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Biology Notes: Topic 8

A2 BIOLOGY UNIT 5 (topic 8) EDEXCEL NOTES Page 1

Topic 8 Grey Matter

The Nervous System and Nerve ImpulsesAll our senses, emotions, memories and thoughts are dependent on nerve impulses. The nervous system

is highly organised, receiving, processing and sending out information, as we saw with temperature and

control of heart rate.

What are nerve cells like?

A neurone is a single cell and a nerve is a more complex structure containing a bundle of the axons of

many neurones surrounded by a protective covering. The nervous system is organised as so:

There are different types of neurones but they all have the same basic characteristics. The cell body

contains the nucleus and cell organelles within the cytoplasm. There are two types of thin extensions

from the cell body:

Very fine dendrites conduct impulses towardsthe cell body A single long process, the axon, transmits impulses away fromthe cell body

Nervous system(NS)

Central nervoussystem (CNS)

Peripheralnervous system

Somaticnervous system

Autonomicnervous system

Sympatheticnervous system

Parasympatheticnervous system

Consisting ofsensory nerves, carrying

sensory information from the receptors to

the CNS, and motor nerves, carrying the

motor commands from the CNS to the

effectors

Consisting of the

brain and the

spinal cord

Involuntary and stimulates smooth

muscle, cardiac muscle and glands.

Voluntary and stimulates

skeletal muscle

Prepares body for

fight or flight

responses

Prepares body for

rest and digest


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There are three main types of neurone:

Motor neuronesthe cell body isalways situated within the central

nervous system (CNS) and the axon

extends out, conducting impulsesfrom the CNS to effectors. The axons

of some motor neurones can be

extremely long, such as those that run

the full length of the leg. Motor

neurons are also known as effector

neurones

Sensory neuronesthey carryimpulses from sensory cells to CNS

Relay neuronesthese are foundwithin the CNS. They can have a largenumber of connections with other

nerve cells. Relay neurones are also

known as connector neurones and as

interneurones.

Reflex ArcsNerve impulses follow routes or pathways through the nervous system. Some nerve pathways are

relatively simple, for example the knee-jerk reflex involves just two neurones: a sensory neurone

communicating directly with a motor neurone to connect receptor cells with effectors cells. These simple

pathways are known as reflex arcs and are responsible for our reflexes.

But most nerve pathways are not simple but have numerous neurones within the CNS. A sensory

neurone connects to a range of neurones within the CNS and passes impulses to the brain to produce a

coordinated response. Even in reflex arcs there are additional connections within the CNS to ensure a

coordinated response. Some synapses with motor neurones will be inhibited to ensure that the desired

response occurs.

1. Receptors detect a stimulus and generate a nerve impulse2. Sensory neurones conduct a nerve impulse to the CNS along a sensory pathway3. Sensory neurones enter the spinal cord through the dorsal route4. Sensory neurone forms a synapse with a relay neurone5. Relay neurone forms a synapse with a motorneurone that leaves the spinal cord through the

ventral route

6. Motor neurone carries impulses to an effector which produces a response. For example, thebicep contracts to raise the arm away from the flame.

THE PUPIL REFLEX

When the eye is exposed from dark to light, there is a reflex arc causing a change in the diameter of their

pupils.


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HOW THE MUSCLES OF THE IRIS RESPONDS TO LIGHT

The iris controls the size of the pupil. It contains a pair of antagonistic muscles: radical and circular

muscles. These are controlled by the autonomic nervous system. The radial muscles are like spokes of a

wheel, and are controlled by a sympathetic reflex. The circular muscles are controlled by a

parasympathetic reflex. The sympathetic reflex dilates and theparasympathetic reflex constricts thepupil.

CONTROLLING PUPIL SIZE

High light levels striking thephotoreceptors in the retina cause nerve impulses to pass along the optic

nerve to a number of different sites within the CNS, including a group of coordinating cells in the

midbrain. Impulses from these cells are sent alongparasympathetic motor neurones to the circular

muscles of the iris, causing them to contract. At the same time the radial muscles relax. This constricts

the pupil, reducing the amount of light entering the eye.

Atropine

The plant deadly nightshade (Atropa belladonna) is the source of the drugatropine which was used inthe Middle Ages by some women to make theirpupils dilate. This was thought to be attractive tomen, hence belladonna, which means beautiful lady in Latin, is the species name.

Atropine inhibits parasympathetic stimulation of the iris, so the circular muscles of the iris relax.

Todayacetylcholine antagonist is used to dilate the pupils for an eye examination.


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How nerve cells transmit impulses

Much of the work done to establish what happens in a nerve fibre was carried out on the giant axons of

the squid. Their large size makes them easier to work with. Hodgkin, Huxley and Eccles carried out

this work in the 1940s and 1950s, and they eventually won a Nobel Prize for their efforts.

