biology notes - topic 8

Biology Notes: Topic 8

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 towards the cell body A single long process, the axon, transmits impulses away from the cell

body

Nervous system (NS)

Central nervous system (CNS)

Peripheral nervous system

Somatic nervous system

Autonomic nervous system

Sympathetic nervous system

Parasympathetic

nervous system

Consisting of sensory 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

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’


There are three main types of neurone:

Motor neurones – the cell body is always situated within the central nervous system (CNS) and the axon extends out, conducting impulses from 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 neurones – they carry impulses from sensory cells to CNS

Relay neurones – these are found within the CNS. They can have a large number 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

pathway


3. 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 motor neurone that leaves the

spinal cord through the ventral route6. Motor neurone carries impulses to an effector which produces a

response. For example, the bicep 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.

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 the parasympathetic reflex constricts the pupil.

CONTROLLING PUPIL SIZE

High light levels striking the photoreceptors 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 along parasympathetic 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.


How nerve cells transmit impulsesMuch 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 1940’s and 1950’s, and they eventually won a Nobel Prize for their efforts.

INSIDE A RESTING AXON

All cells have a potential 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 be polarised. -70 mV is known as the resting potential.

AtropineThe plant deadly nightshade (Atropa belladonna) is the source of the drug atropine which was used in the Middle Ages by some women to make their pupils dilate. This was thought to be attractive to men, 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. Today acetylcholine antagonist is used to dilate the


WHY IS THERE A POTENTIAL DIFFERENCE?

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

The resting potentialOnce the concentration gradients are established and there is no difference in charge between the inside and outside of the membrane, K+ diffuse out of the neurone, through potassium channels, down the potassium concentration gradient. The membrane is permeable to potassium ions but is virtually impermeable to sodium ions. There is some leakage of Na+ into the neurone down the concentration gradient but it does not balance the difference in charge across the membrane caused by the movement of K+. The difference in charge caused by diffusion of K+ causes a potential difference 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 electrical gradient due to the difference in charge. K+

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 by changes in the permeability of the cell 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 as voltage-dependent gated channels. There are three stages in the generation of an action potential.

1. Depolarisation

When a neurone is stimulated some depolarisation occurs. The change in the potential difference across 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 is positive 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 difference reaches +40mV.


2. Repolarisation

After 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 becomes more negative than the outside. This is the falling phase of the oscilloscope trace.

3. Restoring the resting potential

The membrane is now highly 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 by closing of the voltage-dependent K+ channels and potassium ion diffusion into the axon.

If hundreds 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.

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 refractory period. 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

1. At resting potential there is positive 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 potential difference in the membrane adjacent to the first action potential initiates a second action potential. At the site of the first


of firing and the firing of many neurones are usually associated with a strong stimulus.

SPEED OF CONDUCTION

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 µm, conduct impulses at around 0.5 ms-1, whereas the giant axons, with a diameter of 1000 µm, 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 of myelin 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, triggering action 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 the presynaptic 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 containing neurotransmitter to fuse with the presynaptic membrane

4. Neurotransmitter is released into the synaptic cleft

5. Neurotransmitter binds with receptors on the postsynaptic membrane. Cation channels open. Sodium ions flow through the channels

6. The membrane depolarises and initiates an action potential

7. When released the neurotransmitter will be taken up across the presynaptic membrane (whole or after being broken down), or it can diffuse away and be broken down

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 the propagation of the impulse along the next cell. The presynaptic cell expends a considerable amount of energy to produce neurotransmitter 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 three stages 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 they diffuse 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 by exocytosis.

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 of functioning receptors in the postsynaptic membrane will also influence the degree of depolarisation.

INACTIVATION OF THE NEUROTRANSMITTER

Some neurotransmitters are actively taken up by the presynaptic membrane and the molecules are used again. Other neurotransmitters rapidly diffuse away from the synaptic cleft or they are taken up by other 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, allowing flexibility of response Integration of information 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 if several impulses arrive at the same time in a short time frame, there is sufficient depolarisation via the release of neurotransmitter to produce an action potential. Each impulse adds to the effect of the others, known as summation.

There are two types of summation: Spatial summation

o 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

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 open channels 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 of chemical communication with target cells.

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

Nervous control Hormonal control

Electrical transmission by nerve impulses and 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 Blood carries the hormone to all


CO-ORDINATION IN PLANTS

Plants lack a nervous system so must use chemicals to co-ordinate growth, development and responses to the environment. These chemicals are called plant growth substances. They are chemicals produced in the plant in very low concentrations and transported to where they cause a response.

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

A chemical made in the top passed down the coleoptiles. This was demonstrated by removing the tip, placing it on a small block of agar 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 down through the agar jelly. Went provided more evidence by placing the agar blocks on one side of the cut coleoptile top in the dark; this caused the coleoptile to curve away from the side receiving the chemical 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 and found that the total amount did not change compared to a shoot illuminated from all sides; instead more auxin had passed down the shaded side. The increased concentration of auxin caused elongation of the shaded side. Thus, the shoot grows towards the light. This explanation is known as the Cholodny-Went model.

