Topic 8 Flashcards

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1
Q

what does the CNS consist of

A

brain and spinal cord

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2
Q

what is the peripheral nervous system made up of

A
  • sensory neurones
  • motor neurones
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3
Q

what is the peripheral nervous system split into

A

the automatic nervous system
the somatic nervous system

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4
Q

what is the automatic nervous system

A
  • involuntary
  • stimulates smooth muscle, cardiac muscles and glands
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5
Q

what is the somatic nervous system

A
  • voluntary
  • stimulates skeletal muscle
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6
Q

what is the automatic nervous system subdivided into

A

sympathetic and parasympathetic

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7
Q

what does the sympathetic nervous system do

A
  • prepares body for fight or flight responses
  • e.g speed up heart rate
  • norepinephrine
  • epinephrine
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8
Q

what does the parasympathetic nervous system do

A
  • prepares body for rest and digest
  • oxytocin
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9
Q

recall the 3 different types of neurones

A

relay
motor
sensory

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10
Q

draw and describe the structure of the sensory neurone

A
  • cell body seperate
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11
Q

where is the axon and dendron on a neurone

A

where the axon and dendron is depends on direction of impulse
impulse going left to right → dendron before cell body (on the left hand side) , axon after cell body (on the right hand side)
vice versa if the impulse is going from right to left

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12
Q

what does the sensory neurone do

A

carries information from receptors to CNS

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13
Q

what do motor neurones do

A

carry motor commands from the CNS to effectors

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14
Q

draw the structure of the relay neurone

A
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15
Q

draw the structure of motor neurones

A
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16
Q

what is the differences between axons and dendrites

A

axons:

  • unbrached
  • myelinated
  • only one per cell
  • take information away from the cell body
  • branch further from cell body

dendrites:

  • accept neurotransmitters whereas axons dont
  • no myelin sheath
  • branched
  • multiple dendrite
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17
Q

recall the pathway of the reflex arc

A
  1. receptors detect a stimulus and generate a nerve impulse
  2. sensory neurones conduct a nerve impulse to the CNS along a sensory pathway
  3. sensory neurones enter the spinal cord through the dorsal route
  4. sensory neurone form a synapse with a relay neurone
    cell body of sensory neurone found in dorsal route ganglion of the reflex arc
  5. relay neurone forms a synapse with a motor neurone that leaves the spinal cord through the ventral route
  6. motor neurone carries impulses to an effector which produces a response
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18
Q

what is the antagonistic pair in the eye

A

antagonistic pair → radial muscle and circular muscles
circular muscles contract and radial muscles relax to constrict and vice versa

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19
Q

which nervous system controls the radial and circular muscles in the eye

A
  • radial muscles are controlled by sympathetic reflex
  • circular muscles are controlled by parasympathetic reflex
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20
Q

what is the process of the pupils constricting

A

high levels of light hits photoreceptors in retina
causes a nerve impulse
the nerve impulse is passed along the optic nerve
one of the sites it passes is a set of coordinating cells in the midbrain
impulses from these cells are sent through parasympathetic motor neurones
the impulse is sent to the circular muscle in the iris
circular muscles will contract, radial will relax
pupil constricts

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21
Q

what is the process of the pupils dilating

A

low levels of light hits photoreceptors in retina
causes a nerve impulse
the nerve impulse is passed along the optic nerve
one of the sites it passes is a set of coordinating cells in the midbrain
impulses from these cells are sent through the sympathetic motor neurones
the impulse is sent to the radial muscle in the iris
the radial muscle with contract and the circular muscle will relax
pupil dilates

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22
Q

why does the pupil appear black

A

the pupil appears black because the cones and rods at the back of the retina ‘’absorb all the light, so none is reflected back

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23
Q

what is a stimulus

A

any change in the internal and external environment

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24
Q

what are receptors

A
  • receptors detect stimuli
    • they can be cells or proteins on cell surface membranes
      receptors only detect one particular stimulus
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25
Q

what are effectors

A
  • effectors are cells that bring about a response to a stimulus
    • this includes muscle cells and cells found in glands
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26
Q

how do receptors communicate with the effectors

A

receptors communicate with effectors via the nervous or hormonal system

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27
Q

what do the relay neurones do

A

relay neurones transmit electrical impulses between sensory neurones and motor neurones

