Unit 5: Energy, Exercise and Coordination

Topic 8: Grey Matter.

8.1. The nervous system and nerve impulses:

8.1.1.What are nerve cells like?

The nervous system is a highly
organised network of nerve cells
and fibres that transmit nerve
impulses around the body. The
nervous system carries
messages around the body using
neurones.

Nerves
A nerve is a complex structure containing a
bundle of axons of many neurones surrounded
by a protective covering. There is usually a fatty
insulating layer called the myelin sheath around
the axon which is made up of Schwann cells –
the sheath affects how quickly never impulses
pass along the axon. Not all organisms have myelinated axons.

Neurones
Neurones are single cells (although there are different types)
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:
- Most are long – can transmit the action potential over a long distance
- The cell body contains a nucleus and cell
organelles within the cytoplasm
- Contain two types of thin extensions from the
cell body:
o Dendrites which conduct impulses towards
cell body
o Axons which transmits impulses away from
the cell body
- The cell surface membrane has gated ion
channels that control movement of Na, K or Ca
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
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Motor Neurones (effector neurones) – the

cell body is always situated within the CNS
and the axon extends out, conducts impulses
from the CNS to effectors (muscles or glands).
The axons of some motor neurones can be
very long (e.g. in the leg).

 Sensory Neurones – carry impulses from

sensory cells to the CNS.

 Relay Neurones (connector neurones /

interneurones) – found mostly in the CNS.
They have a large number of connections
with other nerve cells.

8.1.2. Reflex Arcs

Nerve impulses follow routes/pathways through the nervous system – these are called reflex
arcs (controlled by the autonomic nervous system).

Reflex arcs are responsible for reflexes

(rapid, involuntary responses to stimuli).
Reflexes are fast and help to avoid
damage to the body.
1. Receptors first detect a stimulus (e.g.
hot cup) and generate a nerve impulse.
2. Sensory neurones conduct nerve
impulses to the CNS along the sensory
pathway.
3. Sensory neurones enter the spinal cord
through the dorsal route.
4. Sensory neurone synapses with a relay
neurone.
5. Relay neurone synapses with motor
neurone which leaves the spinal cord
through the ventral route.
6. Motor neurone carries impulses to an
effector (e.g. muscle) which produces a response (movement).

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

5.2. Exit
3. Enter
2. Sensory 4. Relay 5.1. Motor through
1. Receptor dorsal route 6. Effector
Neurone Neurone Neurone ventral route
of spine
of spine
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The Pupil Reflex

- The iris controls the size of the pupil and it contains a pair of antagonistic muscles: radial
and circular muscles (controlled by autonomic nervous system).
- Radial muscles (like the spokes of a wheel) are controlled by a sympathetic reflex (fight vs
flight).
- Circular muscles are controlled by a parasympathetic reflex (rest & digest).
- When the pupil constricts the radial - When the pupil dilates the radial
muscles relax while the circular muscles contract while the circular
muscles contract (high light). muscles relax (low light).

- When high light strikes the

photoreceptors present in the
retina (back of eye), nerve impulses
pass along the optic nerve to sites
within the CNS (including a group of
coordinating cells in the midbrain).
Photoreceptors are structures
found in sensory cells or sense
organs that respond to light.

- Impulses from these cells from are

sent along parasympathetic motor
neurones to the circular muscles
of the iris, causing them to contract.

- At the same time, the radial

muscles relax which constricts the
pupil and reduces the amount of light
entering the eye.
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8.1.3. How nerve cells transmit impulses:

All cells have a potential difference
(electrical voltage) across their surface
membrane. The inside of an axon is more
negative than the outside (membrane is said
to be polarised) – the value of this is -70 mV
and is known as the resting potential.

Neurones have sodium-potassium pumps

in their surface membranes and these actively
pump Na+ 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+ ions are pumped into the cell
through channels. K+ and Na+ ions diffuse
back down their concentration gradient but K+
diffuses back out faster than Na+ can diffuse
back in – net movement out of cell making the
inside more negative. This is the resting
potential and the membrane is polarised.

There is an uneven distribution of ions across the cell surface membrane of an axon – this is
achieved by the action of sodium-potassium pumps in cell surface membrane.
1. Na+ pumped out of cell while K+ is pumped into the cell – acts against concentration gradients
and uses energy from the hydrolysis of ATP.
2. Once concentration gradients are set up: K+ diffuses out of cell (down the gradient) making the
outside of the cell membrane positive and the inside negative. The membrane is permeable to
K+ ions but virtually impermeable to Na+ ions.
3. The more K+ that diffuses out the larger the potential difference across the membrane. The
increased negative charge inside the cell attracts K+ ions back across the membrane and into
the cell.
4. At -70mV the electrical gradient balances the chemical gradient – no net movement of K+
which maintains the potential difference.
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What happens when a nerve is stimulated?

