Edexcel Categories Archives: Topic 8: Grey Matter

8.4 Brains, the genome and medicine

8.4 Brains, the genome and medicine


Neurotransmitters in the brain

The brain contains neurones, which transmit nerve impulses to each other across synapses. Many different neurotransmitters are involved, including dopamine and serotonin.


Dopamine and Parkinson’s disease

Dopamine is a neurotransmitter secreted by neurones and is in several parts of the brain, including the midbrain. The axons of the neurones extend throughout the frontal cortex, brain stem and spinal cord. Impulses passing between neurones in this region are important for controlling muscular movement and emotional responses. Parkinson’s disease occurs when cells in the basal ganglia die, so dopamine is no longer produced, resulting in the loss of control of movement, stiffness of muscles, tremors, slowness of movement, poor balance, walking problems, depression and difficulties with speech and breathing.


Parkinson’s disease is treated using L-dopa, a precursor in the manufacture of dopamine, which enters the brain and is converted to dopamine. It is not possible to give dopamine as a drug because it cannot enter the brain. This treatment helps in the early stages of the disease but the dose must be increased as the disease progresses because the cells that convert L-dopa to dopamine gradually die. Too much L-dopa results in uncontrolled movement.


The drug selegiline slows the loss of dopamine from the brain. The drug inhibits the enzyme monoamine oxidase, responsible for breaking down dopamine in the brain.


Dopamine agonists mimic the role of dopamine, activating the dopamine receptor directly by binding to them at synapses, activating them and triggering action potentials.


Gene therapy can be used – genes for proteins that increase dopamine production and that promote the growth and survival of nerve cells are inserted into the brain.


Serotonin and depression

Serotonin is a neurotransmitter in many parts of the brain and is involved in functions including mood, appetite, temperature regulation, sensitivity to pain and sleep. Neurones secrete serotonin are in the brain stem and their axons extend into the cortex, cerebellum and spinal cord. A lack of serotonin is linked to the development of clinical depression. Symptoms include sadness, anxiety, hopelessness, loss of interest in pleasurable activities, insomnia and thoughts of death.


The causes are not completely understood and may be multifactoral:

  • There may be a genetic element – it runs in families
  • Could be environmental
  • Fewer nerve impulses than normal are transmitted around the brain, related to low levels of neurotransmitter production


Clinical depression can be treated with drugs that increase serotonin in the brain. The drug MDMA (ecstasy) acts at a serotonin synapse. It binds to a transporter protein which removes serotonin, increasing the effect of serotonin. MDMA can produce feelings of euphoria, friendliness and energy. However side effects cause depression, confusion and anxiety. Animal research shows that regular use of MDMA causes brain damage.


SSSR drugs (selective serotonin reuptake inhibitor) e.g. Prozac inhibits the uptake of serotonin from the synaptic cleft unto the presynaptic cell. This increases the level of serotonin available to bind to the postsynaptic receptor.



  • Some affect synaptic transmission
  • Some are similar shapes to neurotransmitters, so mimic their effects at receptors. These are agonists and activate more receptors
  • Some block receptors, stopping them being activated, these are agonists
  • Some inhibit the enzyme that breaks down neurotransmitters so they are in the system for longer
  • Some stimulate the release of neurotransmitters, so more receptors are activated
  • Some inhibit the release of neurotransmitters, so fewer receptors are activated


How drugs affect synaptic transmission

Ecstasy effects thinking, mood and memory and can also cause anxiety and altered perceptions. It desirable effect is feelings of emotional warmth and empathy.


  • Short term effects – changes in behaviour and brain chemistry, sweating, dry mouth, increased heart rate, fatigue, muscle spasms and hypothermia
  • Long term effects – changes in behaviour and brain structure


Ecstasy increases the concentration of serotonin in the synaptic cleft by binding to molecules in the presynaptic membrane that are responsible for transporting the serotonin back into the cytoplasm. This prevents it being removed from the synaptic cleft. Ecstasy may also cause the transporting molecules to work in reverse, further increasing the amount of serotonin outside of the cell. These higher levels of serotonin cause the mood changes.


The human genome project and drug development

The Human genome project has worked out base sequences of all the DNA (genome) in a human cell. From this, we can work out the amino acid sequences of the proteins they produce, leading to understandings of how the proteins work.  This enables researchers to develop new drugs which target specific proteins, enhancing or lessening their activity.


Not everyone responds in the same way to drugs, knowledge of difference in a person’s base sequences in genes can help us understand this. Knowledge of a particular DNA sequence will enable suitable drugs to be chosen on an individual basis.


1977 – Fred Sanger – first DNA sequencing process. DNA is used as a template to replicate a set of DNA fragments, each differing in length by one base. The fragments are separated according to size using gel electrophoresis and the base at the end of each is identified – allows the sequence of bases in the DNA chain to be determined.


However testing for genetic predisposition has implications:

  • Who should decide about the use of tests and on whom should they be used?
  • Making and keeping records of individual genotypes raises issues of confidentiality
  • Medical treatments through the development of genetic technologies will initially be very expensive
  • Restricted availability of many medical treatments will be a problem to health services in deciding who is eligible for treatment


Using genetically modified organisms to produce drugs

Genetic modification = artificial introduction of genetic material from another organism


Genes for the synthesis of particular proteins can be inserted into an organism’s DNA, so the organism expresses that gene and synthesises the protein. This involves:


  • Identifying and isolating the gene that is inserted by cutting it from DNA using restriction enzymes or by reverse engineering using the sequence of amino acids in the protein to be made and constructing a length of DNA with the appropriate base sequence to code for this protein
  • Inserting the gene into a vector such as bacterial plasmids or a virus
  • Inserting the vector into the organism


First success in genetic engineering was with bacteria:

+ Cheap and easy to culture

+ Rapid reproduction – transferred gene copied rapidly

– Prokaryotic cells do not have the correct biochemistry to make some of the more complex human proteins – so much use eukaryotes e.g. yeast, plants and animals


Bacteria contain simple DNA structures, plasmids, which can be transferred between cells. Using restriction enzymes, the circular plasmid can be cut and using other enzymes, a piece of DNA from another species can be inserted.


