• Created by: Kehaan
  • Created on: 21-05-18 13:28

Nervous system pathways

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A single cell, nerves are a bundle of many axons of many neurones surrounded by a protective coating. Contain a cell body, axon (impulses away from the cell body), and dendrites (towards the cell body).

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Motor/effector - cell body situated in CNS and axon extends out, conducting impulses from CNS to effectors (muscles or glands), axons can be extremely long

Sensory - carry impulses from sensory to CNS

Relay - found mostly within the CNS, can have a large number of connections with other nerve cells

Speed of conduction

Scwann cells - form a fatty insulating layer known as the myelin sheath, not all are myelinated

Wider the diameter, the quicker the impulse. Myelin sheath acts as an electrical insulator, preventing any flow of ions across the membrane, nodes of Ranvier occur in the sheath and are the only places depolarisation can occur, as ions flow across the membrane at one node during depolarisation the next nodes potential difference is reduced, triggering an action potential effectively jumping from node to node, much faster than a wave of depolarisation along the whole membrane - known as saltatory conduction.

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Reflex arc

Rapid, involuntary responses to stimuli

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Pupil reflex

Pair of antagonistic muscle: radial (sympathetic reflex) and circular (parasympathetic reflex), both controlled by the autonomic nervous system

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Controlling pupil size

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Resting potential

K+ diffuses out of the cell due to the concentration gradient, the more potassium ions that diffuse out of the cell, the larger the p.d. across the membrane. The increased negative charge created inside the cell attracts K+ back into the cell when the p.d. is around -70mV the electrical gradient exactly balances the chemical gradient - hence no net movement of K+ (an electrochemical equilibrium for K+ is in place)

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Action potentials

1. The nerve is at resting potential (-70mV)

2. A stimulus depolarises the nerve to the threshold (-50mV)

3. Change in Na+ gate, opening voltage-dependent sodium channels, as sodium ions flow in, depolarisation increases, triggering more gates to open (positive feedback), all-or-nothing

4. Sodium floods into the cell, causing a build-up of positive charge inside the cell, reversing the polarity of the membrane, p.d. reaches +40mV

5. Voltage-dependent Na+ close low permeability returns and voltage-dependent K+ channels open moving K+ out of the axon down the electrochemical gradient - repolarisation as the inside of the cell once again becomes more negative than the outside

6. Membrane now highly permeable to K+, more ions move out than at resting, causing hyperpolarisation of the membrane, re-established by the closing of the voltage-gated K+ channels, and K+ diffuse into the axon 

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How impulses pass along an axon

Domino effect/Mexican wave

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Speed of conduction

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Intensity of impulses

Size of an impulse has no effect as a threshold has to be achieved, all-or-nothing

Size of a stimulus affects:

The frequency of impulses

Number of neurones in a nerve that are conducting impulses

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Synapses explanation

1. An action potential arrives

2. Membrane depolarises, Ca2+ channels open, Ca2+ enter the neurone

3. Cause synaptic vesicles containing NTs (acetylcholine) to fuse with the presynaptic membrane

4. NT released into the synaptic cleft

5. NT binds with complementary receptors on the postsynaptic membrane, causing cation channels to open, Na+ flow through the channels, although several impulses usually required for enough NT to cause depolarisation sufficiently as well as the number of functioning receptors 

6. Membrane depolarises an initiates an action potential (threshold level reached)

7. When released from the receptor the NT will be taken up across the presynaptic membrane (whole or after being broken down), or it can diffuse away and be broken down, in this case, a specific enzyme known as acetylcholinesterase breaks down the NT so it can no longer bind to the receptor, some of the breakdown products are then reabsorbed by the presynaptic membrane and reused

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Role of synapses

Control of nerve pathways, allowing flexibility of response

Integration of information from different neurones, allowing a coordinated response

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Types of synapse


Make the postsynapse more permeable to Na+, need many of these arriving within a short time to produce sufficient depolarisation

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Types of synapse

Inhibitory synapses

Make it less likely that an AP will results, NT from these synapses open channels for chloride and potassium ions, these ions will then move through the channels down their diffusion gradients, chloride ions move into the cell, and potassium ions move out, causing the p.d. to be even lower than usual - hyperpolarisation, making subsequent depolarisation less likely, more excitatory synapses will be required to depolarise the membrane

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Nervous vs Hormonal

Nervous vs Hormonal

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, e.g. muscle contraction // can control long-term changes such as growth

APs carried by neurones with connections to specific cells // blood carries hormones to all cells, but only target cells are able to respond

The response is often very local, such as a specific muscle cell or gland // response may be widespread, such as in growth and development

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Coordination in plants

Plants have no nervous system so rely on chemicals such as plant growth substances

Discovery of auxins

Stimulate growth, the growth response being the result of cell elongation, an increased concentration of auxin moves to the shaded side increasing cell elongation, reduced concentration on the illuminated side inhibited cell elongation, so the shoot grows toward the light - phototropism. Auxin also works in a similar way when gravity is involved - gravitropism.