Neurones are electrically excitable cells; the potential difference across their cell surface
membrane changes when they are conducting an impulse.

What causes an action potential (change in voltage across a membrane)?

Once threshold stimulation occurs, an action potential (large change in voltage across the
membrane) is caused by changes in the permeability of the cell surface membrane to Na+ and K+,
due to the opening and closing of voltage-dependent Na+ and K+ channels. At the resting
potential, these channels are blocked by gates preventing the flow of ions through them.
Changes in the voltage across the membrane cause the gates to open, and so they are referred
to as voltage-dependent gated channels.

There are three stages in the generation of an action potential:

1. Depolarisation: occurs when a neurone is stimulated, changing the potential difference
across the membrane. This causes a change in the shape of the Na+ gate, opening some of
the voltage dependent Na+ channels. Na+ enters the axon, more depolarisation occurs,
triggering more gates to open. This is an example of positive feedback (a change that
encourages further change if the same sort). Action potentials are either there or they are not
(all-or-nothing). The potential difference across the membrane is now +40mV and there is a
higher concentration of Na+ outside of the axon, so Na+ ions flow rapidly inward causing a
positive charge inside the cell membrane.
2. Repolarisation: after about 0.5ms, the voltage dependent Na+ channels spontaneously close
thus restoring permeability to a low level. K+ channels open due to depolarisation of the
membrane, thus K+ ions move out of axon causing a negative charge inside membrane,
3. Restoring Resting Potential: membrane is now highly permeable to K+ ions which continue
to move out of the cell making the potential difference more negative than normal resting
potential – this is called hyperpolarisation of the membrane. Resting potential is re-
established by the closing of K+ channels causing the ions to move back into the axon.
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How is a nerve impulse passed along an axon (propagation of a nerve impulse)?

Stimulation of a neurone causes a sequence of action potentials along the axon (domino effect).
As part of the membrane becomes depolarised at the site of an action potential, a local electrical
current is created as the charged Na+ ions flow between the depolarised part of the membrane
and the adjacent resting region.
The depolarisation spreads to the adjacent region and the nearby Na+ gates will respond to this
by opening as described earlier, triggering another action potential. These events are then
repeated along the membrane.
As a result, a wave of depolarisation will pass along the membrane. This is the nerve impulse.
A new action potential cannot be generated in the same section of membrane for about five
milliseconds - known as the refractory period. It lasts until all the voltage-dependent Na+ and K+
channels have returned to their normal resting state (closed) and the resting potential is restored.
The refractory period ensures that impulses only travel in one direction.

1. At resting potential there is a +ve charge

on the outside of the membrane and -ve
charge on the inside, with higher Na+ ion
concentration outside and higher K+ ion
concentration inside.
2. When stimulated, voltage-dependent Na+
ion channels open and Na+ ions flow into
the axon, depolarising the membrane.
Localised electric currents are generated
in the membrane. Na+ ions move to the
adjacent polarised (resting) region causing
a change in electrical charge (potential
difference) across this part of the
membrane.
3. This change in potential difference in the
membrane adjacent to the first action
potential initiates a second action potential.
At the site of the first action potential, the
voltage-dependent Na+ ion channels close
and voltage-dependent K+ ion channels
open. K+ 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, K+ ions diffuse back into the
axon, restoring resting potential

Are impulses different sizes?

A stimulus must be above threshold level to generate an action potential. The all-or-nothing effect
for action potentials means that the size of the stimulus has no effect on the size of the action
potential. The size of a stimulus affects:
- the frequency of impulses.
- the number of neurones in a nerve that are conducting impulses.

A high frequency of firing and the firing of many neurones are usually associated with a strong
stimulus.
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Speed of impulse conduction:

The speed of nervous conduction is very fast, allowing fast responses to stimuli. They are
affected by 3 factors:
- Temperature – the higher temperature, the faster the speed. Homoeothermic (warm-blooded)
animals have faster responses than poikilothermic (cold-blooded) ones.
- Axon Diameter – the wider the diameter, the faster the impulse travels (less resistance to flow
of ions so depolarisation travels faster). Marine invertebrates lining at low temps have
developed thick axons (1000µm) to speed up their responses. Mammals axons are ± 1-20µm.
- Myelin Sheath – only vertebrates have a myelin sheath which acts as an electrical insulator
and prevents flow of ions across the membrane. Gaps known as nodes of Ranvier occur in
the myelin sheath at regular intervals and are the only places where depolarisation can occur.
The impulse jumps from one node to the next – increases speed of propagation (wave of
depolarisation). The ‘jumping’ conduction is called salutatory conduction.