INSIDE A RESTING AXON

All cells have apotential difference across their surface membrane. At first both electrodes in the

bathing solution, there is no potential difference. But if one of the electrodes is pushed inside the axon,

then the oscilloscope shows that there is a potential difference of around -70 mV. The inside of the axon

is more negative and so the membrane is said to bepolarised. -70 mV is known as the resting potential.

WHY IS THERE A POTENTIAL DIFFERENCE?

The distribution of ions found in the solutions inside and outside a squid giant axon is unequal. Thisis achieved by the action ofsodium-potassium pumps in the cell surface membrane of the axonwhich act against the concentration gradient and are driven by energy supplied by the hydrolysis ofATP. The organic anions are large and stay within the cell, so Cl - move out of the cell to help balancethe charge across the cell surface membrane.

The resting potentialOnce the concentration gradients are established and there is no difference in charge between theinside and outside of the membrane, K+ diffuse out of the neurone, through potassium channels,down the potassium concentration gradient. The membrane ispermeable to potassium ions but is

virtually impermeable to sodium ions. There is some leakage of Na+ into the neurone down theconcentration gradient but it does not balance the difference in charge across the membrane causedby the movement of K+. The difference in charge caused by diffusion of K+ causes a potentialdifference across the membrane.

Why is the resting potential of the axon -70mV?Two forces are involved and result from the concentration gradient generated and the electricalgradient due to the difference in charge. K+ diffuse out of the cell due to the concentration gradientand this causes the electrical gradient as there is a larger potential difference across the cell. Theincreased negative charge created inside the cell as a consequence attracts K+ across the membrane.When the potential difference is about -70mV, the electrical gradient balances the chemicalgradient. There is no net movement of K+, maintaining the resting potential of -70mV. Anelectrochemical equilibrium for potassium is in place and the membrane ispolarised.


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WHAT HAPPENS WHEN A NERVE IS STIMULATED?

Neurones are electrically excitable cells, meaning that the potential difference across their cell surface

membrane changes when they are conducting an impulse.

If an electrical current above a threshold level is applied to the membrane, it causes a massive change in

the potential difference. The potential difference across the membrane is locally reversed, making the

inside of the axon positive and the outside negative. This is depolarisation .

The potential difference becomes +40mV or so for a very brief instant, lasting about 3ms, before

returning to the resting state, as shown by the oscilloscope trace. It is important that the membrane is

returned to the resting potential as soon as possible in order that more impulses can be conducted. This

return to a resting potential of -70mV is known as repolarisation. The large change in the voltage across

the membrane is called action potential.

WHAT CAUSES AN ACTION POTENTIAL?

When threshold stimulation occurs, an action potential is caused bychanges in the permeability of thecell surface membrane to 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 asvoltage-dependent gated channels. There are three stages in

the generation of an action potential.

1. DepolarisationWhen a neurone is stimulated some depolarisation occurs. The change in the potential differenceacross the membrane causes a change in the shape of the Na+ gate, opening some of the

voltage-dependent sodium ion channels. As the sodium ions flow in, depolarisation increases,

triggering more gates to open once a certain potential difference threshold is reached. The

opening of more gates increases depolarisation further. This ispositive feedback; a change

encourages further change of the same sort. It leads to a rapid opening of all the Na+ gates. This

means there is no way of controlling the degree of depolarisation of the membrane; action

potentials are either there or they are not. This is referred to as all-or-nothing.

There is a higher concentration of sodium ions outside of the axon, so sodium ions flow rapidly

inwards through the open voltage-dependent Na+ channels, causing a build-up of positive

charges inside. This reverses the polarity of the membrane. This is where the potential differencereaches +40mV.


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2. RepolarisationAfter about 0.5ms, the voltage-dependent Na+ channels spontaneously close and Na+

permeability of the membrane returns to its usual very low level. Voltage-dependent K+

channels open due to the depolarisation of the membrane. As a result, potassium ions move out

of the axon, down the electrochemical gradient, and the inside of the cell once again becomesmore negative than the outside. This is the falling phase of the oscilloscope trace.

3. Restoring the resting potentialThe membrane is nowhighly permeable to potassium ions, and more ions move out than

occurs at resting potential, making the potential difference more negative than the normal

resting potential. This is known as hyperpolarisation of the membrane. The resting potential is

re-established byclosing of the voltage-dependent K+ channels and potassium ion diffusion into

the axon.

Ifhundreds of action potentials occur in the neurone, the sodium ion concentration inside the cell rises

significantly. The sodium-potassium pumps start to function, restoring the original ion concentrations

across the cell membrane. If a cell is not transmitting many action potentials, these pumps will not have

to be used very frequently. At rest there is some slow leakage of sodium ions into the axon. These

sodium ions are pumped back out of the cell.


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HOW IS THE IMPULSE PASSED ALONG AN AXON?

When a neurone is stimulated, the action potential generated

does not actually travel along the axon but triggers a

sequence of action potentials along the length of the axon.