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28
Q

what happens when a stimulus is detected

A
  • a stimulus is detected by receptor cells and an electrical impulse is sent along a sensory neurone
  • when an impulse reaches the end of a neurone neurotransmitters take the information across to the next neurone which then sends an electrical impulse
  • the CNS processes the info and sends impulses along motor neurones to effectors
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29
Q

what is the hormonal system made up of

A

made up of glands and hormones

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30
Q

what is a gland

A

a gland is a group of cells that are specialised to secrete hormones

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31
Q

what are hormones

A
  • hormones are secreted when a gland is stimulated
    • glands can be stimulated by a change in conc. of a specific substance (sometimes another hormone
    • can also be stimulated by electrical impulses
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32
Q

how are hormones transported and what do they do

A
  • hormones diffuse directly into the blood and then taken around the body by the circulatory system
  • they then diffuse out of the blood all over the blood but only bind to specific receptors on the membranes of target cells
  • the hormones trigger a response in the target cells (which are effectors)
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33
Q

how does the hormonal system increase the concentration of glucose in the blood when the concentration is low

A

receptors in the pancreas detect the low blood glucose conc
the pancreas releases the hormone glucagon into the blood
target cells in the liver detect glucagon and convert glycogen into glucose
glucose is released into the blood so blood glucose conc increases

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34
Q

what are the characteristics of the nervous system

A
  • uses electrical impulses
  • faster response → electrical impulses travel fast
  • localised response → neurones carry electrical impulses to specific cells
  • short-lived response→ neurotransmitters are removed quickly
  • electrical transmission by nerve impulses and chemical transmission at synapses
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35
Q

what are the characteristics of the hormonal response

A
  • uses chemicals
  • slower response→ hormones travel at the ‘speed of blood’
  • widespread response→ targets cell can be all over the body
  • long-lived response → hormones arent broken down very quickly
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36
Q

what happens when the nervous system is in resting state

A
  • (not being stimulated)
    there’s a difference in charge between the inside and outside of the cell
    • this means there’s a voltage across the membrane
    • membrane is polarised
    • voltage across the membrane is called potential difference
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37
Q

what happens when a stimulus is detected in a nerve cell

A
  • when a stimulus is detected → permeability of the cell membrane to ions changes
    if the change in potential difference is big enough → will trigger action potential
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38
Q

what is an action potential

A
  • an action potential is an electrical impulse along a neurone
    • is only triggered if the potential difference reaches a certain level called the threshold level
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39
Q

how is the amount of light that is entering the eye controlled

A

controlled by muscles of the iris

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40
Q

where does light enter the eye

A

light enters the eye through the pupil

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41
Q

what does the lens do

A

the lens focuses light rays onto the retina which lines the inside of the eye

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42
Q

what does the retina contain

A

the retina contains photoreceptors which detects light

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43
Q

what is the fovea

A

an area of the retina where there are lots of photoreceptors

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44
Q

how are nerve impulses carried in the eye

A

nerve impulses from photoreceptor cells are carried from the retina to the brain by the optic nerve which is a bundle of neurones

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45
Q

what is the blind spot in the eye

A
  • where the optic nerve leaves the eye is called the blind spot
    • there arent any photoreceptor cells so its not sensitive to light
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46
Q

describe the process that occurs when light hits the eye

A
  • light enters the eye, hit photoreceptors and is absorbed by light-sensitive pigments
  • light bleaches the pigments which causes a chemical change
  • this triggers a nerve impulse along a bipolar neurone
    bipolar neurones connect photoreceptors to the optic nerve which takes impulses to the brain
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47
Q

what are the two types of receptors in the human eye

A

human eye has two types of photoreceptor→ rods and cones

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48
Q

where are rods found

A

rods are mainly found in the peripheral parts of the retina
over the remainder of the retina, rods outnumber cones by a factor of about 20 to 1
high abundance

