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Biology > Topic 8 > Flashcards

Topic 8 Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

the mammalian nervous system is composed of the …. and …. nervous systems

A

central and peripheral

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2
Q

the peripheral nervous system is divided into the ….. and the … systems

A

autonomic and somatic

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3
Q

the autonomic nervous system is divided into the … and the …. systems, which act antagonistically

A

sympathetic and parasympathetic

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4
Q

the somatic nervous system is concerned with …

A

conscious or voluntary activity

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5
Q

the autonomic nervous system is concerned with…

A

the involuntary actions, such as controlling heart rate

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6
Q

the mammalian nervous system is made up of cells called …

A

neurones

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7
Q

all neurones have…

A

a cell body with organelles such as mitochondria (to provide energy for the active transport of ions in and out of the cell), a nucleus, dendrites (which conduct impulses towards the cell body as well as axons which conduct impulses away from the cell body

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8
Q

there are three neurones that differ in function due to …

A

the positioning of the cell body

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9
Q

sensory neurone

A

transmit impulses from receptors to the central nervous system- cell body in the centre as a seperate blob

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10
Q

relay neurone:

A
  • located within the central nervous system and are involved in transmitting the electrical impulses from sensory neurones to motor neurones- the cell body is a bulge in the middle (doesn’t poke out)
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11
Q

motor neurones:

A

involved in transmitting electrical signals from the central nervous system to muscles and glands (effectors)- the cell body is at the end of the

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12
Q

wider diameter neurones…

A

transmit signals more quickly (however, they take up more space)

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13
Q

myelination:

A

formed by the wrapping of a fatty substance: Schwann cells around a neurone- Schwann cells have little cytoplasm and a lot of cell membrane- the phospholipid abundance causes its insulation of electrical current. It increases the speed of impulses by acting as an electrical insulator allowing impulses to travel by saltatory conductance.

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14
Q

in between schwann cells there are …

A

nodes of ranvier:
- the action potential hops over the schwann cells to each node to spead up the rate of the electrical impulse.

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15
Q

what causes the stimulus to threshold?

A

local current in axon

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16
Q

what happens at threshold?

A

Na+ channels open + Na+ diffuses in

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17
Q

What happens when the axon is depolarised?

A

Na+ channels close. K+ channels open and K+ moves out

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18
Q

what happens when the axon is hyperpolarised?

A

K+ channels close

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19
Q

Hyperpolarised to polarised:

A

local current

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20
Q

what is the polarised milivolts of an axon

A

-70 mV

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21
Q

what is the threshold of an axon in milivolts?

A

-55 mV

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22
Q

what is the depolarised milivolts of an axon?

A

+40 mV

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23
Q

what is the hyperpolarised milivolts of an axon?

A

-90 mV

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24
Q

how many miliseconds does the action potential take?

A

5 miliseconds

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25
Q

what causes the POLarised state of a neurone?

A

Pumping: NoutKin- 3Na+ out and 2K+ in by active transport.
organic ions in the neurone: globular proteins reffered to as organic ions have a slightly negative charge
leakage: K+ leaks out of the potassium channels making the inside slightly more negative

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26
Q

propagation of action potential in neurone

A
  1. local ion currents from the previous deolarised section of the axon change membrane potential
  2. inside becomes less negative and outside becomes less positive (on polarised node)
  3. When the membrane potential reaches -55 mV, (threshold), voltage gated sodium channels open
  4. Sodium ions rush in by diffusion- depolarising the membrane to +40 (action potential is generated)
  5. potassium channels open and sodium channels close
  6. Potassium ions diffuse out of the cell
  7. Inside becomes more neagtive- repolarisation
  8. Membrane potential goes beyond -70mV (hyperpolarised), called the refractory period
  9. Potassium channels close
  10. The sodium-potassium pump restores resting membrane potential by pumping sodoim out and potassium in.
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27
Q

Mark scheme- example past paper question: explain the electrical changes in an axon that allow an action potential to occur:

A
  • the potential difference across the axon is changing
  • due to increased permeability to sodium ions/ sodium channels open
  • sodium ions moce into axon and cause depolarisation
  • followed by an increased permeability to potassium ions/ potassium channels opem
  • potassium ions move out of axon/ cause repolarisation of the membrane
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28
Q