8.1.4. How does a nervous impulse pass between cells?

Where two neurones meet is known as a synapse. The cells do not actually touch - there is a
small gap called the synaptic cleft.

Synapse structure:

How does the synapse transmit an impulse?

There are three stages leading to the nerve impulse
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passing along the post synaptic neurone.

- Neurotransmitter release – when the
presynaptic membrane is depolarised
by an action potential, Ca2+ channels
open and Ca2+ diffuses across the
membrane due to the increased Ca2+
concentration outside the cell. This
causes synaptic vesicles containing
neurotransmitter (e.g. acetylcholine) to
fuse with the presynaptic membrane
and release their contents into the
synaptic cleft by exocytosis.
- Stimulation of the postsynaptic
membrane – the neurotransmitter
takes ±0.5ms to diffuse across the
synaptic cleft and reach the
postsynaptic membrane. Embedded in
the postsynaptic membrane are
specific receptor proteins that have a
binding site with a complementary
shape to the neurotransmitter. The
neurotransmitter binds to the receptor
changing the shape of the protein, and
opening cation channels thus making
the membrane permeable to Na+ ions.
The flow of the Na+ ions across the
postsynaptic membrane causes depolarisation, producing an action potential which is
propagated along the postsynaptic neurone. The extent of the depolarisation depends on the
volume of neurotransmitter.
- Inactivation of neurotransmitter – some neurotransmitters are taken up by the presynaptic
membrane and the molecules are used again. With others, the neurotransmitter rapidly
diffuses away from the synaptic cleft or is taken up by other cells. With acetylcholine,
acetylcholinesterase at the post synaptic membrane breaks it down so it can no longer bind
to receptors. Some breakdown products are reabsorbed by the presynaptic cleft and reused.

8.1.5. What is the role of synapses in nerve pathways?

Control and Coordination
Synapses have two main roles:
- Control of nerve pathways, allowing flexibility of response.
- Integration of information from different neurones, allowing a co-ordinated response.

The posynaptic cell can receive inputs from

many synapses at the same time. The overall
effect of all of these synapses determines
whether an action potential will be generated
The two factors affecting the likelihood that
the postsynaptic membrane will depolarise:
- Type of synapse (excitatory or
inhibitory)
- Number of impulses received (the
balance of excitatory and inhibitory
synapses)
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Types of synapse:
1. Excitatory synapses:
Excitatory synapses make the postsynaptic
membrane more permeable to Na+ ions.
- Summation is the idea that each impulse
adds to the effect of the others – one alone
does not have enough of an effect.
There are two types of summation:
o Spatial Summation: here impulses are
from different synapses, from different
neurones. The number of different sensory
cells stimulated can be reflected in the
control of the response.
o Temporal Summation – here several
impulses arrive at a synapse after travelling
along a single neurone, one after another.
Their combined release of neurotransmitter
generates an action potential in the
postsynaptic membrane.

2. Inhibitory synapses
These synapses make it less likely that an action potential will occur.
The neurotransmitter from these
synapses opens channels for Cl- and
K+ ions in the postsynaptic membrane.
Cl- ions (-ve charge) will enter the
membrane and K+ ions (+ve charge)
will leave the membrane resulting in a
greater potential difference across the
membrane (inside becomes more
negative than usual at ±-90mV) –
hyperpolarisation.
Subsequent depolarisation cannot
occur and more excitatory synapses
will be required to depolarise the
membrane.

Comparing nervous and hormonal coordination:

The body is not only co-ordinated by the nervous system - hormones secreted by endocrine
glands send chemical messages to cells and control long term changes e.g. growth/sexual
development.
Nervous Control Hormonal Control
Electrical transmission by nerve impulse and
Chemical transmission through the blood
chemical transmission at synapses
Fast acting Slower acting
Associated with short term-changes e.g. muscle Can control long term changes e.g.
contraction growth/sexual development
Action potentials carried by neurones with Blood carries hormones to all cells, but only
connections to specific cells specific cells can respond
Response is very local, e.g. in a specific muscle Response may be widespread, e.g. in growth
cell or gland and development
Contrasting nervous and hormonal cells in animals
7|Grey Matter

