by preventing their breathing. It does this by inhibitingthe enzyme acetylcholinesterase at neuromuscular junctions. Explain how this preventsbreathing. 

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(Total 7 marks)

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Q15. Serotonin is a neurotransmitter released in some synapses in the brain. It is transportedback out of the synaptic gap by a transport protein in the pre-synaptic membrane.

(a) Serotonin diffuses across the synaptic gap and binds to a receptor on the post-synapticmembrane.

Describe how this causes depolarisation of the post-synaptic membrane.

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(b) It is important that a neurotransmitter such as serotonin is transported back out ofsynapses. Explain why. 

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(c) Scientists investigated the effect of a drug called MDMA on movement of mice. Theymeasured the amount of movement of three groups of mice, K, L and M. 

•  Group K, mice not given MDMA. 

•  Group L, mice given MDMA. 

•  Group M, mutant mice that did not produce a serotonin receptor on their post-synaptic membranes and were given MDMA. 

The graph shows their results.

The scientists concluded that MDMA affects movement by binding to serotonin receptors. 

How do these results support this conclusion?

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(Total 7 marks)

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Q16. The release of a substance called dopamine in some areas of the brain increases thedesire to eat. 

Scientists measured increases in the release of dopamine in the brains of rats given differentconcentrations of sucrose solution to drink. 

Sucrose stimulates taste receptors on the tongue.

The graph shows their results. Each point is the result for one rat. 

(a) The scientists concluded that drinking a sucrose solution had a positive feedback effect onthe rats’ desire to eat. 

How do these data support this conclusion? 

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(b) In this investigation, the higher the concentration of sucrose in a rat’s mouth, the higher thefrequency of nerve impulses from each taste receptor to the brain. 

If rats are given very high concentrations of sucrose solution to drink, the refractory periodmakes it impossible for information about the differences in concentration to reach thebrain. Explain why. 

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(c) In humans, when the stomach starts to become full of food, receptors in the wall of thestomach are stimulated. This leads to negative feedback on the desire to eat. Suggest whythis negative feedback is important. 

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(Total 8 marks)

Q17. (a)  A myelinated axon conducts impulses faster than a non-myelinated axon. Explain this difference. 

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Doctors investigated the relationship between myelin in brain tissue and different types ofdementia. All types of dementia involve loss of mental ability. 

The doctors measured the mean amount of myelin in samples of brain tissue from:

•  a control group of 12 people without dementia 

•  20 people with vascular dementia (VaD) 

•  19 people with Alzheimer's dementia (AD) 

•  31 people with Lewy body dementia (LD). 

The doctors’ results are shown in the figure. The vertical bars show standard errors.  

Group of people 

(b) The doctors used a statistical test to compare the results for AD and LD.They obtained a value for P of 0.047. 

What does this result show about the difference between the means for AD and LD?  

Use the words probability and chance in your answer. 

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(c) A student who read this investigation concluded that there was a relationship between theamount of myelin in a person ’s brain and whether or not they had dementia. 

Do these data support this conclusion? Give reasons for your answer. 

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(Total 9 marks)

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