Inititation of the action potential- in the synapse:

A
  1. the pre-synaptic membrane depolarises causing Ca2+ channles to open- calcium enters the neurone
  2. Calcium ions cause the synaptic vesicles containing neurotranmitter to fuse with the pre-synaptic membrane.
  3. neurotransmitter is released into the synaptic cleft via exocytosis, diffuses across synapse and binds to receptors sites on chemical-gated sodium channels in the postsynaptic membrane.
  4. these chemical gated channels open and some sodium ions diffude into the cell causing the inside to become less negative
  5. When the membrane potential reaches -55mv (threshold), voltage gated sodium channels open and sodium ions rush in by diffusion, depolarising the membrane to +40mV (action potential is generated)
  6. Potassium channels open and sodium channels close- potassium diffuses out of the cell and the inside becomes more negative- repolarisation
  7. membrane potential goes beyond -70mV (hyperpolarised)
  8. potassium channels close
  9. The soidum-potassium pump restores the resting membrane potential by pumping sodium out and potassium in (NoutKin)
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29
Q

excitatory neurotranmitters:

A

-stimulates next neurone to generate an action potential
- increases permeability of post-synaptic membrane to Na+ (Na+ moves in)- causing threshold and depolarisation
-e.g. acetylcholine

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30
Q

inhibitory neurotranmitters:

A

-inhibits next neurone (more difficult to generate an action potential)
- increased permeability to post-synaptic membrane to Cl- or K+ (Cl- moves in and K+ moves out)
- causing hyperpolarisation (harder to reach the threshold-55mV)

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31
Q

Acetylcholine as a neurotransmitter:

A

-acetylcholine is released at the pre-synaptic membrane
- there are digestive enzymes in the synaptic cleft which break down the neurotranmitter to prevent overstimulation of the post-synaptic membrane.
- following th ebreakdown of the neurotranmitter, it is taken up by the pre-synaptic membrane ands is reused.
- in this cause, the enzyme ‘acetylcholinesterase’ hydrolyses acetylcholine.

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32
Q

what ensures that action potentials can only move in one direction?

A
  • the presence of receptors on one side of the synapse only
  • the refractory period- harder to reach threshold
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33
Q

types of synaptic signal:

A
  1. spacial summation- different pre-synaptic neurones at the same time
  2. temporal summation- the same pre-synaptic neurones at different times
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34
Q

humans have two photoreceptors:

A
  1. cones- allow colour vision in bright light and are clustered in the centre of the retina at the back of the eye
  2. Rods- only provide black and white vision, but are much more sensitive to light intensity than cones and work in dim light conditions.
    - this is due to convergance- three rod cells converge into a single bipolar cell (connecting photoreceptors to the optc nerve) - this acts to amplify the signals triggered by light.
    - only one cone synapses with each bipolar neurone so there is no amplification of the signal- making these photorecpetors less sensitive.
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35
Q

How a rod cell detects light (in light):

A
  1. light energy is absorbed by rhodopsin which splits into retinal and opsin
  2. opsin binds to the membrane of the outer segment of the cell
  3. this causes cation channels to close. The inner segment continues to pump sodium ions out of the cell and the membrane becomes hyperpolarised- more negative.
  4. This means that glutamate (a neurotransmitter) is not released across the synapse- glutamate usually inhibits the neurones that connect the rod cells to the neurones in the optic nerve.
  5. When there is less inhibition, inhibitory gat3es close on bipolar cell
  6. Bipolar cell depolarises
  7. release of excitatory NT from bipolar cell
  8. Ganglion cell sends action potentials to the brain at high frequencies
  9. The information from the optic nerve is processed by the brain in the visual cortex.
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36
Q

Light detection in the rod cell (in the dark):

A
  1. light is not absorbed by rhodopsin pigment (therefore, it is not broken down)
  2. Na+ diffuses in through through open (unblocked) cation channels.
  3. Na+ moves down a concentration gradient
  4. Na+ is actively pumped out
  5. Membrane is slightly depolarised
  6. inhibitory neurotransmitter is released and binds to open inhibitory gates on bipolar cell.
  7. The bipolar cell hyperpolarises
  8. no release of excitatory neurotranmitter from the bipolar cell
  9. Ganglion sends action potentials to the brain at a low frequency.
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37
Q

how is the amount os light entering the eye controlled?