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Stimuli - any changes that occur in an animal's environment

Deteced by receptor cells, which send electrical impulses to the CNS, some types of receptor cells are grouped together into sense organs - eyes, they help to protect the receptor cells and improve efficiency, structures within the sense organ ensure receptor cells are able to receive the appropriate stimuli

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Two types: rods and cones


Allow colour vision in bright light


Only give black and white vision, but work in dim light as well

In the fovea there are only cones, allowing  us to pinpoint accurately the source and detail of what is being observed, over the remainder of the retina, rods outnumber cones by 20:1

Three layers of cells make up the retina, 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 these three layers before reaching rods and cones

Both contain a photochemical pigment which absorbs light - rhodopsin, rod cells have an outer and inner segment, the outer contains many flattened vesicles containing this pigment

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Rods in the light and dark

Dark Sodium ions flow through the outer segment through non specific cation channels (largely sodium ions involved), sodium ions move down the conc gradient into the inner segment where pumps actively remove them, the influx of sodium ions slightly depolarises the cell, triggering the release of neurotransmitters - thought to be glutamate which are released continuously in the dark, binding to the bipolar cell, stopping it depolarising, an inhibitory synapse

Light When light falls on the rhodopsin, it breaks down into retinal and opsin, the opsin causes a series of membrane bound reactions ending in the hydrolysis of a cyclic nucleotide molecule attached to the cation channel in the outer segment, resulting in the closure of the channel, influx of sodium decreases while the inner segment continues to remove sodium ions, making the inside of the cell more negative - hyperpolarised, the release of the NT stops, lack of this results in the depolarisation of the bipolar cell with which the rod synapses, neurones making up the optic nerve are also depolarised and respond by producing an action potential

Once rhodopsin is broken down, vital that it is reformed so subsequent stimuli can be perceived, reforming known as dark adaptation, the higher the light intensity the more rhodopsin molecules have to be reformed and so the longer it takes

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Plant photoreceptors

Phytochromes - protein and non-protein light absorbing pigment, five phytochromes differ in their protein component, non-protein exists in two forms which are isomers, Pr and Pfr                          Pr absorbs red light, and Pfr absorbs far red light, both regulate seed germination, stem elongation, leaf expansion and flowering

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Responses regulated by phytochromes

Germination - red light effective at triggering germination, whereas far red causes inhibition

Photoperiods and flowering - a photoperiod is the relative length of day and night, the ratio of Pr and Pfr allows a plant to determine the length of day and night. Long-day plants only flower when day length exceeds a critical value, so flower when a period of uninterrupted darkness is less than 12 hours (need Pfr to flower), reverse for short day plants (need Pr to flower), however, a flash of red light would negate the effects of the dark period - period of darkness controls flowering!

Greening - once in light, phytochromes promote the development of primary leaves, leaf unrolling and production of pigments, they can also, inhibit certain processes such as elongation of internodes - a result of etiolation

How do they do it?

Involved in activating proteins, either by binding to them or disrupting the binding of a protein, these proteins go on to activate transcription factors, RNA can bind to the promoter region as a transcription initiation complex is formed, transcription and translation occur, synthesising proteins which will then cause changes to the plant

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Plants can detect other environmental cues


Touch and mechanical stress

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The brain

Cortex is the outer part of the brain, composed of grey matter which is mainly nerve cell bodies, synapses and dendrites, the inner part is composed of white matter which is mainly nerve axons, white due to the myelin sheath, both cerebral hemispheres joined by white matter allowing communication

Cerebral hemispheres

Frontal lobe - concerned with higher functions of the brain, involving decision making, reasoning, planning and consciousness of emotions, also with movement, as connects to motors which are connected to muscles

Parietal lobe - concerned with orientation,  movement, sensation, calculations

Occipital lobe - concerned with processing info from the eyes (visual cortex)

Temporal lobe - processes auditory information

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The brain

Thalamus - routes all sensory info to right part of the brain, via axons of white matter

Hypothalamus - thermoregulatory centre, monitors core body/skin temperature, also regulates thirst, sleep and hunger, it also acts as an endocrine gland 