As part of the membrane becomes depolarised and repolarised,

it triggers another action potential. These events are 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. This is the

refractoryperiod. It lasts until all the voltage-dependent

sodium and potassium channels have returned to their normal

resting state, and the resting state is restored. The refractory

period ensures that impulses only travel in one direction.

ARE IMPULSES DIFFERENT SIZES?

A very strong light will produce the same size action

potential in a neurone coming from your eye as does a dim

light. A stimulus must be above a threshold level to generate

an action potential. The all-or-nothing effect for action

potentials means that the size of the stimulus, assuming it is

above the threshold, has no effect on the size of the action

potential.

Different mechanisms are used to communicate the intensity

of the stimulus. The size of the stimulus affects the frequency

of impulses and 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.

SPEED OF CONDUCTION

1. At resting potential there ispositive charge on the outside of

the membrane and negative

charge on the inside, with high

sodium ion concentration outside

and high 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 in the

membrane. Sodium ions move to

the adjacent polarised region

causing a change in the electrical

charge across this part of the

membrane

3. The change in potentialdifference 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 sodium ion

channels close and voltage-

dependent potassium ion

channels open. Potassium ions

leave the axon, repolarising the

membrane. The membrane

becomes hyper polarised

4. A third action potential isinitiated by the second. In this

way local electric currents causethe nerve impulse to move along

the axon. At the site of the first

action potential, potassium ions

diffuse back into the axon,

restoring the resting potential


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The speed of the nervous conduction is in part determined by the diameter of the axon. In general, the

wider the diameter of the axon, the faster the impulse will be. The normal axons of a squid, with a

diameter of 1-20 m, conduct impulses at around 0.5 ms -1, whereas the giant axons, with a diameter of

1000 m, conduct nearer to 100ms-1. The nerve axons of mammals are much narrower than the squid

giant axons, but impulses travel along them at up to 120ms-1. This apparent anomaly is due to the

presence ofmyelin sheath around mammalian nerve axons.

The myelin sheath acts as an electrical insulator along most of the axon, preventing any flow of ions

across the membrane. Gaps known as nodes of Ranvier occur in the myelin sheath at regular intervals,

and these are the only places where depolarisation can occur. As ions flow across the membrane at one

node during depolarisation, a circuit is set up which reduces the potential difference of the membrane at

the next node, triggeringaction potential. In this way, the impulse effectively jumps from one node to

the next. This is much faster than a wave of depolarisation along the whole membrane. This jumping is

called salutatory conduction.

How does a nervous impulse pass between cells?A synapse is the place where two neurones meet. The cell do not touch, there is a small gap called the

synaptic cleft.

SYNAPSE STRUCTURE

A nerve cell may have very large numbers of synapses with other cells, as many as 10,000 in the brain.This is important in enabling the distribution and processing of information.

The synaptic cleft separates thepresynaptic membrane of the stimulation neurone from the

postsynaptic membrane of the other cell. The gap is about 20-50 nm and a nerve impulse cannot jump

across it. In the cytoplasm at the end of the presynaptic neurone there are numerous synaptic vesicles

containing a neurotransmitter.

1. An action potential arrives2. The membrane depolarises. Calcium ion channels open.

Calcium ions enter the neurone

3. Calcium ions cause synaptic vesicles containingneurotransmitter to fuse with the presynaptic membrane4. Neurotransmitter is released into the synaptic cleft5. Neurotransmitter binds with receptors on the

postsynaptic membrane. Cation channels open. Sodium

ions flow through the channels

6. The membrane depolarises and initiates an actionpotential

7. When released the neurotransmitter will be taken upacross the presynaptic membrane (whole or after being

broken down), or it can diffuse away and be broken

down


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HOW DOES THE SYNAPSE TRANSMIT AN IMPULSE?

The arrival of an action potential at the presynaptic membrane causes the release of the

neurotransmitter into the synaptic cleft. The neurotransmitter diffuses across the gap, resulting in events

that cause the depolarisation of the postsynaptic membrane, and hence thepropagation of the impulse

along the next cell. The presynaptic cell expends a considerable amount ofenergy to produceneurotransmitter and put it into vesicles, ready for transport out of the cell. Many neurotransmitters have

been discovered, with 50 identified in the human central nervous system.Acetylcholine was the first to

be discovered.

There are threestages leading to the nerve impulse passing along the postsynaptic neurone:

Neurotransmitter release Stimulation of the postsynaptic membrane Inactivation of the neurotransmitter

NEUROTRANSMITTER RELEASE

When the presynaptic membrane is depolarised by an

action potential, channels in the membrane open and

increase the permeability of the membrane to calcium

ions. These calcium ions are in greater concentration

outside the cell, so theydiffuse across the membrane

and into the cytoplasm.

The increased calcium ions concentration causes synaptic vesicles containing acetylcholine to fuse with

the presynaptic membrane and release their contents into the synaptic cleft byexocytosis.

