Topic 8 · Grey Matter — Edexcel A Level Biology A (SNAB) 9BI0 Revision Notes & Topical Questions

Section 1 of 37Coordination of response

1Why organisms respond

• Why organisms respond to find favourable conditions, find food and avoid harm such as predators or high blood glucose.
  • (avoiding places too hot or cold)

2Pathway

• Pathway a stimulus is detected by specialised receptor cells.
  • (a change in the environment)

3

Receptors lie in sense organs such as the nose and eyes, and inside the body (e.g. pressure receptors in blood vessels).

• They send signals by the nervous or hormonal system to coordination centres in the brain or spinal cord.
• Signals then go to effectors, which are muscles or glands.

4Effector examples

• Effector examples an arm muscle contracts to move the hand from a hot surface;
  • the pancreas secretes insulin in response to high blood sugar.

Section 2 of 37The nervous system

1Structure

• Structure the central nervous system (CNS) is the brain and spinal cord;
  • the peripheral nervous system (PNS) is all the nerves.

2Signals

• Signals electrical impulses pass along neurones; a bundle of neurones is a nerve.

3

Types include sensory, relay and motor neurones.

• Nerves connect receptors to the CNS and the CNS to effectors;
  • the CNS coordinates impulses to and from any part of the body.

4Pathway

• Pathway stimulus → receptor → sensory neurone → CNS → motor neurone → effector.

• Example
  • touching a hot surface; the arm muscle contracts to pull the hand away.

Section 3 of 37The hormonal system

1Hormones

• Hormones chemical messengers made by endocrine glands and carried in the blood.

2

Endocrine glands secrete hormones directly into the blood and may be stimulated by another hormone or a nerve impulse.

• Hormones leave the blood and bind specific receptors on the cell surface membranes of target organs, changing their activity.
• They act more slowly than nerve impulses, so they control functions that do not need an instant response.

3Pathway

• Pathway stimulus → receptor → hormone → effector.

4

Example: high blood sugar → pancreas cells → insulin → liver cells, which convert glucose to glycogen.

Feature	Nervous control	Hormonal control
Transmission	Electrical impulses along neurones	Chemicals in the blood
Speed	Fast	Slower
Duration	Short-lived	Longer-lasting
Target	Specific effectors	Specific target organs with receptors

Section 4 of 37Neurone structure and types

Neurone structure and types

Common features

• Common features a long axon, a cell body containing the nucleus,
  • and an axon terminal with many nerve endings that connect to and receive impulses from other neurones.

Myelinated neurones

• Myelinated neurones the axon is insulated by a fatty myelin sheath made of Schwann cells.

Uninsulated gaps between Schwann cells are the nodes of Ranvier.

• Impulses jump from node to node, which speeds up transmission.
• Non-myelinated axons are not insulated and impulses travel more slowly along the entire length.

Neurone	Function	Structure
Sensory	Carries impulses from receptors to the CNS	Cell body branches off the middle of the axon; dendrites attach to a receptor cell; the dendron links the receptor-end terminal to the cell body, and the axon links the cell body to the CNS
Relay	Lies entirely within the CNS and connects sensory and motor neurones	Short neurone with axon and highly branched dendrites
Motor	Carries impulses from the CNS to effector muscles or glands	Large cell body in the spinal cord or brain with many highly branched dendrites for connections with other neurones’ axon terminals

Section 5 of 37Response to a stimulus: the pupil reflex

1Pathway

• Pathway stimulus → receptor → sensory neurone → CNS → motor neurone → effector.

2Pupil diameter

• Pupil diameter controls how much light reaches the retina using two antagonistic sets of iris muscles.

3

Circular muscles contract to constrict the pupil.

• Radial muscles contract to dilate it.
• When one set contracts the other relaxes.

4Bright light

• Bright light receptors → sensory neurone → CNS → motor neurone → circular muscles contract;
  • the pupil constricts, limiting light and protecting the retina.