Example: bacteria to produce human insulin:

    1. Isolated human gene, modified if necessary
    2. Extracted plasmid is cut with restriction enzyme
    3. Isolated human gene is spliced into plasmid
    4. Modified plasmid placed back into bacterial cells
    5. Cells multiply in fermenter
    6. Bacterium produces human insulin
    7. Insulin protein extracted and purified
    8. Bacterial cells destroyed


To ensure the inserted gene is expressed, a length of DNA called a promoter (region) is inserted for RNA polymerase to begin transcription.


Examples of GMOs used for drug production:

  • Tobacco plants – produce an anti-inflammatory cytokine (interleukin-10) which may treat autoimmune diseases
  • Maize plants – produce human lipase for cystic fibrosis patients
  • Goats – produce antithrombin in their milk for blood clotting disorders


Genes can also be inserted by injecting DNA directly into the nucleus of a fertilised egg which is then implanted into a surrogate female. Retroviruses have also been used to introduce new genes into fertilised eggs. This virus incorporates its DNA into the host DNA.


Genetically modified plants

Genetic engineers introduce new genes with alleles for desired characteristics into a plant’s DNA, resulting in genetically modified plants.


    1. Plasmid carrying desired gene and an antibiotic resistance gene (marker gene) used
    2. DNA insertion of new gene of virus DNA used to incorporate genes into the plant DNA of some cells
    3. incubation in growth medium with antibiotic
    4. Micropropagation: cells grow in sterile culture medium containing sucrose, amino acids, inorganic ions and plant growth substances
    5. Plant growth substances stimulate root and shoot growth
    6. Transgenic plant – all new cells contain the new genes
    7. Plantlets separated and grown into full size plants


Genes can also be inserted into plant cells by

  • A bacterium that infects the species – genes from plasmid DNA are incorporated into the plant chromosome when they infect them
  • Microinjection: DNA injected directly into nucleus of a fertilised egg using a micropipette (only successful in 1% of embryos)
  • Microprojectules: minute pellets carrying the desired genes are shot into the plant cells using a particle gun
  • Retrovirus: virus inflects cells by inserting their DNA/RNA into host’s genome
  • Liposome wrapping: gene wrapped in a lipid bilayer which can then fuse with the cell membrane and deliver the DNA into the cytoplasm


To find out which plant cells have the new gene = insert a marker gene for antibiotic resistance along with the new desired gene. The plant cells are then incubated with the antibiotic which kills unsuccessful cells that have not taken up the new genes. The only cells to survive are the ones that successfully incorporated the new genes and are resistant.  The plantlets are then separated and grow into full size, transgenic plants.


Benefits of GMOsRisks of GMOs
Pest resistant crop plants – reduces the use of pesticides – increases yield, reduces risk of harming beneficial insectsGenes inserted into a crop might spread to others – cause changes in the genotypes of plant populations – affect other organisms in an ecosystem
Resistant crop plants allows the herbicide to kill weeds but not plant cropsPests might develop resistance through natural selection to the substance in GM crops, resulting in ‘super-pests’
Crop plants can be modified to produce high quantities of nutrientsConsuming foods containing GMOs can be considered harmful to health
Could benefit human healthEnvironmental concerns – increased chemical use in crops
Could help to feed the developing worldCould damage organic farmers
GM crops are more cost-effectiveRaises ethical conflicts over the control of food production



Comparison of coordination in plants and animals

Animals Plants
Coordination in both involves receptors, a communication system and effectors
Animals have a nervous system, containing specialised neurones which transmit action potentials very rapidlyPlants do not have a nervous system or neurone, but some parts do transmit action potentials but this is slower than animals and the potential differences are less than those in mammals
Both use chemicals that are produced in one part and travel to other parts where they have their effects
These substances are called hormones and are made in endocrine glands, which secrete them directly to the blood. They affect target organs which have receptors for themThere are no glands where these chemicals are made, but plant hormones are made in one area (e.g. auxins in meristems) and travel to another part where they have their effect. Unlike animal hormones, they do not travel in vessels but move through cells by facilitated diffusion through protein channels or by active transport through protein transporters
Hormones are almost all small protein molecules or steroidsNo protein or steroid plant hormones have been found




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8.3 Brains and behaviour

8.3 Brains and behaviour


The human brain

The brain is part of the CNS, its role is to initiate and coordinate activities of the body. It receives input from receptors inside and outside the body, and the information from these is integrated to produce appropriate responses.

Different parts of the brain have different functions:


The cortex is the top of the brain, made mostly of cell bodies, synapses and dendrites (grey matter). This is the largest brain region and is divided into the cerebral hemispheres.


  • Cerebral hemispheres: Divided into right and left – ability to see, think, learn and feel emotions
  • Mid brain: Relays information to the cerebral hemispheres, auditory information to the temporal lobe and visual information to occipital lobe
  • Corpus callosum: A band of white matter (nerve axons) which connects the two cerebral hemispheres. It also provides connections between the cortex and the brain structures below


Each hemisphere is composed of 4 regions:

  • Frontal lobe: Concerned with higher brain functions such as decision making, reasoning, planning, consciousness of emotions, forming associations and ideas. It includes the primary motor cortex which has neurones that connect to the CNS.
  • Parietal lobe: Orientation, movement, sensation, calculation, some types of recognition and memory
  • Occipital lobe: Processing information from the eyes (vision, colour, shape, recognition, perspective)
  • Temporal lobe: Processing auditory information (hearing, sound, recognition, speech) and memory


  • Cerebellum: Coordination of movements, balance. It receives information from the primary motor cortex, muscles and joints
  • Medulla oblongata: Regulates involuntary processes – control of the heartbeat (cardiovascular centre) and breathing movements (respiratory centre) and blood pressure
  • Hypothalamus: Thermoregulation (maintaining core body temperature), sleep, hunger, thirst, blood concentration. It connects to the pituitary gland which secretes other hormones
  • Thalamus: Routes incoming sensory information to the correct part of the brain via the axons of the white matter
  • Hippocampus: Laying down long term memory
  • Basal ganglia: A collection of neurones responsible for selecting and initiating stored programmes for movement
  • Brain stem: At the top of the spinal column, it extends from the midbrain to the medulla



How the human brain works

Another way to map brain activity is CAT scans (computerised axial tomography). This uses narrow-beam X-rays rotated around a patient to pass through the tissue from different angles. Each narrow beam is reduced in strength depending on the tissue density to produce an image of a thin slice of the brain showing dense and less dense areas. A computer builds up a 3D image. CAT scans are cheaper than fMRI but do not show which tissues are active, so can only show structure not function of the brain. They only give frozen pictures. They are useful in the diagnosis and monitor of conditions such as brain tumours where changes in brain structure are visualised.