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49
Q

draw a diagram of the eye and label the different parts

A
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50
Q

what do cones do

A

cones allow colour vision in bright light
low abundance
high spacial acuity (gives detailed images)

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51
Q

what do rods do

A

rods only give black and white vision and work in dim light aswell as in bright light
low spacial visual acuity (gives less detailed images)

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52
Q

where are cones found and why

A
  • in the centre of the retina there’s only cones
    • this area allows us to pinpoint the source and detail of what were looking at
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53
Q

what does the rods and cones synapse with ?
what does the bipolar neurone synapse with?

A
  • the rods and cones synapse with bipolar neurone cells
  • bipolar neurone cells synapse with the ganglion neurones whose axons together make up the optic nerve
  • light hitting the retina through the layers of neurones before reaching the rods and cones
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54
Q

what is the name of the photochemical pigment which absorbs the light resulting in a chemical change

A

in the rods the molecule is a purplish pigment called rhodopsin

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55
Q

what is the structure of a rod cell?
where are rhodopsin molecules found?

A
  • in the rods, the molecule is a purplish pigment called rhodopsin
  • the rod cell has an outer and inner segment
  • the outer segment contains many layers of flattened vesicles
  • the rhodopsin molecules are located in the membranes of the vesicles
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56
Q

describe the process that occurs in the dark in rod cells

A
  • Na+ flow into the outer segment through non-specific cation channels
  • Ca2+ can also pass through these channels but it is largely sodium involved
  • 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 compared with the -70m resting potential of a cell
  • this slight depolarisation triggers the release of the neurotransmitter glutamate from the rod cells
  • in the dark rods release this neurotransmitter continuously
  • the neurotransmitter binds to the bipolar cell, stopping it depolarising
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57
Q

describe the process that occurs in the light in rod cells

A
  • when light falls on the rhodopsin molecule, it breaks down into the retinal (non protein component) and opsin (protein component)
  • the opsin activates a series of membrane-bound reactions, ending in hydrolysis nucleotide molecule attached to the cation channels
  • the influx of Na+ into the rod decreases while the inner segment continues to pump Na+ out
  • this makes the inside of the cell more negative
  • it becomes hyperpolarised and the release of the glutamate neurotransmitter stops
  • the lack of glutamate results in depolarisation of the bipolar cell with which the rod synapses
  • the neurones that make up the optic nerve are also depolarised and respond by producing an action potential
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58
Q

What happens after rhodopsin has been broken down

A

once the rhodopsin has been broken it is essential that its 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 process

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59
Q

what happens to rhodopsin when theres a higher light intensity

A

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 a maximum of 50 mins

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60
Q

what is dark adaptation

A

this reforming of rhodopsin is called dark adaptation

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61
Q

what do dendrites and dendrons do

A

they carry nerve impulses towards the cell body

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62
Q

what do axons do

A

carry nerve impulses away from the cell body

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63
Q

describe the structure of motor neurones

A
  • many short dendrites
    • carry nerve impulses from the CNS to the cell body
  • one long axon carriers nerve impulses from the cell body to effector cells
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64
Q

describe the structure of sensory neurones

A
  • one long dendron carries nerve impulses from receptor cells to the cell body
  • cell body located which is located in the middle of the neurone
  • one short axon carries nerve impulses from the cell body to the CNS
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65
Q

describe the structure of relay neurones

A
  • many short dendrites carry nerve impulses from the sensory neurones to the cell body
  • an axon carries nerve impulses from the cell body to motor neurones
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66
Q

what is the myelin sheath and what is it made of

A

the myelin sheath is an electrical insulator
- myelin sheath is made of Schwann cell