5Low light

• Low light the same route ends with radial muscles contracting;
  • the pupil dilates to let in the maximum light and improve vision.

Section 6 of 37Resting potential

Nerve impulse

• Nerve impulse not an electrical current like a wire,
• but a momentary reversal of the potential difference across the axon cell surface membrane.
  • (membrane potential or voltage)

Resting potential

• Resting potential in a resting axon the inside is negative compared with the outside, usually about −70 mV, so the membrane is polarised.

Two factors set it up —

Sodium-potassium pumps (carrier proteins) use ATP to pump sodium ions out and potassium ions in, 3 Na⁺ out for every 2 K⁺ in, building concentration gradients for both ions.

• Membrane permeability differssodium and potassium channels let ions diffuse back by facilitated diffusion,
  • but the membrane is less permeable to sodium,
  • so potassium leaves faster than sodium enters.

Result

• Result more positive ions outside than inside, giving the negative inside of about −70 mV.

Some potassium channels stay open at rest; voltage gated channels are closed at rest.

Section 7 of 37Generating an action potential

• Depolarisation
  • reversal of the potential difference, from about −70 mV to about +30 mV;
    • an action potential is produced when a neurone is stimulated.

Generating an action potential

A stimulus opens a small number of sodium channels, so sodium ions diffuse in down their gradient and the inside becomes less negative.

If the potential reaches about −55 mV (the threshold potential), voltage gated sodium channels open and many more sodium ions flood in.

The membrane charge reverses to about +30 mV; the membrane is depolarised and an action potential has been generated.

• Threshold
  • an action potential starts only if the threshold potential is reached.

Section 8 of 37Repolarisation and the refractory period

1

The voltage gated sodium channels close.

2

Voltage gated potassium channels open, so potassium ions diffuse out down their gradient (the sodium-potassium pumps keep working).

3

The inside becomes negative again: repolarisation.

4

There is a brief period more negative than the resting potential: hyperpolarisation.

5

The potassium channels close and the pumps restore resting potential before the membrane can be stimulated again.

Refractory period

• Refractory period while hyperpolarised the membrane is unresponsive, so a new action potential cannot form.

Importance

• Importance it makes action potentials discrete events and ensures impulses travel in one direction.

Section 9 of 37Transmission along the axon and the all-or-nothing principle

Propagation

• Propagation depolarisation at one site makes sodium ions diffuse along the cytoplasm into the next section, depolarising it and opening voltage gated sodium channels there.

This repeats along the axon as a wave of depolarisation.

• Sodium ions that diffuse backwards cannot start a new action potential because that region is hyperpolarised.

All-or-nothing principle

• All-or-nothing principle action potentials are either generated or not; there are no small or large ones.

A weak stimulus opens few sodium channels and the threshold is not reached.

• A strong enough stimulus gives a full action potential.

Coding stimulus size

• Coding stimulus size a stronger stimulus raises the frequency of action potentials;
  • a small stimulus may give one, a large one several in a row.

Section 10 of 37Myelination and saltatory conduction

Unmyelinated axons

• Unmyelinated axons conduction is slow because depolarisation must occur along the whole membrane.

Myelinated axons

• Myelinated axons myelin insulates, blocking ion diffusion, so action potentials occur only at the nodes of Ranvier.

Sodium ions diffusing in local currents (circuits) depolarise the next node.

• The action potential appears to jump from node to node: saltatory conduction.
• This is much faster than in an unmyelinated axon of the same diameter.

Preventing transmission

• Preventing transmission painkillers and anaesthetics can bind sodium channels so they cannot open.

No sodium influx means no depolarisation, so no action potential is generated.

Section 11 of 37Synapse structure and transmission

Synapse structure and transmission

Location

• Location junctions between cells in the nervous system, e.g. between sensory receptor cells and sensory neurones,
  • and between motor neurones and muscle fibres.