Hippocampus - involved in laying down long-term memory

Basal ganglia - responsible for selecting and initiating programmes for movement 

Cerebellum - responsible for balance, coordinates movement as it is being carried out, receiving info from the primary motor cortex, muscles and joints, constantly checks whether the correct movement programme is being carried out 

Medulla oblongata - regulates unconscious control e.g. heart/breathing rate and blood pressure

Midbrain - relays info to the cerebral hemispheres 

Neural plasticity - even after a stroke the neurones can change their structure and function so can recover some abilities, the structure of the brain remains flexible even in later life 

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Brain imaging

CT scans 

X-Rays can only be used for denser material as they are only absorbed by these, can only give 'frozen moment pictures', only have limited resolution so are used to look at structures and not functions within the brain 2D


Use magnetic field and radio waves to detect soft tissues as these are absorbed by high water content in the brain, higher resolution, safer but more expensive and loud, although can be used many times, they also have 'frozen moment pictures' 2D


Brain in real time/action so can study human activities directly. Detects level of uptake of oxygen by certain parts of the brain, deoxy absorbs radio waves, whereas oxy does not, overall larger increase in oxy so fewer radio waves absorbed, which show up as lights - as they are highly active 3D

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Brain imaging


Produce detailed images that allow structure and function to be evaluated, help to diagnose cancers, heart disease and brain disorders, also help to plan heart surgery.

Uses isotopes with short half-lives that are incorporated into glucose or water - called radiotracers. The patient is first injected, as the radiotracer decays it emits positrons, an active area of the brain will have an increased energy use, more oxygen and glucose required so increase in blood flow to that area, that increase will show up on a PET image as more radiotracers in that area, bright spots identify neurones that are highly active 3D

Very expensive, can only be done a few times a year due to safety and cost, but give very detailed images in real time and directly study brain activity 

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Visual development

Axons of neurones from retina grow to the thalamus, axons from here grow towards the visual cortex in the occipital lobe, info from the same part of the retina in each eye synapse next to each other, giving the brain the ability to create one 3D image of what the eyes see

The critical period of growth - incorrect as newborn monkeys were tested and the columns in the visual cortex were formed before the critical period for the development of vision, their formation is therefore genetically determined, nature not nurture. However, periods of time during postnatal development have been identified when the nervous system must obtain specific experiences to develop properly - known as critical periods/windows

Visual cortex needs to receive a full range of light stimulation during the critical period so columns of cells receive impulses from each eye 

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Animal models

Easy to obtain, easy to breed, have short life cycles and a small adult size.

In the study of eye development, kittens and monkeys have been used, due to their similarities to humans

At birth in monkeys there is a great deal of overlap between territories of different axons, in adults there is less overlap, after light deprivation in one eye, columns with axons from the light-deprived eye are narrower than those that aren't, suggesting that visual stimulation is required for refinement of columns and so for full development of the visual cortex 

Axons compete for target cells in the visual cortex, those which do not fire as frequently will have their synapses weakened and eventually will be cut back, so when one eye is deprived of light it's axons will not be stimulated, and so where there is overlap only the one being stimulated will fire, and so the light-deprived will eventually cut back and be lost

Summary: There is a lack of visual stimulation in one eye, axons from deprived eye do not pass impulses to the cortex, non-deprived does send impulses, inactive synapses eliminated, synapses made by active axons strengthened

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Depth perception

Close objects - binocular cells, visual field seen from two different angles, called stereoscopic vision and allows relative position of objects to be perceived 

Distant objects - images on our two retinae are very similar, so visual cues and past experiences are used when interpreting images 

Therefore nature and nurture play a role in depth perception

Different cultures have different beliefs which shape experience and behaviour, correlation not causation

Depth cues in pictures are not innate but learned

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Hippocampus, parietal and temporal lobe are all involved

Created in two ways: pattern of connections and strength of synapses

Image result for habituation diagram (

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Ignore non-threatening stimuli

Save energy and time for maximum feeding and reproductive effort

With repeated stimulation, Ca channels become less responsive so less Ca cross pre synaptic membrane, less NT released, and so less depolarisation as less Na released in the postsynaptic membrane, therefore no AP triggered in motor neurone (effector)

Long term memory

Involves an increase in the number of synaptic connections, repeated use of a synapse also leads to the creation of additional synapses between neurones

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Animal rights (ethics)

Animal rights, if humans have them so should animals, should not be enslaved 

Animal welfare, should treat them to the best of our ability 

Animal suffering, how can we be so sure they do not feel pain

Utilitarianism, expected benefits greater than expected harm

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Blood-brain barrier has small gaps, so large molecules cannot pass, to protect against toxic molecules and effects of changes in blood ion compositions and also disease