A

-muscles in the iris

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38
Q

what focuses the light on the retina?

A

the lens

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39
Q

where are the photoreceptors located on the eye?

A

the retina, specifically the fovea- a point where the photoreceptors are most abundant

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40
Q

what is the point where the optic nerve leaves the eye?

A

blindspot- no photoreceptor cells located there

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41
Q

what is accomodation?

A

the mechism by which the eye changes refractive power by altering the shape of the lens in order to focus on ojects at varying differences

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42
Q

what changes occur when focusing on a far object?

A
  • the lens becomes long and thin.
  • the suspensory ligaments are taught
  • the ciliary muscles are relaxed
  • incoming light is less diverged therefore are refracted less.
  • and vice versa for a near object
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43
Q

photoperiodism:

A

plants flower and seeds germinate in response to changes in day length. The photoreceptor responsible is a blue-green pigment called phytochrome.

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44
Q

on absorbing natural/ red light…

A

phytochrome converts from the inactive form Pr to the active Pfr.

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45
Q

In the dark,..

A

Pfr slowly reverts back to Pr because it is relatively unstable or it can change back rapidly into Pr if exposed to far red light

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46
Q

Pfr is …. to the flowering of short-day plants.

A

inhibitory

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47
Q

Pfr is … to the flowering of long-day plants.

A

stimulatory.

48
Q

what do IAA nad Pfr do?

A
  • bind to protein receptors in the target cells
  • activate intracellular second messenger signal molecules
  • these activate transciption factors, which control the transcription of genes (gene expression)
  • the proteins produced bring about metabolic chnages that result in many responses, including cell expansion, division and differentiation.
49
Q

tropisms:

A

are growth responses in plants where the direction of growth response is determined by the direction of the external stimulus

50
Q

phototropism:

A

is the response of the directional growth of the plant from the direction of light

51
Q

what does IAA cause?

A

cell elongation (lowers pH, elasticating the cell wall (by disrupting bonds between cellulose molecules and allowing cell walls to become stretched) and causing an influx of water by osmosis.

52
Q

when the shoot is iluminated in all directions,…

A

the auxins are distrubuted evenly and diffuse down the shoot tip thus causing even elongation of cells and growth of the shoot upwards (negative geotropism)

53
Q

If the shoot is only iluminated on one side…

A

the auxins move down the sahded side of the shoot (by diffusion) which elongates the cells in the shade, causing the shoot to bend towards the light (positive phototropism)

54
Q

what is the central nervous system made of?

A

brain and spinal chord

55
Q

what is the peripheral nervous system made of?

A

sensory nerves and motor nerves

56
Q

what does the autonomic nervous system do?

A

it stimulates smooth muscle, cardiac muscle and glands

57
Q

what does the somatic nervous system do?

A

stimulates skeletel muscle

58
Q

what does teh sympathetic nervous system do?

A

prepares the body from fight or flight responses

59
Q

what does the parasympathetic nervous system do?

A

prepares body from rest and digest

60
Q

endocrine vs. nervous: what is the messenger?

A

endocrine- chemical messenger
nervous- electrical impulse

61
Q

endocrine vs. nervous- how does it travel?

A

endocrine- blood
nervous- neurones

62
Q

endocrine vs. nervous- how fast is the effect?

A

endocrine- slower
nervous- faster

63
Q

endocrine vs. nervous: how long lasting is the effect

A

endocrine- long
nervous- shorter

64
Q

hypothalumus

A

contains the thermoregulatory and osmoregulatory centres

65
Q

pituitary gland

A

‘master gland’- control of the mentral cycle, releases growth hormone and ADH

66
Q

medulla oblongata:

A

controls breathing and heart rate

67
Q

cerebrum

A

responsible for personality, emotion, visual and auditory processing, speech

68
Q

cerebellum

A

motor control and coordination

69
Q

frontal lobe

A

risk assessment, emotional judgement, personality
- contains the Broca’s region (responsible for the formation of speech) and the motor cortex (initiates movement)

70
Q

parietal lobe:

A

responsible for recieving and processing sensory input such as touch, pressure, heat, cold and pain. Contains the sensory cortex