Coordination in plants:
Plants lack a nervous system so use chemicals to control growth, development and
responses to the environment.
- These chemicals (e.g. auxins), called plant growth
regulators/plant growth substances, are produced in
low concentrations before being transported to where
they cause a response.
- Experiments were conducted on phototropism (bending
of plants towards a light source). These experiments
showed that an oat coleotopile with the tip cut off stops
bending towards the light. Replacing the tip starts re-
growth towards the light again.
- It was concluded that influence (a chemical) made in the
tip was passed down to the rest of the plant causing it to
bend.
- The chemical is indoleacetic acid (auxin) and its main
function is to stimulate grow as a result of cell elongation.
- Experiments show that there is no difference in chemical
production between sides of the plant in light/dark,
however more auxin has passed down the shaded side –
this increased concentration of auxin increases cell
elongation and reduced concentration on the illuminated
side inhibits cell elongation. As a result the shoot grows
towards the light.

Comparison of coordination in plants and animals:

Animals Plants
Coordination in both plants and animals involves receptors, a communication system and
effectors
Plants do not have a nervous system or
neurone, however some parts of plants do
transmit action potentials, but this is done
Animals have a nervous system, containing
very much more slowly than animals, and the
specialised neurones which transmit action
potential differences involve are generally
potentials very rapidly.
less than those in mammals – e.g. Venus fly
trap – action potential brings about it’s closure
when fly lands on leaf
Both animals and plants use chemical that are produced in one part of the organism and travel
to other parts where they have their effects.
In plants, there are no glands where these
chemicals are made, but plant hormones are
In animals, these substances are called made in one area (e.g. auxin made in
hormones and they’re made in the endocrine meristems) and travel to another part of the
glands, which secrete them directly to the plant where they have their effect. Unlike
blood. They’re then carried in solution in the animal hormones, they often do not travel in
blood plasma – they affect target organs vessels but instead move through cells,
which have receptors for them either by facilitated diffusion through protein
channels or by active transport through
protein transporters
Animal hormones are almost all small protein No protein or steroid plant hormones have
molecules or steroids been found
8|Grey Matter

8.2. Reception of stimuli

8.2.1. How does light trigger nerve impulses?

 Receptors
- Stimuli (changes that occur in an animal’s environment) are detected by receptor cells that
send electrical impulses to the CNS.
- Many receptors are spread throughout the body, but some types are grouped together into
sense organs (eg. the eyes) which help protect the receptor cells and improve their efficiency.
- In the eye: the lens and cornea refract (bend) light so that it is focused on the retina where the
photoreceptor cells are located.

Type of receptor Stimulated by Examples of role in body

Taste, smell and regulation of chemical
Chemoreceptors Chemicals
concentrations in the blood
Forces that stretch, compress,
Mechanoreceptors Balance, touch and hearing
or move the sensor
Photoreceptors Light Sight
Temperature control and awareness of
Thermoreceptors Heat or cold
changes in the surrounding temperature
Four main types of receptors

Part of Eye Function

Ciliary muscle Alters the thickness of the lens for focusing
Choroid A black layer that prevents internal reflection of light
Vitreous Humour Transparent jelly
Retina Contains light sensitive cells
Fovea Most sensitive part of retina located within the macula, central area of retina
Optic nerve Sends impulses to the brain
Blind Spot No light sensitive cells where optic nerve leaves the eye
Sclera Protective layer, , allows attachment of external muscles
Iris Controls the amount of light entering the eye by controlling pupil size
Lens Focuses light on the retina
Cornea Refracts (bends) light
Pupil Circular opening for directing light to the lens
Conjuctiva Protects the cornea
9|Grey Matter

Photoreceptors:
The retina contains two types of photoreceptor cells which are sensitive to light: rods and
cones.
- Rods only give black and white vision, but can work in dim and bright light.
- Cones allow colour vision in bright light.

The image below shows the arrangement of the 3 layers of cells which make up the retina: the
rods and cones synapse with the bipolar neurone cells which synapse with ganglion neurone
(whose axons make up the optic nerve).
In both rods and cones, a photochemical pigment absorbs the light entering the eye resulting in a
chemical changes. In rods the pigment is rhodopsin.

How does light stimulate photoreceptor cells?

 In the dark
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) is continuously
released from rod cells and binds to
the bipolar cell, preventing it from
depolarising.