STIMULATION OF THE POSTSYNAPTIC MEMBRANE

The neurotransmitter takes about 0.5 ms 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 part of the acetylcholine molecule. The acetylcholine molecule binds

to the receptor, changing the shape of the protein, opening cation channels and making the membrane

permeable to sodium ions. The flow of sodium ions across the postsynaptic membrane causes

depolarisation, and if there is sufficient depolarisation, an action potential will be produced and

propagated along the postsynaptic neurone.

The extent of the depolarisation will depend on the amount of acetylcholine reaching the postsynaptic

membrane. This will depend in part on the frequency of impulses reaching the presynaptic membrane. A

single impulse will not usually be enough and several impulses are usually required to generate enough

neurotransmitter to depolarise the postsynaptic membrane. The number offunctioning receptors in the

postsynaptic membrane will also influence the degree of depolarisation.


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INACTIVATION OF THE NEUROTRANSMITTER

Some neurotransmitters are actively taken up by the presynaptic membrane and the molecules are used

again. Other neurotransmitters rapidlydiffuse away from the synaptic cleft or they are taken up byother

cells of the nervous system. In the case of acetylcholine, a specific enzyme at the postsynaptic membrane,

acetylcholinesterase, breaks down the acetylcholine so that it can no longer bind to receptors. Some of

the breakdown products are then reabsorbed by the presynaptic membrane and reused.

What is the role of synapses in nerve pathways?

CONTROL AND COORDINATION

Synapses have two roles:

Control of nerve pathways, allowingflexibility of response Integration ofinformation from different neurones, allowing a co-ordinated response

The postsynaptic cell receives input from many synapses at the same time. The overall effect will

determine whether the postsynaptic cell generates an action potential. Two main factors affect the chance

of the postsynaptic membrane depolarising:

The type of synapse The number of impulses received

Some synapses help stimulate an action potential, excitatory synapses, whereas other inhibit the

postsynaptic membrane from depolarising, inhibitory synapses. There might be numerous excitatory

and inhibitory synapses and so the action potential relies on the balance of these synapses at any given

time.

TYPES OF SYNAPSE

EXCITATORY SYNAPSES

Excitatory synapses make the postsynaptic membrane more permeable to sodium ions. A single

excitatory synapse does not depolarise the membrane enough to cause an action potential but ifseveral

impulses arrive at the same time in a short time frame, there is sufficient depolarisation via the release

ofneurotransmitter to produce an action potential. Each impulse adds to the effect of the others,

known as summation.

There are two types of summation:

Spatial summationo Impulses are from different synapses, usually from different neurones. The number

of different sensory cells stimulated can be reflected in the control of the response


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Temporal summationo Several impulses arrive at a synapse having travelled along a single neurone one after

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

postsynaptic membrane

INHIBITORY SYNAPSES

Inhibitory synapses make it less likely that an action potential will occur in the postsynaptic membrane.

The neurotransmitter from these synapses openchannels for chloride and potassium ions in the

postsynaptic membrane, moving through the channels down their diffusion gradient. Chloride ions will

move into the cell and the potassium ions will move out. Thus, there is a greater potential difference, like

hyperpolarisation. This makes subsequent depolarisation less likely.

COMPARING NERVOUS AND HORMONAL CO-ORDINATION

The nervous system is not the only means by which the activities of the body can be co-ordinated.Hormones, which secrete into the bloodstream by endocrine glands, act as a means ofchemicalcommunication with target cells.

Many hormones are produced steadily over long periods to control long-term changes in the bodysuch as growth and sexual development.Adrenaline is more short term in its action, but takes longerthan the nervous system to produce a response.

Nervous control Hormonal control

Electrical transmission by nerve impulsesand chemical transmission at synapses

Chemical transmission through the blood

Fast acting Slower acting

Usually associated with short-term changes Can control long-term changes

Action potentials carried by neurones withconnections to specific cells

Blood carries the hormone to all cells, butonly target cells are able to respond

Response is often very local Response may be widespread


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CO-ORDINATION IN PLANTS

Plants lack a nervous system so must use chemicals to co-ordinate growth, development andresponses to the environment. These chemicals are calledplant growth substances. They arechemicals produced in the plant invery lowconcentrations and transported to where they cause a

response.

The Discovery of AuxinsCharles Darwin completed experiments onphototropism, which are considered to be some of theearliest work on the effects of auxin. Their experiments showed that an oat coleoptiles with its topcut off stops bending towards the light. Replacing the top starts growth towards the light again. Theyconcluded that some influence was transmitted from the shoot top to the lower part of theseedlings, causing them to bend. Boysen-Jensen and Went would later identify the nature of theinfluence.