Structure

• Structure the synaptic cleft is the gap; the presynaptic neurone has a rounded synaptic knob containing vesicles of neurotransmitter; the next cell is postsynaptic.
  • (e.g. acetylcholine)

1

An action potential arrives and depolarises the presynaptic membrane, opening voltage gated calcium channels.

2

Calcium ions diffuse into the synaptic knob.

3

Calcium makes vesicles move to and fuse with the presynaptic membrane, releasing neurotransmitter (e.g. ACh) by exocytosis.

4

Neurotransmitter diffuses across the cleft and binds receptors on the postsynaptic membrane, opening sodium channels so sodium diffuses in.

5

If enough sodium enters to reach threshold, an action potential travels down the postsynaptic axon.

6

The neurotransmitter is broken down (acetylcholine by acetylcholinesterase) to stop continued stimulation.

• More action potentials
  • more neurotransmitter released, more sodium channels open, a larger sodium influx and a greater chance of reaching threshold.

Section 12 of 37Roles of synapses

One-way transmission

• One-way transmission neurotransmitter is released on one side and receptors are on the other, so chemical transmission cannot go backwards.

Divergence

• Divergence one presynaptic neurone can connect to several others, sending signals in many directions.

Summation

• Summation a single impulse may release too little ACh, open too few sodium channels and not reach threshold, so effects are added.

Synaptic convergence: several presynaptic neurones meet one postsynaptic neurone.

• Temporal summationmany action potentials arrive in quick succession at one knob.

Section 13 of 37Detection of light

Detection of light

Eye structure

• Eye structure light enters through the pupil and is focused onto the retina’s fovea; iris muscles control the amount of light,
  • and the lens shape is changed by ciliary muscles attached by suspensory ligaments to focus objects at different distances.

Photoreceptors

• Photoreceptors the fovea contains many; the retina has two kinds.

Optic nerve

• Optic nerve carries action potentials to the brain and leaves at the blind spot, which has no photoreceptors.

Feature	Rod cells	Cone cells
Location	Mainly the outer retina	Mostly grouped in the fovea
Sensitivity	Light intensity (presence and brightness)	Wavelength of visible light (colour)
Image	Black and white	Colour; red-, green- or blue-sensitive types, and the mix stimulated decides the colour seen

Section 14 of 37How rod cells generate impulses

1

Pigment

• Pigment rod cells contain rhodopsin, which breaks into retinal and opsin in light (bleaching);
  • this causes a chemical change in the photoreceptor.

2

Pathway

• Pathway information goes from rods and cones to the optic nerve by bipolar neurones.
  • (ganglion cells are not needed)

3

In the dark —

4

Sodium ions are pumped out of the rod, then diffuse back through sodium (cation) channels.

• The rod is depolarised (the inside is only slightly negative) and releases an inhibitory neurotransmitter onto the bipolar neurone.
• The bipolar neurone is inhibited and no impulse goes to the optic nerve.

5

In the light —

6

Rhodopsin bleaches and the sodium channels close, so sodium cannot return while pumping continues.

• The inside becomes more negative than −70 mV: the rod is hyperpolarised.
• It stops releasing inhibitory neurotransmitter, so an action potential is generated in the bipolar neurone and sent to the optic nerve.

7

Summary

• Summary rod membranes are depolarised in the dark and hyperpolarised in the light.

Section 15 of 37Plant responses and tropisms

Why respond

• Why respond growing towards light raises photosynthesis, harmful or foul-tasting chemicals deter herbivores,
  • and roots growing toward water increase water uptake.

Stimuli

• Stimuli light, gravity, physical objects, herbivory, water and touch.

Tropism

• Tropism a directional growth response;
  • phototropism is a response to light and geotropism (gravitropism) to gravity.

Positive tropisms grow towards a stimulus; negative tropisms grow away, e.g. negative geotropism is upward growth.