MRI (magnetic resonance imaging) uses a magnetic field and radio waves to detect soft tissues. When placed in a magnetic field, the nuclei of atoms line up with the direction of the magnetic fields. In an MRI scanner, the magnetic field runs down the centre of the tube in which the patient lies. Another magnetic field comes from the high frequency radio waves. These combined fields cause the direction and frequency of the hydrogen nuclei to change, taking energy from the radio waves. When the radio waves are turned off, the hydrogen nuclei return to their original alignment and release the absorbed energy. This is detected and a signal is sent to a computer to analyse it to produce an image. It is used to diagnose tumours, strokes, brain injuries and infections of the brain and spine.


One way to investigate the functions of brain parts following oxygen uptake is using fMRI (functional magnetic resonance imaging). A person lies inside a huge cylindrical magnet. The magnetic field affects the nuclei of atoms in the body, causing them to line up in the direction of the filed. This sends a signal to a computer, which builds up an image by mapping the strengths of signals from different brain parts. Deoxyhaemoglobin absorbs the radio wave signal and oxyhaemoglobin does not. Increased neural activity requires increased oxygen demand so an increase in blood flow – there is a large increase in oxyhaemoglobin levels in the blood so less signal is absorbed. The less radio signal, the higher the level of activity – active areas of the brain light up. By comparing images of a person doing different activities, the areas of the brain involved in these tasks can be identified.


Visual development

We see because the brain processes the image formed from the retina, using past experience and other sensory inputs. They capacity of the brain to process and interpret the action potentials that arrive along the optic nerve is acquired in early childhood. Newborn babies have little ability to interpret information but this is highly developed by the age of 5 or 6 years. The experiences determine the way brain cells are wired up during development.


Evidence for a critical period in visual development:

1960s – Hubel and Wiesel – experiments using monkeys and kittens because they are similar to humans. If they prevented light reaching the retina of one or both eyes as the animals matured they did not develop normal visual abilities. Depriving them at different stages of development affected different aspects. Monkeys deprived of light in one eye (monocular deprivation) were blind in that eye. They concluded that there are specific windows during development, known as critical periods/windows during which particular types of visual input are needed for visual capacities to develop.


More information has been obtained from the development of human babies. Some are born with cataracts, which prevent light patterns from reaching the retina, depriving normal visual input. These can be removed to give normal vision. However they can have a permanent impairment of their ability to perceive shape such as difficulties in face recognition. However elderly people who develop cataracts in later life have normal vision after they are removed.

Researchers tested their visual abilities as they grow up and looked for correlations between the time of visual deprivation and visual abilities that fail to develop. They found three different critical periods:

  • Sensitive period: Developmental changes in the eyes and brain do not occur if a particular visual input is not experienced
  • Period after sensitive period: Even if visual ability has developed properly, it can be damaged if abnormal visual input is experienced
  • Period after above: When any damage by earlier deprivation can be reversed if normal visual input is given


One visual ability is visual acuity – the ability to distinguish objects of small sizes. It is tested by the ability to tell the difference between a plain grey square and one divided by striped. The narrower stripes distinguished, the better the visual acuity.


In human babies:

  • A newborn’s visual acuity is very poor
  • Visual acuity improves during the first 6 months and reached adult values at around 5 years of age
  • Babies born with cataracts that are not treated until 9 months have the visual acuity of a newborn baby when they are removed
  • These babies then improve their visual acuity so by 1 year old they have the same of a normal baby
  • They then fall behind in development, so by 5 years old their visual acuity is 3 times worse than normal and they never develop normal adult acuity


There are a range of visual critical windows in which deprivation of normal visual input has different effects on development.


Similar results have been shown from binocular vision and peripheral vision. For example a young boy who had an eye infection had his eyes bandaged for two weeks and when removed, he had permanently impaired vision.


During the critical period:

The axons of the ganglion cells that make up the optic nerve pass out of the eye and extend to several brain areas, including the thalamus. Impulses are then sent along other neurones to the primary visual cortex where information is processed. Before reaching the thalamus, some neurones in each optic nerve branch off to the midbrain. Here they connect to motor neurones involved in controlling the pupil reflex and eye movement. Audio signals also arrive at the midbrain so you can quickly turn your eyes in the direction of a visual or auditory stimulus.


Retina à thalamus à visual cortex


The human nervous system begins to develop at birth. There is no large increase in the number of brain cells but there is a large increase in brain size due to the elongation of axons, myelination and the development of synapses. Once neurones have stopped dividing, the immature neurones migrate to their final position and wire themselves. Axons lengthen and synapse with the cell bodies of other neurones. Neurones must make correct connections to function properly.


Axons of the neurones from the retina grow to the thalamus where they form synapses with neurones. Axons from these thalamus neurones grow towards the visual cortex in the occipital lobe. The visual cortex is made of a column of axons which are overlapping at birth and receive stimulation from the retina. Normally, the critical period produces the distinctive patterns of columns but those that receive input from a light deprived eye become narrower. This is because dendrites and synapses from the light-stimulated eye take up more space in the visual cortex. Axons compete for target cells in the visual cortex and every time a neurone fires onto a target cell, the synapses of another neurone sharing the target cell are weakened and they release less neurotransmitter.