The model has been widely criticised due to the small sample sizes and the difficulty of measuring the small concentrations. However, many plant physiologists maintain that the basic features 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 it possible to visualise the location of the auxin.

Auxins are synthesised in actively growing plant tissues (meristems). The auxins are actively transported away to where they bring about a range of responses through their effect on cell elongation. By binding with


Reception of Stimuli

How does light trigger nerve impulses?RECEPTORS

Stimuli are detected by receptor 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 to protect 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 detect light 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 elongationAuxins have many other effects in plants. They inhibit growth of side branches down the plant (apical dominance). This effect can be seen if the growing tip at the top of a plant (apical meristem) is removed. The side branches down the plant will start to grow. Auxins also initiate growth of lateral roots, fruit development and leaf fall.

Many synthetic 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 auxins accumulate in cells, cuasing rapid growth that kills the plant. Hence why it can be sprayed to kill weeds but not grass.

Commercial fruit growers spray plants with synthetic auxins to induce fruiting. This means that the fruit will be seedless due to the lack of pollination. Auxin

Different types of receptorsReceptors can be cells that synapse with a sensory neurone, or can themselves be part of a specialised sensory neurone, 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


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 source and detail of what they are looking at. The remainder of the retina have a rod-cone ratio of about 20-1.

Three layers 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 UKThe central part of the retina (macula) receives light entering the yes from ‘straight ahead.’ The delicate cells of the macula sometimes becomes damaged from causing progressive deterioration of sight. Age-related macular degeneration is the most common cause of blindness in the UK. A drug, Lucentis, was approved for treatment of the wet type of the condition in 2008. The drug binds to a protein growth factor, stopping the growth of new abnormal blood vessels under the retina that leak fluid and blood. However,


HOW DOES LIGHT STIMULATE PHOTORECEPTOR CELLS?

In rods and cones, a photochemical pigment absorbs 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 of flattened 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 back out 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 of membrane-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 is dark adaptation.

Plants can also detect and respond to environmental cuesPlants contain several families of photoreceptors, one of which are phytochromes, which absorb red and re-red light. Five different phytochromes have been identified.

PhytochromesA phytochrome molecule consists of a protein component bonded to a non-protein light-absorbing pigment molecule. The five phytochromes differ in their protein component. The non-protein component exists in two forms, which are different isomers:

Pr – phytochrome red; absorbs red light (660nm) Pfr – phytochrome far-red; absorbs far-red light (730nm)

Why you should eat your carrotsPoor night vision, sometimes called night blindness, has been known for many years to be one of the symptoms of the disease caused by a shortage of vitamin A in 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 A and thus why it is said that you can


These two isomers are photoreversible. Plants synthesise phytochromes in the Pr form; absorption of red light converts Pr into Pfr. Absorption of far-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.

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

The photoperiod 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.

Red Light

Red Light

Far-Red Light

Far-Red Light

Development Processes

Reverts in the Dark


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, phytochromes promote the development of leaves, 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 may bind to the protein or disrupt the binding of a protein complex. These signal proteins may act as transcription factors or activate transcription factors that bind to DNA to allow transcription of light-regulated genes. The transcription and translation of proteins result in the plant’s response to light.

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 cuesGRAVITY

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 of nerve 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

Component FunctionFrontal lobe Concerned with the higher brain functions like decision making,

reasoning, planning and consciousness of emotions. It is responsible for the formation of associations and ideas.


Parietal lobe

Concerned with orientation, movement, sensation, calculation, recognition and memory

Occipital 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 the brain

Hypothalamus

Monitors core body temperature and skin temperature. Controls sleep, thirst and hunger. Also acts as an endocrine gland (antidiuretic hormone) and links to the pituitary gland

Hippocampus

Long-term memory

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

Midbrain Relays information to the hemispheresMedulla oblongata

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, using animal models and studying human patients during surgery. Individuals with brain damage still provide valuable information but neuroscientists now have a wide range of non-invasive imagining techniques.

STUDIES OF INDIVIDUALS WITH DAMAGED BRAIN REGIONS

Studying the consequences of accidental 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, his personality changed where he became nasty, foul-mouthed and irresponsible. He was impatient 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 can see facial features but they all 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.

THE EFFECTS OF STROKES

Brain damage caused by a stroke can cause problems with speaking, understanding speech, reading and writing. 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 brain’s structure and functioning is affected by both nature and nurture, remaining flexible even later in life.

BRAIN IMAGING

CT SCANS

Computerised Axial Tomography was developed in the 1970’s 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 a picture 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 magnetic field 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 wave signal but oxyhaemoglobin 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 visual or auditory stimulus.

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 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, proven in staining techniques and by using electrical 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 using labelled 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 developmentMEDICAL 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 person’s 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 the eye.

PowerPoint’s include:

Nerve Impulses - Over all story

The Brain - scans and imaging

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

biology notes - topic 8

Education