• A seedling bends towards light because there is more growth on the shaded side.

Section 16 of 37Plant growth factors

Plant hormones

• Plant hormones chemical messengers (growth factors) made in growing parts and moved to other tissues to regulate cell growth in response to a directional stimulus.

Auxin

• Auxin stimulates cell elongation in shoots and inhibits growth in roots.

Others and their roles —

Gibberellins: stem elongation, flowering, seed germination.

• Cytokininscell growth and division.
• Abscisic acidleaf loss and seed dormancy.
• Ethenefruit ripening and flowering.

Section 17 of 37IAA in shoots and roots

IAA (indoleacetic acid)

• IAA (indoleacetic acid) a type of auxin; it probably acts by altering transcription of genes for cell growth.

It is made in growing parts and redistributed by diffusion and active transport between cells, and over longer distances in the phloem.

• Uneven distribution gives uneven growth.

Shoots (phototropism) —

A higher IAA concentration increases cell elongation.

• Light from one side moves IAA to the shaded side, giving a gradient with more on the shaded side.
• Faster elongation there bends the shoot towards the light.

Roots (geotropism) —

IAA moves to the lower side of the root, where high concentration inhibits elongation (the opposite of its effect in shoots).

• The lower side grows more slowly than the upper, so the root bends downwards.
• The role of amyloplasts in sensing gravity is not required.

Section 18 of 37Phytochrome and flowering

1

Night length

• Night length controls flowering; nights are short in spring and summer and long in autumn and winter,
  • and some plants flower with short nights, some with long.

2

At a certain night length, genes controlling flowering are switched on or off; expressed genes make their polypeptides.

• Plants detect night length through the forms of the pigment phytochrome in the leaf.

3

Two forms —

4

P_R is inactive and absorbs red light (660 nm).

• P_FR is active and absorbs far-red light (730 nm).
• P_R absorbing red light becomes P_FR;
  • P_FR absorbing far-red light returns to P_R, and in the dark unstable P_FR slowly reverts to P_R.

5

Day and night —

6

In the day sunlight has more 660 nm than 730 nm light, so P_R converts to P_FR faster and P_FR rises.

• At night no red light is available and P_R levels rise as P_FR reverts slowly.

7

Long day plants

• Long day plants flower when nights are short (summer).

8

Long days convert P_R to P_FR faster than the reverse, so high levels of P_FR activate flowering genes.

• The gene is transcribed and translated and the protein causes flowers instead of stems and leaves.

Section 19 of 37Brain regions and their functions

Brain regions and their functions

The brain

• The brain with the spinal cord it forms the CNS and is made of billions of interconnected neurones, with different regions for different functions.

Cerebrum

• Cerebrum the largest part controlling conscious activities such as vision, hearing, speech, thinking and memory.
  • (about 80% of the mass)

It has two cerebral hemispheres joined by the corpus callosum; the right controls the left side of the body and the left the right.

• The cerebral cortex (grey matter) is a thin, highly folded outer layer of neurone cell bodies;
  • folding increases surface area for more neurones and connections, enabling more complex behaviour.
• White matter below the cortex consists of myelinated axons.

Hypothalamus

• Hypothalamus monitors blood and releases hormones or stimulates the pituitary; it works in homeostasis.

Regulates body temperature.

• Osmoregulationmonitors blood water balance and releases ADH if the blood is too concentrated, which increases water absorption in the kidneys.
• Regulates digestive activity, appetite hormones and enzyme secretion.
• Controls endocrine functions by making the pituitary release hormones for metabolism, growth, puberty, sexual functions, sleep and mood.

Cerebellum

• Cerebellum coordinates movement, including balance, which needs eyes, semicircular canals and many muscles.

Medulla oblongata

• Medulla oblongata has coordination centres: the cardiac centre controls heart rate and the respiratory centre controls breathing rate.