Nature v nurture

The effect of genes is nature and the environment (experiences) is nurture. Most behaviour patterns are determined by the interactions of both. Any behaviour shown at birth is innate and is considered to be caused by genes. Newborn babies show reflex reactions such as the startle reflex to a sudden loud noise or when they are dropped a short distance. The baby responds by flinging out their arms and legs and contracting the neck muscles. This response is innate but may be influenced by the experiences of the baby whilst a foetus in the uterus.


One way to investigate is using identical twins as they have identical genes. Brain development and behaviour of twins brought up in different families and environments are compared – these differences were caused by the environment.


Animal studies confirm that innate behaviour patterns can be modified by experience.


Development of the brain

The effects of strokes:

  • Drain damaged caused by a stroke can cause problems with speaking, understanding speech, reading and writing
  • Some patients can recover some abilities showing the potential of neurones to change in structure and function (neural plasticity)
  • The brain structure remains flexible even in later life and can respond to changed in the environment


Depth perception:

  • Close objects – depend on presence of cells in visual cortex that obtain information from both eyes – visual field is seen from 2 angles – stereoscopic vision, allows relative position of objects to be perceived
  • Distant objects – the images on the retinas are similar – visual cues and past experienced used to interpret the images


Cross cultural studies

People from different cultures may not share the same beliefs and behaviours. Carpentered world hypothesis – those who live in a world dominated by straight lines and right angles perceive depth cues differently to those who live in a circular culture. When surrounded by straight buildings unconsciously we tend to interpret images with acute and obtuse angles as right angles. People who live in a circular culture with few straight lines or right angles have little experience of interpreting acute and obtuse angles on the retina as representations of right angles – they are rarely fooled by optical illusions.


Studies with newborn babies:

The visual cliff – babies are encouraged to crawl across a transparent table, which is a visual cliff. Patterns placed below the glass create the appearance of a steep drop. If the perception of depth is innate the babies should be aware even if they have not previously experienced this stimulus. Young babies were reluctant to crawl over the ‘cliff’ even when the mothers encouraged them.


Learning and memory

The nervous system changes when there are changes in the synapses that underpin learning and memory changes. Memory is in different parts of the cortex and short-and long term memory is controlled by different parts of the brain.



Learning is when organisms modify their behaviour as a result of experience. One of the simplest types of learning is habituation, defined as a decrease in the intensity of a response when the same stimulus is given repeatedly. For example humans show habituation when hearing a loud bang repeatedly.


Snails withdraw their body when it is touched on the shell. This response helps avoid damage by predators. If it is touched repeatedly and nothing unpleasant happens, it stops withdrawing its body. This is useful because it avoids energy being wasted on an unnecessary action and enables the snail to stay fully active.


How is habituation achieved?

With repeated stimulation, calcium ion channels become less responsive:

  1. Less calcium ions cross presynaptic membrane into presynaptic neurone
  2. Fewer synaptic vesicles fuse with presynaptic membrane
  3. Less neurotransmitter released into synaptic cleft
  4. Less sodium ion channels on posysynaptic membrane open
  5. Less sodium ions flow into postsynaptic membrane
  6. Less or no action potential is triggered in postsynaptic motor neurone


For example, sea slugs have less neurones than humans so their neurobiology is simpler than that of humans. They also have large accessible neurones so those involved in behaviours can be identified. The sea slug breathes through a gill in a cavity on the upper side of its body and water is expelled through a siphon tube. If the siphon is touched, the gill is withdrawn into the cavity – a protective reflex. Sea slugs are habituated to waves which stimulate the siphon. After a few minutes of repeated stimulation, the siphon no longer withdraws. Habituation allows animals to ignore unimportant stimuli so that limited sensory, attention and memory can be concentrated in more threatening or rewarding stimuli.


Practical – investigating habituation in pond snails:

  1. Collect pond snails of the same species and place them in the same tank and leave for a few days to acclimatise
  2. Place a snail in a dish and leave to rest for 5 minutes until active
  3. Using a small implement, gently touch the snail between the tentacles. The snail will withdraw and then slowly extend again.
  4. Repeat the stimulus several times, with set intervals of less than one minute. Record the time for the tentacle to be returned to its fully extended position
  5. Plot a graph of time against number of stimuli given


Sensitisation: Sensitisation is the opposite of habituation, when an animal develops an enhanced response to a stimulus. For example if a predator attacks sea slugs, they become sensitised to other changes in its environment and responds strongly. There is a greater calcium ion uptake, more neurotransmitter released, greater depolarisation and a higher frequency of action potentials.


Animal testing – ethical issues

May be the only way to fully test new drugs and substances or find out about an aspect of physiology or behaviour which may lead to less suffering of humans and animalsWe have no right to submit animals to procedures that may cause discomfort or make their lives unpleasant
Only done when necessary – humans have a greater right to lifeThere is no need to use animals in research as there are other ways of conducting the same investigations
Only way to study how a drug affects the whole bodyAnimals are different to humans – no certainty that drugs tested on animals will have the same effect on humans


Institutions in the UK that test on animals follow the same codes of conduct:

  • Limit the use of animals to circumstances where there is no alternative method (such as using cells grown in tissue culture)
  • Only allow research after thorough scrutiny of the proposal, which must show no other method is possible and the animal welfare will be given high priority at all times
  • All people involved, including scientists, are given fully training in ensuring the health and wellbeing of the animals


Utilitarianism – the belief that the right action is the one that maximises the overall happiness – a utilitarian framework allows certain animals to be used in medical experiments provided the overall expected benefits are greater than the harms.

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8.2 How the nervous system works

8.2 How the nervous system works


The nervous system ­


The nervous system is the network of nerve cells and fibres that transmits impulses around the body. The nervous system is divided into the central and peripheral nervous systems.