A chemical made in the top passed down the coleoptiles. This was demonstrated byremoving thetip, placing it on a small block ofagar jelly and putting the agar on top of the cut end of the

coleoptile. The coleoptile started to grow again; a chemical produced by the top had diffused downthrough the agar jelly. Went provided more evidence by placing the agar blocks on one side of the cutcoleoptile top in the dark; this caused the coleoptile to curve away from the side receiving thechemical messenger from the agar. The chemical was identified as the auxin, indoleacetic acid(IAA) and its major function is to stimulate growth.

Went measured the amount of chemical being produced on the shaded and lit side of the shoot andfound that the total amount did not change compared to a shoot illuminated from all sides; insteadmore auxin had passed down the shaded side. The increased concentration of auxin causedelongation of the shaded side. Thus, the shoot grows towards the light. This explanation is known asthe Cholodny-Went model.

The model has been widely criticised due to the small sample sizes and the difficultyofmeasuring the small concentrations. However, many plant physiologists maintain that the basicfeatures of the model still hold. New techniques being used to study tropisms include the use of

genetically modified plants that produce fluorescent proteins in the presence of auxin, making itpossible to visualise the location of the auxin.

Auxins are synthesised in actively growing plant tissues (meristems). The auxins are activelytransported away to where they bring about a range of responses through their effect on cellelongation. By binding with receptorson the plasma membranes in the zone of shoot elongation,auxins produce second messenger signal molecules that bring about changes in gene expression.

Transcription of genes coding for enzymes then result s in metabolic changes. It is through that theauxin causes acidificationof the cell wall by indirectly stimulating the activity ofproton pumps,moving H+ out of the cytoplasm. The low pH is thought to affect an enzyme in the cell walls thatcauses bonds between the cellulose microfibrils to break, expanding the cell wall. The increasedpotential difference across the membrane enhances uptake of ions into the cell. This causes the

uptake of water, resulting in cell elongation.


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Reception of Stimuli

How does light trigger nerve impulses?

RECEPTORS

Stimuli are detected byreceptor cells that send electrical impulses to the central nervous system. Many

receptors are spread through the body, but some are grouped together into sense organs, like the eye.

These help toprotect the receptor cells and improve their efficiency; structures within the sense organ

ensure that the receptor cells are able to receive the appropriate stimulus. The receptor cells that detectlight are found in the eye. The lens and cornea refract the light so that it focuses on the retina where the

photoreceptor cells are located.

More than just shoot elongation

Auxins have many other effects in plants. Theyinhibit growth of side branches down the plant (apicaldominance). This effect can be seen if the growing tip at the top of a plant (apical meristem) isremoved. The side branches down the plant will start to grow. Auxins also initiate growth of lateral

roots, fruit development and leaf fall.

Manysynthetic auxins have been produced for agriculture. 2,4-dichlorophenoxy acetic acid (2,4-D)is an effective herbicide. Monocotyledons, inactivate synthetic auxins whereas in dicotyledons the auxinsaccumulate in cells, cuasing rapid growth that kills the plant. Hence why it can be sprayed to kill weedsbut not grass.

Commercial fruit growers spray plants with synthetic auxins to induce fruiting. This means that the fruitwill be seedless due to the lack of pollination. Auxin is also used to help initiate rooting of currings forplant propagation. Agentorange was a mixture of synthetic auxins, seen used during the Vietnam

War to defoliate the rainforest.

Different types of receptors

Receptors can be cells that synapse with a sensory neurone, or can themselves bepart of aspecialised sensoryneurone, like the temperature receptors in the skin.

Type of receptor Stimulated by Examples of role in body

Chemoreceptors Chemicals Taste, smell, etc.

Mechanoreceptors Pressure, force Balance, touch, hearing, etc.Photoreceptors Light Sight

Thermoreceptors Temperature Temperature control, awareness of surroundings

Except for photoreceptors, the receptors all work in a similar manner. At rest, the cell surfacemembrane has a negative resting potential. Stimulation of the receptor causes depolarisation of thecell. The stronger the stimulus, the greater the depolarisation. When depolarisation exceeds thethreshold, it triggers an action potential. This is either relayed across the synapse usingneurotransmitters or passed directly down the axon of the sensory nerve.


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PHOTORECEPTORS

The retina contains rods and cones. Cones allow colour vision in bright light whereas rods only give

black and white vision. However, unlike cones, rods work in dim light as well as in bright light. In

the centre of the retina, there are only cones. This area allows people to pinpoint accurately the sourceand detail of what they are looking at. The remainder of the retina have a rod-cone ratio of about 20-1.

Threelayers of cells make up the retina. The rods and cones synapse with bipolar neurone cells, which

in turn synapse with ganglion neurones, whose axons together make up the optic nerve. Light hitting

the retina has to pass through the layers of neurones before reaching the rods and cones.