 In the light
1. Light energy breaks down
rhodopsin into opsin and retinal.
2. This breakdown causes Na+
channels to close, reducing influx of
Na+ into the rod.
3. Na+ still actively pumped out but
cannot diffuse into outer segment
therefore inside of cell is more
negative.
4. Membrane is hyperpolarised (-90mV) and release of neurotransmitter stops.
5. Lack of neurotransmitter results depolarisation of bipolar cell and neurones of optic nerve,
resulting in an action potential.
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‘Dark Adaptation’
- Once the rhodopsin molecule has been
broken down it needs to be converted back
so that more stimuli can be received (this
takes a few minutes).
- The higher the light intensity the more
rhodopsin molecules are broken down and
the longer it takes for all the rhodopsin to
reform.
- The reforming of rhodopsin – ‘dark
adaptation.’

8.2.2. Plants and Environmental Cues

- Plants can also detect and respond to stimuli, adapting their growth and development to make
sure they survive and reproduce.
- Plants detect the quantity (duration), intensity, direction, and wavelength (quality) of light using
photo receptors and respond to changes in light conditions. They also respond to
environmental cues such as gravity, touch, and mechanical stress.
- All messages in a plant are chemical so responses are slower.
- Plants contain several types of photoreceptor; the most extensively studied being
phytochromes – 5 of which have been identified.

 Phytochromes – plant photoreceptors

- Phytochromes consist of a protein component bonded to a non-protein light absorbing
pigment molecule.
- The five phytochromes differ in their protein component while the non-protein component
exist in the form of two different isomers which are photoreversible:

Pr Phytochrome Red (absorbs red light (660nm))

Pfr Phytochrome Far-red (absorbs far-red light (730nm))

- Plants synthesise phytochromes in the Pr form – absorption of red light converts Pr into Pfr
and absorption of far-red light converts Pfr into Pr.
- White light, including sunlight, contains both red
and far-red light.
- After daylight there is more Pfr. After darkness
there is more Pr.
- Phytochromes regulate: seed germination,
stem elongation, leaf expansion, chlorophyll
formation and flowering.
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Germination:
- Red light triggers germination while far-red inhibits germination, therefore the effects are
reversible.
Flowering:
- The photoperiod (relative length of the day and night) determines time of flowering.
- The ratio of Pr and Pfr present enables the plant to determine the length of day and night.
- Long day plants only flower when day length exceeds a critical value (period of
uninterrupted darkness is less than 12 hours). Pfr stimulates flowering.
- Short day plants only flower when the period of uninterrupted darkness is greater than 12
hours. Pr is required, and any Pfr inhibits flowering.
Greening:
 Changes in form and biochemistry due to exposure to sunlight.

How do phytochromes switch processes on or off?

- Exposure to light causes the molecules to change
form and shape.
- Activated phytochromes then interact with other
proteins, binding to them or disrupt the binding of a
protein complex.
- These signal proteins act as transcription factors, or
activate transcription factors, which bind to DNA
allowing transcription of genes.
- The transcription and translation of proteins results in
the plant’s response to light.

8.3. The Brain

The cerebral hemispheres:
- The outer layer of the brain is called grey matter.
- The cortex at the top of the brain is made mostly of cell
bodies, synapses and dendrites (grey matter). It is
divided into left and right cerebral hemispheres.
Each hemisphere is composed of 4 regions: frontal
lobe, pariental lobe, occipital lobe and temporal
lobe.
- Each lobe interprets and manages its own sensory
inputs. The two cerebral hemispheres are connected by
white matter (nerve axons) called corpus callosum.
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Each cerebral hemisphere is composed of 4 regions:

1. Frontal lobe
2. Parietal lobe
3. Occipital lobe
4. Temporal lobe

Other structures lying directly below

the corpus callosum include:
- Cerebellum: Coordinates
movement and balance. It
receives information from the
primary motor cortex, muscles
and joints.
- Medulla oblongata: Regulates
involuntary body processes e.g.
control of heart rate
(cardiovascular centre), breathing
movements (respiratory centre)
and blood pressure.
- Hypothalamus:
Thermoregulation (maintaining core body temperature at ± 37.8°C). Controls sleep, hunger,
thirst, and blood concentration. Connects directly to the pituitary gland which secretes other
hormones.
- Thalamus: Responsible for routing all
incoming sensory information to the correct
part of the brain (via axons of white matter).
- Hippocampus: Involved in laying down long
term memory.
- Basal ganglia: A collection of neurones
responsible for selecting and initiating stored
programmes for movement.
- Brain stem (reptilian brain): Top of the spinal
column; it extends from midbrain to medulla.
- Mid brain: Relays information to the
cerebral hemispheres, including auditory
information to the temporal lobe and visual
information to occipital lobe.
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The effects of strokes:

- Brain damage caused by a stroke can cause problems with speaking, understanding speech,
reading and writing.
- Some patients can recover some abilities after a stroke, showing the potential of neurones to
change in structure and function (neural plasticity).
- Brain structure remains flexible even in later life & can respond to changes in the environment.