71
Q

occipital lobe

A

responsible for visual processing, perception, depth, colour, including visual cortex

72
Q

temporal lobe:

A

auditory processing. Contains the Wernicke’s region (responsible for stringing words together)

73
Q

MRI (magnetic resonance imaging)

A

-anatomical (reveals structure)
- shows tissue structure based on the water content
- higher water content in tissue (e.g. blood, brain, skeletal muscle, spinal cord)
- lower water content tissue (e.g. bone, teeth)

74
Q

advantages and disadvantages of MRI:

A

advantages:
- doesn’t use radiation
- better detail for soft tissues
- high image resolution
- smaller structures can be seen
disadvantages:
- can cause claustrophobia
-cant wear or contain metal
- more expensive
- takes a while
- noisy
- have to stay still

75
Q

CT scanning (computed tomography)

A
  • anatomical (reveals structure)
  • shows tissue structure based on how dense the tissue is- less dense is lighter
  • higher density tissue (e.g. bone)
  • lower density tissue (e.g. blood or lungs- water and air)
  • uses radiation in the form of x-rays to produce cross-section images of the brain.
    -can detect injuries such as brain bleeding after a stroke
76
Q

advantages and disadvantages of CT scanning:

A

advantages:
- better detail shown for bony structures
- very quick therefore, good for emergency diagnosis
- less expensice
- quiet
- more open design
disadvantages:
- uses radiation therefore repeated scanning not good
- not as much detail shown

77
Q

fMRI (functional magnetic resonance imaging)

A
  • metabolic (reveals function)
  • measures metabolic activity based on blood flow and oxygenation status of haemoglobin.
  • BOLD= blood oxygen level dependent
  • brain can be seen in action whilst performing tasks as it monitors the uptake of oxygen.
  • can be used for medical diagnosis of conditions which are caused by abnormal activity of the brain such as seizures.
78
Q

advantages and disadvantages of fMRI:

A

advantages:
- brain activity measured in real time
- images produced faster (every 4 seconds)
- higher image resolution
- less expensive than PET
disadvantages:
- can cause claustrophobia
- can’t wear or contain metal
-patient has to minimise movement

79
Q

PET (positron emission tomography)

A
  • metabolic activity based on usage of a particular metabolite (most commonly glucose in brain scanning)
  • uses radiactive isotopes (such as carbon-II in glucose) with a short half life to monitor areas of activity in the brain
  • detected by the emissions of positrons as the radioisotopes decay
80
Q

advantages and disadvantages of PET:

A

advantages:
- easy to interpret due to colour coding
- patient doesn’t have to stay still
- good for early cancer detection
disadvantages:
- images produced slower (1 per 40 seconds)
- uses radiation therefore repeated scanning isn’t good
- lower image resolution
- more expensive than fMRI

81
Q

critical windows:

A

critical windows for development are periods of time where it is thoguht that the nervous system needs specific stimuli in order to order to develop properly

82
Q

when eyes are deprived of light during critical window:

A

-axons do not pass nerve impulses to cells in the visual cortec
- inactive synapses are eliminated

83
Q

eyes that remain open in the critical window:

A
  • axons pass nerve impulses to cells in the visual cortex
  • synapses used by active axons are strengthened
  • synapses only present for axons coming from the light-stimulated eye, so the visual cortex can only respond to the eye.
84
Q

evidence from the critical windows:

A

-medical observations (e.g. children who develop cataracts before the age of 10 days may suffer from permanent visual impairment even if the cataracts are repaired at a later date- however, if cataracts are removed in adults, there is no visual imairment)
-animal models (e.g. work in monkeys has shown that both light and patterns are needed for full visual capacity development)

85
Q

Hubel and Wiesel experiments:

A

-kittens and monkeys were used as models to investagate the critical window (for critical period) in visual development because of the similarity of their visual systems to that of humans. They were deprived of light in one eye from birth and after 6 months were found to be blind, providing evidence for the critical window and evidence for the chiasmata in the optic nerve)

86
Q

supporting animal testing:

A

-they are easy to breed
- they have short life cycles
- small adult size
- similarity to humans
- reducing the ethical problems faced if drugs were to be tested on humans alone.