The most common cause of blindness in the UK

The central part of the retina (macula) receives light entering the yes from straight ahead. The delicate

cells of the macula sometimes becomes damaged from causingprogressive deterioration of sight. Age-related macular degeneration is the most common cause of blindness in the UK. A drug, Lucentis, wasapproved for treatment of thewet type of the condition in 2008. The drug binds to a protein growthfactor, stopping the growth ofnew abnormal blood vessels under the retina that leak fluid and blood.However, only10% of cases are the wet type. The more common dry type is caused by accumulation offatty deposits beneath the retina which cause it to dry out.


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HOW DOES LIGHT STIMULATE PHOTORECEPTOR CELLS?

In rods and cones, aphotochemical pigmentabsorbs the light resulting in a chemical change. In

rods, the molecule is a purple colour and called rhodopsin. The rod cell has an outer and inner

segment; these contain many layers offlattened vesicles. The rhodopsin molecules are located in the

membranes of the vesicles.

IN THE DARK

In the dark, sodium ions flow into the outer segment through non-specific cation channels. The

sodium ions move down the concentration gradient into the inner segment where pumps continuously

transport them backout of the cell. The influx of Na+ produces a slight depolarisation of the cell. The

potential difference across the membrane is about -40mV. This slight depolarisation triggers the release

of a neurotransmitter, glutamate, from the rod cells. In the dark, rods release this neurotransmitter

continuously. The neurotransmitter binds to the bipolar cell, stopping it depolarising.

IN THE LIGHT

When light falls on the rhodopsin molecule, it breaks down into retinal and opsin, non-protein and

protein compounds. The opsin activates a series ofmembrane-bound reactions, ending in hydrolysis

of a molecule attached to the cation channel in the outer segment. The breakdown of this molecule

results in the closing of the cation channels. The influx of Na+ into the rod decreases, while the inner

segment continues to pump Na+ out. Thus, the insider of the cell is more negative and becomes

hyperpolarised, preventing the release of the glutamate. The lack of glutamate results in depolarisation

of the bipolar cell. The neurones that make up the optic nerve are also depolarised and respond by

producing an action potential.

Once the rhodopsin has been broken down, it is essential that it is rapidly converted back to its original

form so that subsequent stimuli can be perceived. Each individual rhodopsin molecule takes a few

minutes to do this. The higher the light intensity, the more rhodopsin molecules are broken down and

the longer it can take for all the rhodopsin to reform, up to 50 minutes. The reforming of rhodopsin isdark adaptation.


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Plants can also detect and respond to environmental cues

Plants contain several families of photoreceptors, one of which are phytochromes, which absorb red

and re-red light. Five different phytochromes have been identified.

Phytochromes

A phytochrome molecule consists of aprotein component bonded to a non-protein light-absorbingpigment molecule. The five phytochromes differ in theirprotein component. The non-protein

component exists in two forms, which are different isomers:

Prphytochrome red; absorbs red light (660nm) Pfrphytochrome far-red; absorbs far-red light (730nm)

These two isomers arephotoreversible. Plants synthesise phytochromes in the Pr form; absorption of

red light converts Pr into Pfr. Absorption offar-red light converts Pfr back into Pr. In sunlight Pr is

converted into Pfr, and Pfr into Pr. The former reaction dominates in sunlight because more red than far-

light is absorbed. Pfr accumulates in the light whereas, in the dark, Pfr is slowly converted to Pr.

PHYTOCHROMES TRIGGER GERMINATION

Phytochromes were discovered through germination experiments. Experiments with lettuce indicate

that a flash of red light will trigger germination, but if followed by a flash of far-red light, germination is

inhibited. When repeated, the same effect can be observed. This suggests that the effects of red light and

far-red light are reversible. The finial flash of light determines whether germination occurs. Red light

is particularly effective at triggering germination whereas far-red light seems to inhibit germination.

Why you should eat your carrots

Poor night vision, sometimes called night blindness, has been known for many years to be one of thesymptoms of the disease caused by a shortage of vitamin Ain the diet. Retinal, a derivative of vitamin

A, is part of the rhodopsin found in rods. A shortage of vitamin A leads to a lack of retinal and thus

rhodopsin, which means poor vision in low light conditions.

Carrots are a good source of vitamin Aand thus why it is said that you can see in the dark if you eatcarrots.

Red LightRed Light

Far-Red Light

Far-Red Light

Development

Processes

Reverts in the Dark


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When lettuce seeds are exposed to red light, Pr is covered to Pfr, stimulating responses that lead to

germination. In lettuce seeds kept in the dark, no Pr converts into Pfr. The seeds do not germinate

because it is the appearance of Pfr that triggers stimulation. When exposed to far-red light, Pfr is

converted back to Pr, inhibiting germination.

PHOTOPERIODS, FLOWERING AND PHYTOCHROMES

Thephotoperiod is the environmental cue that determines time of flowering. The ratio of Pr to Pfr in a

lplant enables it to determine the length of day and night. Long winter nights give ample time for Pfr to

convert back to Pr, so that by sunrise all phytochrome will be Pr. Summer nights may not be long enough

to do so, so some Pfr, may still be present in the morning.