Brain Imaging
 CAT scans (CT scans – Computerised Axial Tomography):
- Use thousands of narrow beam X-rays rotated around the
patient to pass through tissue from different angles.
- Each narrow beam is attenuated (reduced in strength)
according to the density of the tissue in its path.
- The X-rays are detected and used to produce an image of the
brain in which different soft tissues can be distinguished.
- Are cheaper than MRI’s.
- Don’t show which tissues are active; can only show structure,
not function of the brain.
- Used to detect brain disease and monitor changes in tissue over
the course of an illness.

 MRI (Magnetic Resonance Imaging):

- Use 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 field.
- Hydrogen atoms in water are monitored in MRI as there is a
high water content in the tissues under investigation.
- In a scanner: a magnetic field runs down the centre of the tube
in which a patient lies, while another magnetic field is
superimposed on this, which comes from the magnetic
component of high frequency radio waves. The combined fields
cause the direction (axis) and frequency of spin of the hydrogen
nuclei to change, taking energy from the radio waves to do so.
- When the radio waves are turned off, hydrogen nuclei return to their original alignment and
release the absorbed energy – this energy is detected and sent to a computer for analysis.
- Different tissues respond differently to the magnetic field and so produce contrasting signals
and distinct regions in the image.
- Used in: diagnosis of tumours, strokes, brain
injuries and infection of the brain and spine.
 fMRI (Functional Magnetic Resonance Imaging):
- Looks at the function of the different areas of the
brain by following the uptake of oxygen in active
brain areas.
- Deoxyhaemoglobin absorbs the radio wave
signal, whereas oxyhaemoglobin does not.
- Increased neural activity in a brain area results in
an increased demand for oxygen and hence an
increase in blood flow.
- The less radio signal there is absorbed, the
higher the level of activity in that area, so
different areas of the brain will ‘light up’ when
they are active.
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8.3.1. From the eye to the brain

The axons of the ganglion cells that make up the optic nerve pass out of the eye and extend to
several areas of the 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 of the neurones in each optic nerve branch off to the midbrain where they
connect to motor neurones involved in controlling the pupil reflex and eye movement. Audio
signals also arrive at the midbrain so we can quickly turn our eyes in the direction of a visual or
auditory stimulus.

8.4. Visual Development

8.4.1. Axon growth:
- Axons of the neurones from the retina grow to the thalamus where they form synapses with
neurones in the thalamus in a very ordered arrangement. Axons from these thalamus
neurones grow towards the visual cortex in the occipital lobe.
- The visual cortex is made of columns of cells and axons from the thalamus synapse within
these columns.
- Columns are formed before the critical period for development of vision in which dendirites
and synapses are stimulated by light
- During the critical period, axons compete for target cells in the visual cortex. Every time a
neurone fires onto a target cell, the synapses of another neurone sharing the target cell are
weakened and release less neurotransmitter. Synapses not firing will be cut back.
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.
We ‘see’ because our brain processes the image formed from the retina, using past
experience and other sensory inputs. The capacity of the brain to process and interpret the
action potentials that arrive along the optic nerve is acquired during early childhood. Newborn
babies have little ability to interpret information, but this is highly developed by age of 5 or 6. The
experiences the child has determines the way the brain cells are ‘wired up’ during development.

1960s – Hubel and Wiesel carried out important experiments using monkeys and kittens. They
found that if they prevented light reaching the retina of one or both eyes as the young animals
matured, this stopped them developing normal visual abilities. Depriving them of vision at
different stages of development affected different aspects of vision. They concluded that there
were specific ‘windows’ during development, known as critical periods/windows during which
particular types of visual input were needed in order for particular visual capacities to develop
normally.
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8.5. Making sense of what we see

Depth perception:
- Close objects (<30m away) – we depend on the presence of cells in the visual cortex that
obtain information from both eyes at once – the visual field is seen from 2 angles which allows
comparison of the view from one eye to the other. This is stereoscopic vision and it allows
relative position of objects to be perceived.
- Distant objects (>30m away) – the images on our retinas are similar, so visual cues and past
experiences are 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.’
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.

8.6. Learning and memory

Learning is when organisms modify their behaviour as a result of experience. One of the simplest
types of learning is habituation: a decrease in intensity of a response when the same stimulus is
given repeatedly (e.g. humans show habituation when hearing a loud bang repeatedly).
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.