87
Q

against animal testing:

A
  • against basic animal rights (right to freedom/ not captivity), to have food and health support, consent)
  • it prevents them from expressing natural behaviours
88
Q

3 views of animal ethics:

A

relativist: humans should minimise harm to animals (prioritising animal welfare)
absolutism: animals should never be wed
utiltarianism: animals are used in research in the cases where the overall expected benfits of the study outweigh the harm done to the animal.

89
Q

learning:

A

a relatively permanent change in behaviour or knowledge that comes from experience

90
Q

memories are formed by…

A

-changing or making new synapses in the nervous system

91
Q

habituation:

A

a very simple type of learning that involves the loss of a response to a repeated stimulus that fails to provide any form of reinforcement (reward or punishment). It allows animals to ignore important stimuli so that they can concentrate more on rewarding or threatening stimuli.

92
Q

with repeated stimulation:

A
  1. Ca2+ channels become less repsonsive- so less Ca2+ crosses the pre-synaptic membrane
  2. Less neurotransmitter is released by exocytosis (so less diffuses)
  3. There is less depolarisation of the post-synaptic membrane so no action potential is trigegred in the motor neurone. (AP is less likely to occur as the neurone is less likely to reach threshold)
93
Q

by habituating ….

A

an organism can prevent energy expenditure and free up energy capacity more more relevent stimuli

94
Q

habituation specifically for the snail:

A
  1. The snail’s eye stalk is touched
  2. Impulses pass along a sensory neurone from the eye stalk
  3. The sensory neurone synapses with a motor neurone that connects the tentacle muscle
  4. Impulses pass along the motor neurone
  5. The eye stalk muscle contracts and the eye stalk is withdrawn
  6. With repeated stimulation, the calcium ion channels of the presynaptic neurone become less responsive to the changes in voltage associated with action potentials
  7. Fewer calcium ions enter the presynaptic neurone
  8. Less neurotransmitter is released from the presynaptic neurone
  9. Fewer sodium ion channels are opened in the postsynaptic neurone, so there is less depolarisation of the membrane
  10. An action potential is not generated in the postsynaptic neurone
  11. The eye stalk muscle does not contract and is not withdrawn
95
Q

Parkinsons disease: how does it work?

A

-insifficient dopamine levels due to the loss of dopamine-producing neruones in the basal ganglia
- the motor cortex in people with parkinsons disease recieve little dopamine and there is a loss of control of muscular movements.
- less dopamine released in the synaptic cleft meaning less can bind with receptors on the post synaptic membrane.
- fewer sodium channels on the membrane are opened so depolarisation of the post synaptic neurone does not occur.
-fewer sodium channels on the membrane are opened so depolarisaltion of the postsynaptic neurone does not occur
- fewer action potentials which creats symptoms such as tremours and slow movement.

96
Q

Symptoms of Parkinsons disease:

A
  • a tremor to specific parts of the body
  • slow movement
  • stiff and inflexible muscles
  • difficulties with balance
  • changes to speech
97
Q

Schizophrenia:

A

-excess dopamine in the brain is believed to be a major cause of schizophrenia.
- this can be treated with drugs that block the binding of dopamine to its post synaptic receptor sites.
- these drugs are usually similar to dopamine in structure, but unable to stimulate its receptos.
- a side effect in patients taking these drugs is to induce symptoms of Parkinsons.

98
Q

Treatment of Parkinsons:

A
  • Dopamine cannot be given directly to those who have Parkinson’s disease as it cannot cross the barrier between the blood and brain.
  • Dopamine agonists- produce the same effect as dopamine by binding to and activating the dopamine receptors on the post synaptic membrane e.g. a MAO inhibitor
    -Dopamine precursors- these are chemicals that can be converted into dopamine in the neurones e.g. L-dopa. This drug is transported from the blood into the brain, where it is converted into dopamine which means more nerve impulses can be transmitted and thus control symptoms.
    -Deep brain stimulation: A device like pacemaker is placed in the body. The electrodes deliver high frequency stimulation to the basal ganglia to produce dopamine
    -Gene therapy: Genes for proteins that increase dopamine production and promote growth and survival of nerve cells are inserted into the brain.
99
Q

Depression:

A

-low levels of seratonin- seratonin transmits nerve impulses through areas of the brain that control mood. Neurones that secrete seratonin are in the brain stem. Therefore low levels of seratonin increase episodes of depression.
- depression is a multifactorial condition; several genes can increase suseptability to the condition with environmental factors also contributin.
- depression is associated with feelings of sadness, anxiety, hopelessness. Loss of interrest in pleasurable activities and reduced energy levels are common, as are insomnia, restlessness and thoughts of death.