Central nervous system = brain and spinal cord


Peripheral nervous system =

  • Sensory nerves – carry sensory information from the receptors à CNS
  • Motor nerves – carry motor commands from CNS à effectors


Peripheral nervous system is sub-divided into:

  • Somatic nervous system – voluntary, stimulates skeletal muscle
  • Autonomic nervous system – involuntary, stimulates smooth muscle, cardiac muscle and glands


Autonomic nervous system divided into:

  • Sympathetic – Prepares body for fight or flight response – increases activity e.g. speeding up heart rate
  • Parasympathetic – Prepares body for rest and digest – decreases activity e.g. lowering breathing rate


The nervous system carries messages around the body using neurones. Neurones are nerve cells which are highly specialised and adapted for the rapid transmission of electrical impulses (action potentials) around the body. Most neurones have a similar basic structure – they:

  • Most are long – can transmit the action potential over a long distance
  • The cell surface membrane has gated ion channels that control the movement of Na, K or calcium ions
  • Have Na/K pumps that use ATP for active transport
  • Maintain a potential difference across their cell surface membrane
  • Have a cell body containing the nucleus, mitochondria and ribosomes


Sensory neurones:

  • Carry impulses from receptors to CNS
  • Cell body is attached to the middle


Motor/effector neurone:

  • Conducts impulses from CNS to effectors (muscles or glands)
  • In CNS
  • Can have long axons
  • Cell body is at the end


Relay/connector neurones:

  • Connect sensory and motor neurones
  • Mostly in CNS
  • Large number of connections with other nerve cells
  • Cell body is in the middle of the axon


Stimulus à Receptor cells à Sensory neurone à CNS à Motor neurone à Effectors à Response


There are two types of main extensions from the cell body of a neurone:

  • Dendrites – Conduct impulses towards cell body
  • Axons – Transmits impulses away from cell body


Myelin sheath:

  • Some neurones have a fatty insulating layer around the axon
  • Made of many layers of Schwann cells wrapped around the axon
  • Acts as an electrical insulator
  • Between Schwann cells are exposed patches of membrane – nodes of Ranvier
  • Speeds up the transmission of action potentials – impulse jumps from node to node (saltatory conduction)


Nerve impulses


Neurones have sodium-potassium pumps in their surface membranes. These actively pump Na+ (sodium) ions out of the cell by active transport. This uses ATP as ions are moved against their concentration gradients.


When a neurone is not transmitting impulses, it is at rest. K+ (potassium) ions are pumped inside through channels. K+ and Na+ ions diffuse back down their concentration gradient but K+ diffuses faster back out than Na+ can diffuse back in – there is a net movement out of the cell, making the inside more negative. This is the resting potential (-70mV) and the membrane is polarised.


Generation of action potential:


  • Depolarisation…
    • There is a change in permeability, causing Na+ channels to open so Na+ to enter the cell down the concentration gradient – inside of cell becomes more positive than outside
    • This reverses the resting potential, the membrane depolarises. The potential difference is +40mV (action potential)
    • If this reaches the threshold level, an action potential is generated and an impulse is fired. If it does not, nothing happens
  • Repolarisation…
  • Na+ gates close and membrane permeability to Na+ ions decreases
  • Voltage-dependent K+ channels open, K+ ions move out of cell down electrochemical gradient
  • Inside of cell becomes more negative – drops below the resting potential value (hyperpolarisation)
  • Restoring resting potential…
  • K+ channels close, sodium-potassium pump restarts, restoring the normal distribution of ions either side of the cell surface membrane
  • Potassium ions diffuse into axon


The refractory period is a time delay between action potentials, when the axon restores its resting potential after the action potential. Ion channels are recovering and cannot be opened and the axon is unable to generate another action potential until the refractory period is over and all voltage-dependent K+ and Na+ channels are closed, ensuring impulses only travel in one direction.


When the threshold is reached, the action potential always fires with the same voltage, no matter the size of the stimulus. If it isn’t reached, the action potential will not fire. A larger stimulus does not cause a larger action potential but it causes more frequent action potentials.



  1. Membrane is polarised (resting state)
  2. Ion channels open, Na+ ions diffuse into cell
  3. Membrane depolarises – less negative
  4. Voltage-dependent Na+ channels open – more enter – positive
  5. Potential difference reaches -40mV
  6. Na+ ion channels close and K+ channels open
  7. K+ ions diffuse out – negative inside – repolarisation
  8. Potential difference overshoots – hyperpolarisation
  9. Potential difference restored – returns to resting state



The action potential travels rapidly along the axon or dendron. This is because the repolarisation of one part of the membrane sets up local currents with the areas either side of it – these regions depolarise too as some Na+ flow sideways.


Propagation of an impulse along an axon:

  1. At resting potential there is a positive charge on the outside of the membrane and negative charge on the inside, with higher sodium ion concentration outside and higher potassium ion concentration inside
  2. When stimulated, voltage-dependent sodium ion channels open and sodium ions flow into the axon, depolarising the membrane. Localised electric currents are generated. Sodium ions move to the adjacent polarised (resting0 region causing a change in electrical charge (potential difference) across this part of the membrane
  3. This change in potential difference initiates a second action potential. At the site of the first action potential, the voltage-dependent sodium ion channels close and voltage-dependent potassium ion channels open. Potassium ions leave the axon, repolarising the membrane. The membrane is hyperpolarised
  4. A third action potential is initiated by the second. In this way, local electric currents cause the nerve impulse to move along the axon. At the site of the first action potential, potassium ions diffuse back into the axon, restoring resting potential


In a myelinated neurone, local currents cannot be set up where the myelin sheath is as the Na+ and K+ cannot flow through the fatty myelin sheath. Instead the action potential jumps from one node of Ranvier to the next where the ions move through the cytoplasm (saltatory conduction). This increases the speed at which it travels along the axon.


How is the impulse propagated along a myelinated axon?

  • Depolarisation occurs at Node of Ranvier
  • Local electric currents occur between nodes
  • Potential difference is reduced at next node, initiating another action potential
  • Impulses jump between nodes by saltatory conduction


Action potentials are conducted faster along axons with large diameters, as there is less resistance to the flow of ions so depolarisation travels faster.  They also are faster at higher temperatures (up to 40oc).



Two neurones are not in direct contact, there is a small gap called the synaptic cleft. The synapse is the junction between the two neurones. The presynaptic neurone has a swelling, called a synaptic knob which contains vesicles filled with neurotransmitter. The presynaptic knob has mitochondria to provide energy to make neurotransmitters and vesicles. The electrical impulse cannot cross the synaptic cleft, so a neurotransmitter is released at the end of the first neurone from the presynaptic membrane. It diffuses across the synapse, binds with the second neurone on the postsynaptic membrane, generating an action potential.