8.6.1. How memories are stored

Memory can be created by altering: the pattern of connections, and
the strength of synapses.
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
repeated stimulation, the siphon no longer withdraws. Habituation
allows animals to ignore unimportant stimuli so that limited sensory,
attention and memory resources can be concentrated on more
threatening or rewarding stimuli.
How is habituation achieved?
With repeated stimulation, calcium ion channels become less
responsive:
1. Less Ca+ ions cross presynaptic membrane into
presynaptic neurone.
2. Fewer synaptic vesicles fuse with presynaptic
membrane.
3. Less neurotransmitter released into synaptic cleft.
4. Less Na+ ion channels open on posysynaptic
membrane.
5. Less Na+ ions flow into postsynaptic membrane.
6. Less or no action potential is triggered in
postsynaptic motor neurone.
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Practical – investigating habituation in pond snails:

1. Collect pond snails of the same species and place them in the same tank. Leave for a few
days to acclimatise.
2. Place one snail in a dish and leave to rest for 5 minutes until active.
3. Gently touch snail between tentacles. Snail will withdraw and then slowly extend again.
4. Repeat stimulus several times with set intervals of < 1min. Record and time the time taken for
the tentacles to be returned to fully extended position.
5. Plot a graph of time against number of stimuli given.

More connection – longer

memory:
Long-term memory storage
involves an increase in the number
of synaptic connections. Repeated
use of a synapse leads to creation of
additional synapses between
neurones.

Sensitisation: the opposite of

habituation. Happens when an
animal develops an enhanced response to a stimulus. Humans can learn by sensitisation. E.g. if
a predator attacks sea slugs, they become sensitised to other changes in their environment and
respond strongly to them. There is a greater calcium ion uptake, more neurotransmitter released,
greater depolarisation and a higher frequency of action potentials.

Nature vs nurture
There’s a long standing interest as to the extent to which the behaviour of animals is determined
by genes or by the environment – that is, the experiences an animal has whilst it develops. The
effect of genes is sometimes known as nature and the effect of the environment as nurture.
We understand today that most patterns of behaviour are determined by the interactions of both.

A behaviour pattern that is shown at the very beginning of an organism’s life is said to be innate,
and is considered to be caused entirely by genes. However, in humans, its environment has
influenced even a newborn baby, as it was developing in the uterus. Newborn babies show
various reflex reactions, such as the startle reflex. This happens when a baby hears a sudden
loud noise, or is dropped a short distance. The baby responds by flinging out arms and legs
and contracting the neck muscles. This response is largely innate but it may also be
influenced by the experiences of the baby while it was 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.

8.6.2. Animal testing – ethical issues

For
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 animals
Only done when necessary – humans
have a greater right to life
Only way to study how a drug affects the
whole body
Against
We have no right to submit animals to
procedures that may cause discomfort or
make their lives unpleasant
There is no need to use animals in
research as there are other ways of
conducting the same investigations
Animals are different to humans – no
certainty that drugs tested on animals will
have the same effect on humans
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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 (e.g. 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 course of action is the one that maximises the overall
happiness in the world. A utilitarian framework allows certain animals to be used in medical
experiments provided the overall expected benefits are greater than the overall expected harms.

8.7. Problems with synapses

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

8.7.1. Dopamine and Parkinson’s disease

Dopamine is a neurotransmitter secreted by neurones, including many located in the midbrain.
The axons of the neurones in this area extend throughout the frontal cortex, brain stem and
spinal cord. Parkinson’s disease occurs when dopamine-secreting neurones in the basal ganglia
die so dopamine is no longer produced, resulting in loss of control of muscular movement.
Symptoms of the disease include stiffness of muscles, tremors, slowness of movement, poor
balance, walking problems, depression and difficulties with speech and breathing.

Treatment for Parkinson’s disease:

- Slowing the loss of dopamine from the brain with the use of drugs like selegiline. This inhibits
enzyme monoamine oxidase, which is responsible for breaking down dopamine in the brain.
- Treating symptoms with drugs. Dopamine itself cannot treat Parkinson's because it cannot
cross into the brain from the bloodstream, but L-dopa (a precursor in the manufacture of
dopamine) can be given. Once in the brain, L-dopa is converted into dopamine, increasing the
concentration of dopamine and controlling the symptoms of the disease.
- Use of dopamine agonists. Dopamine agonists are drugs that activate dopamine receptors
directly. These drugs mimic the role of dopamine in the brain, binding to dopamine receptors
at synapses and triggering action potentials. They are useful in the treatment of Parkinson's
disease since they avoid higher than normal levels of dopamine in the brain. Abnormally high
dopamine levels can have unpleasant side effects.
- Results of gene therapy trials in animals & phase I trials in humans show promise. Genes for
proteins that increase dopamine production and promote growth and survival of nerve cells are
inserted into brain. Cell therapy where proteins themselves are injected is also being trialled.
- New surgical approaches are being trialled, some of which are generating encouraging results.