Section 20 of 37Studying the brain: CT and MRI

Studying the brain: CT and MRI

The difficulty

• The difficulty the brain is complex and delicate and its regions work together, so it is hard to study;
  • scanners avoid surgery.

CT (computerised tomography)

• CT (computerised tomography) x-rays aimed from all angles give cross-section images.

Detectors pick up x-rays leaving the body; dense tissue absorbs more and appears lighter.

• Shows structure and damage;
  • blood is less dense than brain tissue so CT locates bleeding and damaged vessels after a stroke.
• It does not show function directly, but linking symptoms to damage locations shows which regions control what.
• Not recommended for pregnant women or children because of higher radiation than a normal x-ray, though the risk is very low.

MRI (magnetic resonance imaging)

• MRI (magnetic resonance imaging) a magnetic field and radio waves produce images;
  • the patient lies still in a large magnet.

Soft tissue is clear and resolution is higher than CT; it is especially useful for finding tumours.

• Function is again deduced only by linking damage to symptoms.
• It is more expensive than CT but uses no x-rays, and is often chosen for long-term therapies.
• The magnet interferes with pacemakers and insulin pumps, so such patients cannot be scanned.

Section 21 of 37Studying the brain: fMRI and PET

Studying the brain: fMRI and PET

fMRI (functional MRI)

• fMRI (functional MRI) uses the same method but studies function in real time.

It measures the ratio of oxygenated to deoxygenated haemoglobin to show active regions.

• Patients do actions, answer questions or think about a topic and the active region lights up.
• Usesfinding the cause of seizures and psychology research.

PET (positron emission tomography)

• PET (positron emission tomography) radioactive tracers collect where blood flow, metabolism or neurotransmitter activity is high.

The tracer is given before the scan, e.g. radioactively labelled glucose, which accumulates in metabolically active brain areas.

• Areas of high radioactivity show tracer movement and accumulation, indicating whether a region is active.
• It can show reduced activity in regions in Alzheimer’s disease.

Summary

• Summary some scans show only structure (CT, MRI) while others show structure and function in real time (fMRI, PET).

Section 22 of 37Development of the visual cortex

1Visual cortex

• Visual cortex the part of the cerebral cortex that processes visual information.
  • (at the back of the brain)

2Critical period

• Critical period soon after birth in baby mammals the neurones in the visual cortex form synapses;
  • both eyes must be stimulated for correct organisation.

3

Synapses that pass nerve impulses during this period are strengthened and become permanent.

• Synapses that receive no impulses are lost and cannot be re-formed.
• Lack of visual stimulation can cause blindness in one or both eyes.

4Evidence

• Hubel and Wiesel’s animal model studies (below).

Section 23 of 37Animal models and the work of Hubel and Wiesel

1Why animal models

• Why animal models the human brain is delicate and complex,
• so surgery risks damage; some animals have a similar brain structure,
• so findings apply to humans, and animal experiments are widely thought more ethically acceptable than human ones.

2

A scientific model represents real events, e.g. computer models of global warming, balls for particles, scaled-down vehicles for safety testing.

3Hubel and Wiesel (1960s–70s)

• Hubel and Wiesel (1960s–70s) studied the long-term effect of depriving one eye of vision.

4

Kittens had one eye stitched shut soon after birth; after 3 months they were blind in that eye.

• Electrodes showed that ocular dominance columns for the closed eye were smaller and those of the open eye larger than normal, i.e. they switched dominance.
• Ocular dominance columns are stripes of neurones that receive input from one eye only (right or left).
• Adult cats given 3 months of deprivation were not blinded and their columns did not change.
• The results were repeated in young and adult monkeys, showing that light stimulation in early development is essential.

• Ethics
  • animal research allows testing of new medicines and study of anatomy and physiology without risk to humans,
  • but it raises welfare and suffering concerns that must be weighed against the benefits.