Neurotransmitter release à stimulation of postsynaptic membrane à inactivation of neurotransmitter


  1. Action potential arrives at presynaptic membrane/synaptic knob
  2. Membrane depolarises causing voltage-dependent calcium ion channels to open – calcium ions enter neurone down their concentration gradient
  3. Calcium ions cause synaptic vesicles containing neurotransmitter to fuse with presynaptic membrane
  4. Neurotransmitter released into synaptic cleft by exocytosis and diffuses across the cleft
  5. Neurotransmitter binds with complementary receptor proteins on postsynaptic membrane, causing cation channels to open so Na+ ions flow through into the cytoplasm of the neurone
  6. Postsynaptic membrane depolarises, setting up an action potential in the postsynaptic neurone
  7. To stop action potentials, the released neurotransmitter is taken up by the presynaptic membrane or diffuses away and is broken down by enzymes


Two examples of neurotransmitters are acetylcholine (ACL) and noradrenalin. They are synthesised in vesicles, which requires energy. Therefore the synaptic knobs have many mitochondria to produce ATP.


Although synapses slow the transmission of impulses, they are useful:

  • Ensure impulses travel only in one direction because receptors are only on the postsynaptic membrane
  • Allows neurones to connect with many other neurones – increases range of possible responses to a particular stimulus
  • Control nerve pathways an give flexibility of response
  • Integrate information from different neurones to give a coordinated response


Extent of depolarisation:

  • Depends on how much neurotransmitter reaches the postsynaptic membrane
  • – Depends partly on the frequency of impulses reaching the presynaptic membrane
  • A single impulse usually won’t release enough neurotransmitter to depolarise and postsynaptic membrane
  • Also depends on the number of receptor sites on the postsynaptic membrane


Excitatory synapses (depolarise)

Make the postsynaptic membrane more permeable to Na+ ions

Makes it more likely that an action potential will be generated

Several impulses together release enough – summation


Inhibitory synapses (hyperpolarise)

Inhibitory synapses make it less likely that an action potential will result.

  • The neurotransmitters open channels for Cl- and K+ ions in the postsynaptic membrane
  • These move through the channels down their diffusion gradients
  • Cl- ions move into the cell and K+ ions move out
  • This causes a greater potential difference across the membrane as the inside becomes more negative than usual (-90mV)
  • This makes depolarisation less likely as more excitatory synapses are needed


If the stimulus is small, little neurotransmitter will be released and this might not be enough to excite the posysynaptic membrane to the threshold level – more than one synapse/neurone is needed to provide sufficient depolarisation – summation is when each impulse adds to the effect of another


  • Spatial summation: Impulses are from different synapses connect to one neurone, there is enough neurotransmitter for an action potential
  • Temporal summation: Several impulses arrive at a synapse one after another


The combined release of neurotransmitter generates an action potential in the postsynaptic membrane.


Generator potentials

Receptor cells respond to changes in the environment.

When a stimulus is detected, the membrane becomes more permeable – gated Na+ ion channels open and Na+ ions diffuse into the cell

Small change in potential – generator potential

The larger the stimulus, the more gated channels will open – the larger the generator potential

If enough Na+ ions enter, the potential difference changes significantly and will initiate an impulse or action potential.


Synapses can amplify or disperse information – one neurone connects to many other neurones – information dispersed around the body – synaptic divergence or many neurones connect to one neurone – information amplified (made stronger) – synaptic convergence.


Sensory receptors


  • Specialised cells that detect changes in the environment. They are specific to one type of stimulus
  • Energy transducers – convert one form of energy to another. Each type of transducer is adapted to detect changes in a particular energy form
  • May be a change in light levels/pressure on the skin
  • Each change in energy levels in the environment is a stimulus
  • Sensory receptors can convert any stimulus energy into a form of electrical energy (a nerve impulse)


Examples of receptors:


Receptors Energy changes detected
Light sensitive cells (rods and cones) in eye retinaLight intensity and range of wavelengths
Olfactory cells lining the inner surface in the nasal cavityPresence of volatile chemicals
Taste buds in the tongue, hard palate, epiglottis & oesophagusPresence of soluble chemicals
Pressure receptors (pacinian corpuscles) in the skinPressure on skin
Sound receptors in the inner ear (cochlea)Vibrations in air
Muscle spindles (proprioceptors)Length of muscle fibres


The human eye

Light enters the eye through the pupil. The amount of light is controlled by the muscles of the iris. Light rays are focused by the lens onto the retina, which lines the inside of the eye and contains photoreceptor cells that detect the light. Nerve impulses are carried from the retina to the brain by the optic nerve.


  • Conjunctiva: Protects the cornea
  • Cornea: Bends light
  • Lens: Focuses light on retina
  • Iris: Controls amount of light entering eye by controlling pupil size
  • Sclera: Protective layer, allows attachment of external muscles
  • Blind spot: No light sensitive cells where optic nerve leaves eye
  • Fovea: Most sensitive part of retina
  • Retina: Contains light-sensitive cells
  • Vitreous humour: Transparent jelly
  • Choroid: Black layer prevents internal reflection of light
  • Cilary muscle: Alters thickness of lens for focusing
  • Optic nerve: Transmits impulses to brain
  • Pupil: Circular opening for directing light to the lens


How do photoreceptors convert light into an electrical impulse?

  • Light enters the eye, hits the photoreceptors and is absorbed by light-sensitive pigments
  • Light bleaches the pigments, causing a chemical change and a change in membrane permeability to sodium
  • A generator potential is created, if it reaches threshold, a nerve impulse is sent along a bipolar neurone
  • Bipolar neurones synapse with ganglion neurones whose axons make up the optic nerve – bipolar neurones connect photoreceptors to the optic nerve
  • Optic nerve extends to several brain areas including the thalamus
  • Before reaching the thalamus, some of the neurones branch off to the mid brain
  • At the mid brain they connect to motor neurones that control pupil reflex and eye movement


There are two types of photoreceptors in the retina – rods cells and cone cells:

  • Rods – sensitive to dim light because many join to one neurone. They give low visual acuity and only give information in black and white. Rods are found in the peripheral parts of the retina.
  • Cones – Can only respond in bright light (less sensitive) as only one joins one neurone. They give high visual acuity because they are close together. They give information in colour. Cones are found packed together in the fovea.