8.7.2. Serotonin and depression

Serotonin is a neurotransmitter involved in functions including mood, appetite, temperature
regulation, sensitivity to pain and sleep. Neurones that secrete serotonin are situated in the brain
stem and their axons extend into the cortex, cerebellum and spinal cord. A lack of serotonin is
linked to clinical depression. Symptoms include sadness, anxiety, hopelessness, loss of interest
in pleasurable activities, insomnia, restlessness and thoughts of death.
When someone is depressed, fewer nerve impulses than normal are transmitted around the
brain, related to low levels of neurotransmitter production.

The causes are not completely understood, but depression may be multifactorial:
 There may be a genetic element – it runs in families
 Could be environmental – trauma or stress related
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Treatment for depression:

SSRI drugs (selective serotonin reuptake inhibitor) e.g. Prozac, inhibit 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.

8.7.3. How drugs affect synaptic transmission

Clinical depression can be treated with drugs that increase serotonin in the brain. The drug
MDMA (ecstasy) increases the concentration of serotonin in the synaptic cleft by binding to
molecules in the presynaptic membrane that are responsible for transporting serotonin back into
the cytoplasm. This prevents its removal from the synaptic cleft. The drug may also cause the
transporting molecules to work in reverse, further increasing the amount of serotonin outside the
cell. These higher levels of serotonin bring about the mood changes seen in users of the drug. It
is possible that ecstasy has a similar effect on molecules that transport dopamine as well.

Effects of using ecstasy

MDMA can produce feelings of euphoria, friendliness, well-being, enhanced senses and
energy. However, it has many other side effects on the body, causing depression, clouded
thinking, agitation, muscle spasms, hyperthermia, confusion and anxiety. Animal research
shows the regular use of MDMA causes damage to several parts of the brain.
- 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

8.7.3. Better treatments

The Human Genome Project and drug development
The Human Genome Project (HGP) has deciphered the base sequence of the human genome
(all DNA of an organism). 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. 1977 –
Fred Sanger – first DNA sequencing process.

Not everyone responds in the same way to drugs, knowledge of differences in a person’s base
sequence can help understand this. Knowledge of a particular DNA sequence will enable suitable
drugs to be chosen on an individual basis. Issues surrounding the Human Genome Project:
- 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 treatment 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

8.7.4. Using genetically modified (GM) organisms to produce drugs

Genetic modification (artificial introduction of genetic material from another organism) produces
transgenic or genetically modified organisms (GMOs). GM is also known as genetic
engineering, genetic manipulation, or recombinant DNA technology.

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 a 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
- A bacterium that infects the species – genes from plasmid DNA are incorporated into the plant
chromosome when they infect them
- Inserting the vector into the organism using microprojectules: tiny pellets carrying the desired
genes are shot into the plant cells using a particle gun
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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.

E.g. 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

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 into a virus,
used to incorporate genes into DNA of
plant 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
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Benefits of GMOs Risks of GMOs

Pest resistant crop plants – reduces the use
of pesticides – increases yield, reduces risk
of harming beneficial insects
Herbicide resistant crops allow the herbicide
to kill weeds but not crops
Crop plants can be modified to produce high
quantities of nutrients
Could benefit human health
Could help to feed the developing world
GM crops are more cost-effective
Genes inserted into a crop might spread to
others – cause changes in the genotypes of
plant populations – adversely affect other
organisms in an ecosystem
Pests might develop resistance through natural
selection to the substances in GM crops,
resulting in ‘super-pests’ or ‘superweeds’
Consuming foods containing GMOs can be
considered harmful to health
Environmental concerns – increased chemical
use in crops
Could damage organic farmers
Raises ethical conflicts over the control of food
production

Genetically modified animals:

Several techniques can be used to artificially introduce genes into animal cells. For example:
- Retroviruses: 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
- Microinjection: DNA injected directly into nucleus of a fertilised egg using a micropipette (only
successful in 1% of embryos)

Concerns about genetic modification:

The main health concerns that have been raised are:
- Transfer of antibiotic-resistance genes to microbes -
- Formation of harmful products by new genes
- Transfer of viruses from animals to humans.

The main environmental concerns about GMOs are:

- Transfer of genes to non-GM plants (cross-pollination)
- Increased chemical use in crops.
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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; affects speed of impulse, 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 / not enough depolarisation 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 neurotransmitter and 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 & release neurotransmitter into 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