LONG-DAY PLANTS

Long-day plants only flower when day length exceeds a critical value. They flower when the period off

uninterrupted darkness is less than 12 hours. They need Pfr to stimulate flowering.

SHORT-DAY PLANTS

Short-day plants tend to flower in spring or autumn when the period of uninterrupted darkness is

greater than 12 hours. They need long hours of darkness to convert all Pfr to Pr. Pfr inhibits flowering in

short-day plants. In most short-day plants, a flash of red light in the middle of the dark period negates

the effect of the dark period.

PHYTOCHROME AND GREENING

In light, phytochromespromote the development ofleaves, leaf unrolling and the production of

pigments. They can inhibit processes like elongation of internodes.

HOW DO PHYTOCHROMES SWITCH PROCESSES ON OR OFF?

Exposure to light causes phytochrome molecules to change shape. Each activated phytochrome then

interacts with other proteins; the phytochromes maybind to the protein or disrupt the binding of a

protein complex. These signal proteins may act as transcription factors or activate transcription factors

that bindto DNAto allow transcription of light-regulated genes. The transcription and translation of

proteins result in the plants response to light.


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OTHER PHOTORECEPTORS

Scientists working with a mutant member of the cabbage family have discovered at least three pigments

used by plants to detect blue light, including phototropins that determine phototropic responses.

Plants detect other environment cues

GRAVITY

Light cannot be the cue for the shoot to grow upwards and the root to grow downwards as the seed is

more than a short distance under the soil. The stimulus for this is gravity. The response ensures that

developing shoots reach the light while roots grow in the soil.

TOUCH AND MECHANICAL STRESS

It is thought that the mechanical stimulus activates signal molecules whose end result is the activation

of genes that control growth. When touched, specialised cells lose potassium ions. Water follows by

osmosis and the cells become flaccid, so no longer support the leaf and keep it upright.

The BrainTHE CEREBRAL HEMISPHERES

From the top down, the cortex of the brain can been seen. It is grey and highly folded, composing mainly

ofnerve cell bodies, synapses and dendrites. It is also known as the grey matter. The cortex is the

largest region of the brain. It is positioned over and around most other brain regions. It is divided into the

left and right cerebral hemispheres. The two cerebral hemispheres are connected by a broad band of

white matter (nerve axons), called the corpus callosum. The hemispheres are divided into lobes.

Frontal lobe Parietal lobe Occipital lobe Temporal lobe


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Component Function

Frontal lobe Concerned with the higher brain functions like decision making, reasoning, planningand consciousness of emotions. It is responsible for the formation of associationsand ideas.

Parietal lobe Concerned with orientation, movement, sensation, calculation, recognition and

memoryOccipital lobe Concerned with vision, colour, shape recognition and perspective

Temporal lobe Concerned with hearing, sound recognition, speech and memory

Thalamus Responsible for routing incoming sensory information to the correct part of thebrain

Hypothalamus Monitors core body temperature and skin temperature. Controls sleep, thirst andhunger. Also acts as an endocrine gland (antidiuretic hormone) and links to thepituitary gland

Hippocampus Long-term memory

Cerebellum Responsible for balance, co-ordinating movements, receiving information from theprimary motor cortex, muscles and joint, checks motor programmes

Midbrain Relays information to the hemispheres

Medullaoblongata

Regulates body processes like heart rate, breathing and blood pressure

Basal ganglia Responsible for selecting and initiating stored programmes for movement

Discovering the function of each brain regionUntil recently, neuroscientists were only able to study the brain by looking at pathological specimens,

by examining the effect of damage to particular areas of the brain, usinganimal models and studying

human patients during surgery. Individuals with brain damage still provide valuable information but

neuroscientists now have a wide range ofnon-invasive imagining techniques.

STUDIES OF INDIVIDUALS WITH DAMAGED BRAIN REGIONS

Studying the consequences ofaccidental brain damage can determine the functions of certain regions

of the brain. Researchers have also studied the consequences of injuring or destroying neurones to

produce lesions in non-human animal models, and the consequences of the removal of brain tissue.

THE STORY OF PHINEAS GAGE

Gage was the foreman of a railway construction company who was popular and responsible. He was

working with dynamite when an explosion propelled a three and a half foot long iron bar through his

head. He did not die but most of the front part of the left hand side of his brain was destroyed. After the

accident, hispersonality changed where he became nasty, foul-mouthed and irresponsible. He wasimpatient and obstinate, unable to complete any plans for future action. He died 12 years later.

Harvard University have used photographs and X-rays to come up with computer graphics showing that

it is highly probable that the accident severed connections between the midbrain and frontal lobes.

Thus, the reduced ability to control his emotional behaviour was related to damage at this site.