Rods Cones
Number in retina20:1
Where in retinaAll over retina but not foveaOnly fovea
Light-sensitive pigmentRhodopsinIodopsin
Vision Black and white vision

Both dim and bright light

Colour vision

Only bright light

Sensitivity IntensityWavelength



Rod cells

The outer segment of a rod cell contains membranes, staked up parallel. Sodium-potassium pumps act across the membranes and cation channels remain open, so some sodium and potassium ions leak back through.


The membranes also contain a pigment called rhodopsin (in vesicles) which is made of a retinal molecule and an opsin molecule.   When light hits rhodopsin, the retinal changes shape. This causes sodium and potassium ion channels in the membrane to close, but the sodium-potassium pump keeps working. As the ions cannot leak back in or out of the neurone, a greater potential than usual builds up (negative inside) and the membrane is hyperpolarised.


When no light falls onto a rod cell and the potential difference is normal, it constantly releases transmitter substances, which diffuses to the next neurone. This stops that neurone generating action potentials. When light falls on the rod cell and hyperpolarises the membranes, it stops releasing the transmitter substances and the neighbouring neurone can generate action potentials. These are transmitted along axons to the optic nerve, which carry them to the visual centre in the brain.


The change in shape of retinal makes it unstable and it separates from opsin. If this happens to all the rhodopsin in all rod cells, you cannot see in dim light. If you walk from a sunny area to a dim room you cannot see much because our cones stop functioning in low intensity light and the rod pigments have become bleached. In dim light, retinal and opsin gradually combine again, forming rhodopsin – this is dark adaptation. Until rhodopsin is reformed, no more action potentials can be created in the bipolar cells so no more stimuli can be detected. This takes a few minutes. The brighter the light, the more rhodopsin molecules break down and the longer it takes for them to reform.



  1. Na+ diffuses through open cation channels into outer segment
  2. Na+ move down concentration gradient into inner segment
  3. Na+ is actively pumped out of cell using ATP and ion pumps
  4. Membrane slightly depolarised -40mV
  5. Inhibitory neurotransmitter (glutamate) released from rod cells and binds to bipolar cell, preventing it from depolarising.



  1. Light energy breaks rhodopsin à opsin + retinal
  2. Opsin binds to membrane of outer segment
  3. Na+ cation channels close
  4. Na+ still actively pumped out but cannot diffuse into outer segment
  5. Inside of cell is more negative – membrane hyperpolarised (-90mV)
  6. No inhibitory neurotransmitter (glutamate) is released
  7. Cation channels in bipolar cell open and membrane is depolarised, generating an action potential in the neurone of the optic nerve à brain


Controlling pupil size

The iris is the coloured part of the eye surrounding the pupil and it controls the pupil size. Light passes through the pupil on its way to the retina. In bright light, the pupil is small (contracted) to limit the amount of light passing through to prevent damage to rods and cones. In dim light the pupil is large (dilated) to allow more light to reach the retina.


When bright light hits the retina, it is detected by photoreceptors which send nerve impulses along the optic nerve to the CNS of the brain along a sensory neurone. This causes action potentials to be sent along parasympathetic motor neurones to the muscles in the iris. Circular muscles contract and radial muscles relax, making the iris wider and the pupil narrower (pupil constricts).


In dim light, the circular muscles relax and the radial muscles contract to widen the pupil – the opposite reaction.


The radial muscles are controlled by sympathetic reflex

The circular muscles are controlled by parasympathetic reflex


Reflex arcs

Nerve impulses follow routes/pathways through the nervous system, these reflex arcs are responsible for our reflexes and they are controlled by the autonomic nervous system. Reflexes are fast and help to avoid damage to the body.


  1. Receptors detect stimulus and generate nerve impulse
  2. Sensory neurones conduct nerve impulse to CNS along sensory pathway
  3. Sensory neurones enter spine
  4. Sensory neurone synapses with relay neurone
  5. Relay neurone synapses with motor neurone which leaves spine
  6. Motor neurone carries impulse to effector producing a response


If there is a relay neurone involved, the reflex can be overridden by the brain.


Hormonal system

  • Made up of glands and hormones
  • Gland = group of cells specialised to secrete a useful substance
  • Hormones = chemical messengers, many are proteins or peptides
  • Hormones are secreted when a gland is stimulated
  • Hormones diffuse into the blood and diffuse around the body
  • Hormones trigger a response in target cells
  • Stimulus à Receptor à Hormone à Effectors à Response
  • Hormones are not released directly to the target cells, they travel in the blood which is slower
  • They aren’t broken down as fast as neurotransmitters – long-lasting
  • They are widespread – hormones are transported all over the body