Section 24 of 37Habituation

Habituation

Why animals ignore stimuli

• Why animals ignore stimuli detecting and responding requires energy, so animals conserve energy for survival.

Habituation

• Habituation learning not to respond to a repeated stimulus that has no negative outcome.

Examples: humans no longer noticing a smell or sound, wild animals losing fear of humans after harmless contact, animals ignoring non-predatory species.

• If the stimulus changes (e.g. a constant sound gets louder) the nervous system responds again.

Mechanism

• Mechanism changed synaptic transmission.

Fewer calcium ions enter the presynaptic neurone when an impulse arrives.

• Less neurotransmitter is released.
• Fewer sodium channels open on the postsynaptic membrane and less sodium enters, so the inside stays negative.
• Threshold is not reached, no impulse reaches the effector and there is no response.

Section 25 of 37Practical: investigating habituation in snails

Principle

• Principle snails withdraw into their shell after a touch;
  • as they become habituated, re-emergence time gets shorter.

Apparatus

• Apparatus a snail, a soft object and a stopwatch.
  • (damp cotton bud or blade of grass)

1

Place a snail on a clean flat surface (the same surface throughout, with constant humidity because snails withdraw in dry conditions) and let it emerge.

2

Gently brush the snail’s head with the damp cotton bud or grass; it should withdraw.

3

Start the stopwatch and time how long until it re-emerges and fully extends its eye-stalks (the same end-point every time).

4

Repeat 10–15 times, recording the time each trial, using the same object and touch location.

Expected result

• Expected result a graph showing re-emergence time gradually falling.

Welfare

• Welfare handle snails gently and quickly, avoid heat and dry conditions,
  • and return them to a suitable habitat,
  • or the exact place they were collected from.

Section 26 of 37Parkinson’s disease

Parkinson’s disease

Neurotransmitter imbalance

• Neurotransmitter imbalance some disorders are linked to imbalances of neurotransmitters such as dopamine (Parkinson’s) and serotonin (depression).

Parkinson’s disease

• Parkinson’s disease a movement disorder caused by loss of neurones in parts of the brain.

Symptoms: tremor, slow movement, stiff and inflexible muscles, balance problems and speech changes.

• The lost neurones normally make dopamine, which is involved in muscle control.
• Less dopamine in the synaptic cleft means less binds postsynaptic receptors, fewer sodium channels open, the postsynaptic neurone does not depolarise,
  • and fewer action potentials cause the symptoms.

Treatments —

Dopamine agonists produce the same effect as dopamine by binding and activating dopamine receptors,

• or are chemicals that can be converted to dopamine in neurones, e.g. L-dopa.
• Enzyme inhibitorsMAOB inhibitors block enzymes that break down dopamine in the synaptic cleft, raising dopamine levels.

Future treatments —

Gene therapy: adding genes to affected brain cells to increase dopamine production or protect dopamine-producing cells.

• Stem cell therapyreplacing lost dopamine-producing cells.

Section 27 of 37Depression

Serotonin

• Serotonin low levels are linked to depression because serotonin carries impulses through brain areas that control mood and low levels increase episodes.

Other chemicals

• Other chemicals noradrenaline and dopamine are also linked.

Antidepressants

• Antidepressants drugs that raise levels of relevant neurotransmitters.

SSRIs (selective serotonin reuptake inhibitors) prevent uptake of serotonin at synapses, raising its overall level.

• TCAs (tricyclic antidepressants) raise both serotonin and noradrenaline.
• MAOB inhibitors block enzymes that break down neurotransmitters in the synaptic clefts.

Section 28 of 37Action of drugs on synapses

Effect	How drugs achieve it
Increase transmission	Cause more neurotransmitter to be made in the synaptic knob; cause more to be released at the presynaptic membrane; imitate the neurotransmitter by binding and activating postsynaptic receptors; prevent enzymes breaking it down; prevent reuptake by the presynaptic cell
Decrease transmission	Prevent neurotransmitter production in the knob; prevent its release; let it leak gradually out of the knob where enzymes destroy it, leaving little when an action potential arrives; bind postsynaptic receptors and block neurotransmitter binding

• Context
  • prescription drugs can help neurological disorders, while recreational drugs can damage the nervous system or even kill.