THE STRANGE CASE OF LINCOLN HOLMES

A car crash left Holmes with damage to an isolated part of his temporal lobe and now he cannot

recognise a face. He cansee facial features but theyall appear as a jumble, which he is unable to put

all the component parts together. He cannot even recognise a photograph of himself. This has revealed

that recognition of faces is at least partly carried out by a specific face recognition unit in the temporal

lobe.


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THE EFFECTS OF STROKES

Brain damage caused by a stroke can cause problems with speaking, understanding speech, reading

andwriting. Paul Broca concluded that lesions in a small cortical area in the left frontal lobe were

responsible for deficits in language production.

Some patients can recover some abilities after a stroke, showing that neurones have the potential to

change in structure and function, known as neural plasticity. The brains structure and functioning is

affected by both nature and nurture, remainingflexible even later in life.

BRAIN IMAGING

CT SCANS

Computerised Axial Tomographywas developed in the 1970s in order to view images of soft tissue.

CT scans use thousands of narrow-beam X-rays to pass through the tissue from different angles. Each

narrow bean is attenuated according to the density of the tissue in its path. The X-rays are detected and

used to make apicture of slices of the brain.

CT scans only give a still image meaning that it is used to look at structures rather than functions of the

brain. They can be used to detect brain disease but small structures cannot be distinguished.

MRI

Magnetic resonance imaging uses a magneticfield and radio waves to detect soft tissues. The atoms

line up with the direction of the magnetic field. Hydrogen atoms in water are monitored as they have

the strong tendency to line up with the magnetic field and there is a high water content.

A magnetic component of high frequency radio waves is superimposed onto a magnetic field causing

the direction and frequency of spin of the hydrogen nuclei to change. The nuclei take energy from the

radio waves, so when there are no more radio waves, the hydrogen nuclei return to their original

alignment and release energy. The energy is detected and sent to a computer, which produces image

slices. Different tissues respond differently, producing contrasting signals and distinct regions in the

image. MRI is used to diagnose tumours, strokes, brain injuries and infections of the brain and

spine. It can produce much more detailed images than CT scans can.

FMRI

Functional Magnetic Resonance Imaging can provide information about the brain in action. It is used to

study human activities like memory, emotion, language and consciousness.

fMRI records the uptake of oxygen in active brain areas as deoxyhaemoglobin absorbs the radio

wavesignalbutoxyhaemoglobin does not. Increased neural activity in the brain results in an increase

in blood flow for oxygen, so there is an increase in oxygaemoglobin. The less radio signal there is

absorbed, the higher the level of activity.

From the eye to the brainThe axons of the ganglion cells that make up the optic nerve pass out of the eye and extend to several

areas of the brain, including the thalamus. Before reaching the thalamus, some neurones in each optic

nerve branch off to the midbrain to connect to motor neurones involved in controlling the pupil reflex

and movement of the eye. Audio signal arrive at the midbrain to turn our eyes in the direction of a visualor auditory stimulus.


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Visual DevelopmentThe human nervous system begins to develop soon after conception. By the 21st day, the neural tube

had formed, developing into the spinal cord while the front part of the tube develops into the brain. The

rate of brain growth can be 250,000 neurones per minute to reach a total of about 100,000 million

neurones. There is not a huge increase in the number of brain cells after birth but the brain increases in

size because of several factors. These factors are mainly the elongation of axons, myelination and the

development of synapses.

Axon growthAxons of the neurones from the retina grow to the thalamus where they form synapses with neurones in

the thalamus in a veryordered arrangement. Axons from these thalamus neurones grow towards the

visual cortex in the occipital lobe.

The visual cortex is made ofcolumns of cells, proven in staining techniques and by usingelectrical

stimulation. Axons from the thalamus synapse within these columns while adjacent columns receive

stimulation.

The columns were thought to be a result of nurture rather than nature but Crowley and Katz proved that

it is not the case. They saw, by usinglabelled tracers, that ferrets and newborn monkeys both have these

columns, suggesting that their formation was genetic. However, periods during postnatal development

have been identified when the nervous system must gain specific experiences to develop properly, known

as critical windows or sensitive periods.

Evidence for a critical period in visual development

MEDICAL OBSERVATIONS

One case is that of a young Italian boy who had a minor eye infection, it was bandaged up for two weeks.

Afterwards, he was left with permanently impaired vision.

People born with cataracts contributed to the understanding of critical periods in development. Cataract

is the clouding of the lens of the eye, affecting the amount of light to the retina. If it is not removed by

the age of 10, it can cause permanent impairment of the persons ability to perceive shape. However,

elderly people report normal vision if the cataract is removed despite having them for years. This suggests

that there is a specific time in development when it is crucial for a full range of light stimuli to enter theeye.

Radioactive label moves from one eye and is

concentrated into distinct bands in the visual cortex,

showing the columns of cells that receive input from

that eye. These banding patterns have been observed

in animals that have received no visual stimulation.


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