100
Q

Treatment for depression:

A

-antidepressants work by increasing levels of seratonin in the brain.
SSRIs (selective seratonin reuptake inhibitors) are a class of antidepressants:
1. SSRIs bind to channel proteins that are responsible for the reuptake of seratonin
2. Seratonin levels remain high in the synapse
3. Seratonin bind to receptor proteins in the post-synaptic membrane
4. post synaptic membrane depolarises
5. action potential/ impulse transmission continues

101
Q

MDMA: how does it work and side effects

A

-MDMA inhibits the reuptake of seratonin into the presynaptic neurone by binding to the specific proteins that enable seratonin reuptake, located on the presynaptic membrane; this increases the amount of seratonin present in the synaptic cleft.
- the drug has stimulated so much seratonin release that the cells cannot synthesise enough ti meet the demand once it has gone- resulting in feelings of depression
side effects:
- clouded thinking/ agitation
- sweating/ dry mouth
- increased heart rate
- muscle spasms (and jaw clenching)
- hyperthermia

102
Q

animal experiments exploring nature vs nurture:

A
  • the environment in which animals live in can be manipulated to allow the investagation of the impact of the environment on brain development
  • animals of the same species would have similar genes, therefore making it more likely that differences in brain development would be due to the changed environment factors.
103
Q

twin studies- exploring nature versus nurture:

A

Identical (monozygotic twins) develop from one fertilised egg, so share 100% of their genes. Non-identical (fraternal/ dizygotic twins) develop from two eggs, so share around 50% of genes. If genes influence the development of a characteristic, then identical twins should show a greater similarity in that characteristic than non-identical twins. Phenotypic differences in identical twins will be due to environemental factors.
-scientists will often use non-identical twins raised in similar environment as a control group when studying identical twins raised in the same environement

104
Q

Cross cultural studies:

A

People brought up in different cultures have different environmental influences. Scientists can study the effects of different upbringing on brain development by comparing large groups of people who are the same age but from different cultures. Any differences due to nurture, any similaritties due to nature.

105
Q

Newborn studies:

A
  • brains of newborn babies haven’t been exposed to the external environment for a long period of time. Studying the brains of newborn babies can help us understand which behaviours are learnt or innate and to what extent different parts of the brain have developed without environmental influences.
106
Q

brain damage studies:

A

brain damage in adults cannot be easily repaired as the brain is fuly developed, however, since a childs brain is still developing, they provide an opportunity for scientists to study the effects of brain damage on development.
- scientists can choose a particular characteristic and then compare the development of that trait in children born with and without brain damage.
- if children born with brain damage show the development of that characteristic, then is is more likely due to nurture rather than nature

107
Q

human genome project:

A

A 13-year old long project that identified all the genes found in human DNA (plants and bacteria have since been sequenced)

108
Q

Single nucelotide polymorphisms:

A

A DNA variation that occirs when a single nucleotide in the genome sewuences is altered in at least %of the population, with one base substituted for another.

109
Q

Pharmacogenomics:

A

analysis of organism responses to drugs based on genetics

110
Q

personalised medication:

A

personalised medicine involves the development of targeted drugs to treat a variety of human diseases in individuals with different genotypes.
- provided us with the information about the identification of new genes associated with disease and the development of drugs that target specific proteins e.g. if an enzyme is involved with a disease, a drug that acts as an enzyme inhibitor can be developed.
- by combining information about the genome with other clinical and diagnostic information, patterns can be identitfied that can help to determine an individuals risk of developing a disease.

111
Q

social/ moral/ ethical issues surrounding personalised medicine:

A

-increased research costs for drug companies could increase the price of new medicines and mean that only wealthier people have access to personalised medicine
- there is fear thqt insurance companies and employers may use personalised medicine data against individuals to unfairly discriminate against them- e.g. insurance costs might increase for people with some genetic variants
-some patients may be refused personalised medicine if it is not predicted to be that effective for them, even if there is no other treatment
-knowing that the iny medication available may not work could be very distressing for the individual being treated and their families.