Dopamine secreting neurones in basal ganglia die, they normally release dopamine in the motor cortex, but no longer can so a loss of muscular movements: stiffness of muscles, tremor of muscles, slowness of movement, poor balance and walking problems, depression and difficulties with speech/breathing can also arise

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Slowing the loss of dopamine from the brain, inhibit the enzyme which breaks down dopamine, and so availability of dopamine increases - a MAO inhibitor

Dopamine itself cannot be given as it cannot cross the barrier, however, L-Dopa (a precursor) can which, once in the brain, can convert into dopamine, thereby increasing the concentration of dopamine - main therapy 

Use of dopamine agonists, drugs which mimic dopamine and bind to dopamine receptors, triggering action potentials, useful as they can avoid higher than normal levels of dopamine in the brain

Gene therapy can produce genes which increase the synthesis of dopamine and promote the growth and survival of nerve cells

Deep brain stimulation used to treat the symptoms of the disease - a person can reduce medications and so lessen effects of side effects 

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Excess dopamine

Believed to be a major cause of schizophrenia

Treated with drugs that block the binding of dopamine, have a similar structure to dopamine but unable to stimulate the receptors

Side effects include inducing the symptoms of Parkinson's

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Linked with serotonin

Thought to be a multifactorial condition, many genes involved and environment can be a trigger

Fewer impulses than usual are transmitted around the brain, low levels of NT produced, the molecules needed for protein synthesis often present in low conc, but the number of receptor sites increases possibly to compensate


MAOIs, rarely used as they have adverse side effects

SSRIs, inhibits reuptake of only serotonin from synaptic clefts, reducing some symptoms of depression, and so maintaining a higher level of serotonin and so increases the rate of nerve impulses in serotonin pathways 

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How drugs affect synaptic transmission

NT synthesis and storage

NT release

NT-receptor binding site

NT reuptake

NT breakdown

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Ecstasy (MDMA)

Affects thinking, mood and memory, can also cause anxiety

MDMA increases conc of serotonin in the synaptic cleft, by binding to molecules in the presynaptic membrane responsible for transporting serotonin back into the cytoplasm, drug may also cause the reuptake molecule to work in reverse, the higher levels of serotonin cause the mood changes MDMA users experience 

As the drug has stimulated so much serotonin release, the cells cannot synthesise enough to meet demand once it has gone, resulting in a feeling of depression

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Better treatments

Due to the HGP, we are gaining a much better insight into the ways our genes control our phenotypes, leading to major advancements in our understanding of diseases with a genetic basis to improve treatments, hoped that it will also allow us to be in a better position to avoid risk factors specific to our own genetic make-up

HGP - the deciphering of the base sequences in the human genome (all the DNA in the organism)

Personalised medicine - preventative medicine and improved drug treatment, pharmacogenomics is the study of drugs that are for specific individuals, by identifying certain genes they can predict what the person is prone to and how risk factors can be reduced

Ethical dilemmas - people patent fragments of DNA, making them inaccessible to the public, which is who it was meant for initially, allowing any biologist to use the information provided. Also, is it acceptable for insurers to have this information about certain people (i.e. health insurance)? Who decides whether a person is tested for genes and what this information is used for? Making and keeping of records of individual genotypes raises problems for confidentiality. Who is eligible for such treatments and what will the prices be, may also cause extra strain on NHS type services

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Genetic modification

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Plant GMOs

Can be used to mass produce antibodies, better than bacteria as lots can be grown, no need for antiseptic conditions

Bacterium infects plants, genes from the plasmid DNA become incorporated into the chromosomes of the plant

Minute pellets that are covered in DNA carrying the desired genes are shot into the plant cells, using a particle gun 

Viruses can be used, infect cells by inserting their DNA or RNA, used to transfer new genes into the cell

Gene insertion not 100% successful, so scientists therefore need to screen to find which have the gees, generally done by incorporating a gene for antibiotic resistance, called a marker gene, along with the new desired gene, antibiotics destroy any plants or cells which have not incorporated the gene - those who survive have the gene, the GMOs can then be cultured in agar micropropagation

Same REs are used to produce sticky ends, which will end up forming complementary bases with one another (the plasmid and DNA which is incorporated into it)

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Concerns with GMOs


Transfer of antibiotic-resistance genes to microbes, formation of harmful products by new genes, transfer of viruses from animals to humans, people should have a choice


Transfer of genes to non-target species, possible breeding of superweeds, possibility that GM crops will lead to the increased use of chemicals in agriculture 

Who owns these new organisms?

Are patented, so small time farmers may not be able to buy them, causing them to lose out to more competitive GM crops etc

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