Section 29 of 37Examples: MDMA and L-dopa

MDMA (ecstasy)

• MDMA (ecstasy) a recreational drug whose use and sale are criminal offences in most places;
  • it affects several neurotransmitters, mainly serotonin.

It binds the reuptake proteins on the presynaptic membrane, inhibiting serotonin reuptake (serotonin is normally recycled),

• so more stays in the brain.
• It also triggers release of further serotonin from presynaptic neurones.
• Serotonin affects mood, anxiety and sleep;
  • users may feel extreme euphoria and heightened touch and bodily sensation.

L-dopa

• L-dopa a drug for Parkinson’s disease with a structure very like dopamine.

It is converted to dopamine in a reaction catalysed by dopa-decarboxylase, raising dopamine levels.

• Dopamine itself cannot be given because it cannot cross the blood-brain barrier.
• More impulses in movement-control brain areas give better control and lessen symptoms.

Section 30 of 37Personalised medicine

Definition

• Definition development of targeted drugs for diseases in individuals with different genotypes.

Drugs can be tested on synthetic tissues, groups of lab-cultured cells genetically identical to certain patients.

Genomics

• Genomics information from the Human Genome Project, stored in databases of gene and protein sequences, is used for genomic medicine.
  • (sequencing the whole human genome)

Knowing the sequence and structure of disease proteins allows drugs that target them, e.g. an enzyme inhibitor for a disease-causing enzyme.

• Genome data combined with clinical data shows patterns that indicate an individual’s disease risk.

Genetic screening

• Genetic screening identifies people at high risk so preventive steps can be taken.

Known mutations raise breast cancer risk, so carriers can have surgery in advance.

• People may choose diet and lifestyle based on genetic risks of cancer and heart disease.

Treatment choice

• Treatment choice doctors can use an individual’s genome to predict how well they will respond to specific treatments.

Personalised medicine

Social, moral and ethical issues

• Social, moral and ethical issues higher research costs may raise prices, so only wealthier people may get access.

Discrimination

• Discrimination insurers and employers might use genetic data unfairly, e.g. raising insurance costs for certain variants.

Refusal

• Refusal patients may be denied treatment predicted to be less effective, even with no alternatives,
  • which can be distressing for them and their families.

Section 31 of 37Producing drugs using GMOs: micro-organisms

Genetic engineering

• Genetic engineering deliberately modifying a characteristic by removing a gene for the desired trait from one organism and transferring it to another where it is expressed.

The organism has recombinant DNA and is a genetically modified organism (GMO).

• Micro-organisms, plants and animals have been engineered to make medical proteins.

1

Restriction enzymes cut out the gene for the desired protein (e.g. insulin) from the genome.

2

Many copies are made by PCR, in which DNA polymerase joins free nucleotides into new complementary strands.

3

The copies are inserted into plasmids (small loops of DNA), which act as DNA vectors; DNA ligase joins the gene to the plasmid.

4

The plasmids carry the gene into micro-organisms.

5

The GM micro-organisms grow in large fermenters with nutrients and make large quantities of the protein.

6

The protein is isolated, purified, packaged and distributed.

• Examples
  • human insulin and human blood clotting factors made by genetically modified bacteria.

Section 32 of 37Producing drugs using GMOs: plants and animals

Plants

• Plants a gene is put into a plasmid, then into a bacterium, which infects plant cells and acts as the vector.

An alternative is a gene gun, firing tiny pellets coated with DNA into plant cells.

• The gene moves into the plant cell nucleus and the cell is stimulated to grow into an adult plant, every cell of which carries the gene.
• Exampleshuman insulin and a cholera vaccine produced by modified plants.