112
Q

Genetically modified organisms:

A

the technique involves removing a gene that codes for a desired charcteristic from one organism and transferring the gene into another organism where the desired gene is then expressed
- the genetically engineered organism is said to contain recombinant DNA and will be a genetically modified organism
-micro-organisms, plants and animals have been genetically engineered to produce proteins used in medicine

113
Q

Process of Genetic Modification:

A
  1. Restriction enzymes are used to remove the gene coding for a desired protein from an organisms genome
  2. many copies of the gene are made using the polymerase chain reaction, or PCR. The enzyme DNA polymerase is used to join free nucleotides into new strands of DNA that are complementary to the original strand
  3. These copies are inserted into small loops of DNA called plasmids, which are vectors of DNA (viruses are another example)
  4. The restiction enzyme is used to cut the plasmid so that the ends are complementary. DNA ligase catalyses the joining of the desired gene to the plasmid.
  5. The now genetically modified micro-organisms are grown in large fementers containing nutrients, enabling them to multiply and produce largw quantities of the new protein.
  6. The protein can be isolated and purified before being packaged and distributed e.g. insulin to treat diabetes or blood clotting factors to treat haemophilia.
114
Q

Genetically modified plants:

A
  • a similar process can be used to insert desired genes from other organisms into plant cells.
    -after the gene is inserted into a plasmid and then transferred to a bacterial cell, there are two ways to transfer the plasmid to plants:
  • the bacteria can be used to infect plants; the bacterium acts as a vector for introducing the gene into the plant DNA. this is done by inserting a gene for antibiotic resistance- a marker gene along with the new desired gene. The antibiotic is toxic to plant cells at high doses, so the plant cells are incubated with the antibiotic which kills off any new cells that have taken up the new genes.
  • another method involves a ‘gene gun; tiny pellets are coated with the desired DNA and then fired into the plant cells
  • the gene is transferred from the bacterial cell into the plant cell nucleus, after which the plant is stimulated to multiply and grow into an adult plant. The GM plant cells become plants using micropropagation where they are grown in a sterile culture medium containing amino acids, inorganic ions and plant growth substances.
  • each cell of the plant contains a copy of the gene coding for the desired protein
  • the protein can now be purified from the plant tissues, or the plant can be eaten to deliver the drug. (e.g. insulin and the cholera vaccine)
115
Q

Genetically Modified Animals:

A
  • the gene that codes for the desired protein is injected into the nucleus of a zygote.
  • The zygote is implanted into the uterus of a surrogate animal where it develops into an adult animal.
  • retorviruses hae also been used to introduce new genes into fertilised eggs. The type of virus incorperates its DNA into the host’s DNA.
  • every cell of this genetically modified animal will contain a copy of the gene coding for the desired protein.
  • the protein can be purified from e.g. the milk of an animal
  • human antithrombin (used to treat people with a clotting factor) has been produced from genetically modified goats
116
Q

Concerns about genetic modification: Benefits-

A

-crops can be modified to produce higher yileds and have increased nutritional value, reducing famine and malnutrition
- crops can be modified to be resistant to pests and reduced pesticide use; this lowers production costs and decreases environmental damage
- enzymes used in industrial processes can be produced from genetically modified organisms; this is very cost effective
- diseases can be treated with human proteins produced by genetically modified plant tissues; these do not need refridgeration, making them more accessible to people living in rural areas
- genetically modified organisms guarentee a low-cost suopplu of some human medications

117
Q

risks of genetically modified organisms:

A

there are concerns about the long-term impacts of using genetically modified good organisms on human health
- some are concerned that pests may develop resistance to the modified crop defences, leading to increased use of pesticides
- genetically modified crops are often grown in large fields, creating monocultures that are bad for biodiversity
- there could be transmission of genetic material between genetically modified and non- GM organisms. This could lead to resistance to pesticides/ antibiotics or development of super weeds
- geneticalle modified crop varieties are usually owned by the companies that develop them, so seeds can be expensive. Developing countries would be unfairly affected.

Biology (9 decks)

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