Nervous system keywords

  • Nerve impulse: An electrical impulse sent along a nerve to allow information to travel to effectors to carry out a response to a stimulus
  • Neurone: A single cell which has dendrites, an axon, a cell body and terminal branches, making up part of the nervous system
  • Nerve: Contains a bundle of the axons of many neurones surrounded by a protective covering
  • Cell body: Contains the organelles and is found in different locations for different neurones with extensions called dendrites and the axon
  • Dendrites: Conduct impulses towards the cell body. Each neurone has many
  • Axon: Conducts impulses away from the cell body, a single long process
  • Motor neurone: Carry impulses from CNS to effectors
  • Sensory neurone: Carry impulses from sensory cells to CNS
  • Relay neurone: Have a large number of connections with other nerve cells
  • Myelin sheath: Fatty insulating layer around the axon. It affects the speed of the impulse. It is made of Schwann cells
  • Effector: Produce a response when an impulse is received from motor neurones
  • Reflex arc: Nerve impulses follow simple pathways
  • Reflexes: Rapid, involuntary responses to stimuli
  • Photoreceptors: Receptors in the retina that respond to light levels
  • Resting potential: -70mV, when the inside of the axon membrane is more negative due to the movement of potassium ions
  • Repolarisation: The charge is reversed, becoming positive on the inside (+40mV) because voltage-dependent Na+ channels open and Na+ flow in
  • Repolarisation: The Na+ channels close and K+ channels open, allowing K+ ions to flow out making the inside more negative
  • Action potential: The change in voltage across the axon membrane
  • Positive feedback: The opening of Na+ ion gates makes more open
  • All or nothing: There is either enough depolarisation or not enough to create an action potential
  • Hyperpolarisation: The K+ ion gates open to re-polarise the membrane and too many are left out, the potential reaches -90mV
  • Refractory period: A new action potential cannot be generated for a few milliseconds until all the gates are closed and resting potential is restored. This ensures the impulse only travels in one direction
  • Nodes of Ranvier: Gaps at regular intervals in the myelin sheath on the axon. They are the sites of depolarisation
  • Saltatory conduction: The action potential jumps across the axon to  each node of Ranvier, making the impulse travel faster
  • Synapse: Where two neurones meet
  • Synaptic cleft: The gap between the two meeting neurones
  • Presynaptic neurone: Has Ca+ ion channels and neurotransmitter vesicles. It is the stimulating neurone that passes on the impulse
  • Postsynaptic membrane: Receives the neurotransmitter and the impulse, it fires off another impulse
  • Synaptic vesicles: Contain the neurotransmitter to depolarise the membrane
  • Neurotransmitter: When Ca+ ions enter the presynaptic membrane, vesicles fuse with the membrane and release the neurotransmitter into the synaptic cleft. They bind with channels on the postsynaptic membrane
  • Acetylcholine: A neurotransmitter, the first to be discovered
  • Summation: Each impulse adds to the effect of the others
  • Spatial summation: Impulses from different neurones
  • Temporal summation: Several impulses along one neurone
  • Inhibitory synapses: Make it less likely that an impulse will be fired in the postsynaptic neurone by allowing it to hyperpolarise by letting Cl- ions in and allowing K+ ions out
  • Excitatory synapses: Make the postsynaptic neurone more permeable to Na+ ions meaning it is more likely that depolarisation will occur and lead to an action potential


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8.1 Sensitivity in plants

Topic 8: Grey matter

8.1 Sensitivity in plants


Photoreceptors: A structure in living organisms, especially a sensory cell or sense organ that responds to light.



The interaction of cells enables them to coordinate their activities appropriately. Organisms have specialised cells or molecules that are sensitive to changes in the environment (stimulus), called receptors. These then trigger events to bring about coordinated responses to environmental changes.


Plant photoreceptors:

Plants use light as their sole energy source in photosynthesis. Light gives plants information about the seasons and respond by moving into different stages of their life cycles.


Plants respond to:

  • Light intensity
  • Light direction
  • Light quality (wavelength)
  • Light duration (day length)



Proteins that are sensitive to red light found in leaves. Phytochromes exist in two forms which are changed from one form to another when they absorb light. Phytochrome red P(R) absorbs red light and is changed to far-red P(FR) which absorbs far-red light. This changes it back to P(R) in a reversible reaction.


White light, including sunlight, contains both red and far-red light. This causes more P(FR) to be produced from P(R). In the dark, P(FR) slowly changes to P(R):


  • After daylight there is more P(FR)
  • After darkness there is more P(R)


In some plant species, phytochromes affect seed germination. Dormant seeds only germinate when they contain plenty of P(FR) which happens when normal sunlight falls onto them. This is valuable because it prevents germination in unsuitable conditions when there is not enough light for photosynthesis. If a light-sensitive seed is provided with the correct conditions (water, temperature) and then is given a short burst of far-red light, it won’t germinate. If the burst of far-red light is followed by a burst of red light it will germinate because the red light converts P(R) to P(FR).


Phytochromes also determine if the plant produces flowers. Some plants adapt to flower in spring, when the days are longer. Others are adapted to flower in late summer or autumn when the days are shorter. The photoperiod determines flowering.


During darkness, P(FR) converts back to P(R). Short-day plants require P(R) in their tissues to flower, which occurs when they have long uninterrupted nights. If white or red light is shone on them even briefly during the night, they will not flower because this converts P(R) back to P(FR).


Long-day plants need an abundance of P(FR) which only happens when they have short nights because not all of the P(FR) has been converted and the sun begins the conversion of P(R) back to P(FR) again.


Phytochromes activate other molecules in plant cells which affect various metabolic pathways. The phytochromes also act as transcription factors in the nucleus, switching genes on and off.



A growth response to directional light. Shoots are positively phototrophic, growing towards the source of light. Roots are negatively phototropic, growing away from the source of light. This response involves an auxin (IIA), a plant hormone promoting elongation of stems and roots. Auxin is a plant hormone/growth regulator. It is synthesised by cells in the meristem of a shoot and then transported downwards through the shoot tissues. Auxin binds with receptors in the plasma membranes in the zone of shoot elongation, producing a second messenger signal molecule that brings about changes in gene expression. An increased potential difference across the membrane enhances uptake of ions into the cell, causing uptake of water by osmosis causing cell elongation.


Auxin activates transcription factors in the nucleus, switching different sets of genes on or off. Some code for the production of proteins (expansins) which act on cellulose cell walls, enabling them to stretch and expand when the cell takes in water. This is probably due to the disruption of hydrogen bonds between the cellulose molecules. Auxin stimulates cell expansion.


The distribution of auxin in a shoot is affected by photoropin. When unidirectional light falls onto the shoot, this affects the auxin distribution, causing it to accumulate on the shady side. This causes the cells on the shady side to grow more rapidly, so the shoot bends towards the light.


When the tip is removed and placed on some agar jelly and then placed back on the plant, it started to grow again, showing the chemical diffused through the agar jelly.


Geotropism – a growth response by a plant to gravity. Shoots are negatively geotropic, roots are positively geotropic.

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