Animals

• Animals the gene is injected into the nucleus of a zygote,
• which is implanted into a surrogate mother and develops into an adult in which every cell has the gene.

The protein can be purified from, e.g., the animal’s milk; human blood clotting proteins are produced this way.

Risks and benefits

• GMOs can be medically beneficial,
  • (reliable supply of human proteins, large quantities)
• but there are concerns about the effects of changing genes and the ethics of modifying animals, especially for crop plants eaten by humans.

Section 33 of 37Nature versus nurture in brain development

1Brain development

• Brain development growth of the brain and formation of connections, measured by brain size, number of neurones and functional level.
  • (neural pathways)

2Nature and nurture

• Nature and nurture development is influenced by genetic (nature) and environmental (nurture) factors, which interact and are hard to separate.

3

One factor would have to be removed completely to study the other, which is almost impossible, and many genes and environmental factors exist.

Section 34 of 37Methods for investigating nature and nurture

Method	Approach	What the results suggest
Animal experiments	Vary the environment of the same species (similar genes), or switch off a gene and raise altered and unaltered animals in similar environments (acceptable in mice, not humans)	Differences are due to the environment in the first case and to genes in the second
Identical twins raised apart	Genetically identical, different environments	Differences are nurture; similarities are nature, e.g. very similar IQ scores imply nature matters in intelligence
Twins raised together	Similar environments, so hard to separate effects; non-identical twins act as a control	Traits more common in identical than non-identical twins are largely genetic; traits showing little difference are largely environmental
Cross-cultural studies	Compare large groups of children of the same age from different cultures	Differences are more likely nurture and similarities nature
Newborn studies	Newborns have not been shaped by the outside environment	Basic abilities (crying, feeding, recognising faces) suggest nature; lack of speech suggests nurture matters
Brain damage studies	Compare a trait in children with and without brain damage in the relevant area	Development despite damage suggests nurture; no development suggests nature. Children with damage to language areas were delayed but caught up by age 5, suggesting nurture matters in language

Section 35 of 37Worked examples

1. Describe how the resting potential of an axon is maintained. [4]4 marks

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2. Explain how the myelin sheath increases the speed of conduction. [3]3 marks

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3. Describe the sequence of events at a cholinergic synapse after an action potential arrives. [5]5 marks

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4. Explain why rod cells send an impulse when light falls on them, although they are inhibitory in the dark. [4]4 marks

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5. Explain how IAA causes a shoot to bend towards light. [3]3 marks

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6. Compare CT and MRI scans. [3]3 marks

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Section 36 of 37Key terms

Term	Meaning
Resting potential	Potential difference across an unstimulated axon membrane, about −70 mV.
Threshold potential	Membrane potential, about −55 mV, that triggers an action potential.
Saltatory conduction	Jumping of the action potential between nodes of Ranvier.
Neurotransmitter	Chemical that carries an impulse across a synapse, e.g. acetylcholine.
Summation	Adding effects of impulses to reach threshold at a synapse.
Tropism	Directional growth response to a stimulus.
Phytochrome	Pigment existing as PR and PFR that detects night length.
Habituation	Learning to ignore a repeated harmless stimulus.
Recombinant DNA	DNA containing a gene transferred from another organism.
Personalised medicine	Treatment matched to an individual’s genotype.

Section 37 of 37Exam technique

1

Describing a nerve impulse as an electric current flowing like in a wire — it is a wave of changing membrane potential.

2

Thinking a stronger stimulus gives a bigger action potential — it raises the frequency, since action potentials are all-or-nothing.

3

Saying PFR is the inactive form of phytochrome — PR is inactive and PFR is active.

4

Saying IAA stimulates elongation in roots — it inhibits it, unlike in shoots.

5

Confusing MRI (structure) with fMRI (function in real time) and PET (tracer activity).