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67
Q

what are the nodes of ranvier

A
  • between Schwann cells there are tiny patches of bare membrane which is called the nodes of Ranvier
  • sodium ion channels are concentrated at the nodes
    in a myelinated neurone, depolarisation only happens at the node of ranvier
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68
Q

what is saltatory conduction

A
  • the cytoplasm of the neurone conducts enough electricity charge to depolarise the next node, so the impulse jumps from node to node
  • this is called saltatory conduction and its really fast
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69
Q

what happens in a non myelinated neurone

A

in a non-myelinated neurone, the impulse travels as a wave along the whole length of the axon membrane
this is slower than saltatory conduction

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70
Q

what is conduction velocity

A
  • the speed at which an impulse moves along a neurone is known as conduction velocity
    • a high conduction velocity means that the impulse is travelling quickly
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71
Q

describe an experiment design to measure the potential difference across the membrane of an axon

A
  • with both electrodes in the bathing solution there’s no potential difference
  • if one electrode is pushed inside the axon then the oscilloscope shows a potential difference of around -70mV (millivolts)
  • inside of axon is more negative than outside → the membrane is said to be polarised
  • value of -70mV is known as resting potential
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72
Q

what does the sodium/potassium pumps in the cell surface membrane of the axon do

A
  • these carry Na+ out of the cell and K+ into the cell
    • these pumps act against the concentration gradients of these 2 ions and are driven by energy supplied by hydrolysis of ATP
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73
Q

what are the two forces involved in the movement of potassium ions which keeps the axon at resting potential

A
  • the concentration gradient generated by Na+/K+ pump
  • the electrical gradient due to the difference in charge on the two sides of the membrane resulting fro K+ diffusion
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74
Q

describe how resting potential is brought about

A
  • the Na+/K+ pump creates concentration gradients across the membrane
    • inside the cell → high K+, low Na+ conc.
    • outside the cell → low K+, high Na+ conc.
    • 3Na+ leaves the axon for every 2K+ that enters the axon using active transport
    • once Na+ leaves the axon during resting state, it doesn’t come back in
    • membrane is x100 more permeable to K+ than Na+
  • K+ diffuse out of the cell down the K+ concentration gradient, making the outside of the membrane positive and the inside negative → creates a potential difference
  • the potential difference/ concentration gradient will put K+ back into the cell
    • amount that leaves = amount that comes back in → to reach an equilibrium
    • causes outside to be more positive than the inside
    • inside the axon → overall negative charge due to presence of organic anions that cant cross the membrane
  • at -70mV potential difference, the two gradients counteract and each other and there is no net movement of K+
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75
Q

what causes an action potential

A
  • once threshold stimulation occurs, an action potential is caused by the change in the permeability of the cell surface membrane to Na+ and K+ → due to the opening and closing of voltage-dependent Na+ and K+ channels
  • threshold is -55mV
    once this threshold is reached it causes the voltage gated channels to open
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76
Q

what are the three stages of the generation of an action potential

A

depolarisation
repolarisation
hyperpolarisation/ restoring resting potential

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77
Q

what happens in the depolarisation stage of an action potential

A
  • when neurone is stimulated some depolarisation occurs
  • change in potential difference across the membrane causes a change in the shape of Na+ gate → opens some of the voltage-dependent sodium ion channels
  • as sodium ions flow in depolarisation increases → triggers more gates to open once a potential difference threshold is reached
  • opening of more gates increases depolarisation further → an example of positive feedback
  • influx of sodium ions into the cell
    -voltage reaches +40mV
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78
Q

what happens in the repolarisation stage of an action potential

A
  • after 0.5ms, the voltage-dependent Na+ channels spontaneously close and Na+
  • permeability of membrane to Na+ returns to usual (very low level)
  • voltage-dependent K+ channels open due to the depolarisation of the membrane so potassium ions move out of the axon, down the electrochemical gradient (are attracted by the negative charge outside the membrane)
  • inside of the cell becomes more negative than the outside again
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79
Q

what happens in the restoring resting potential stage of an action potential

A
  • membrane is now highly permeable to potassium ions
  • more ions move out than occurs at resting potential
  • makes potential difference more negative than the normal resting potential
    • known as hyperpolarisation
  • resting potential is re-established by closing of the voltage-dependent K+ channels and potassium ions diffuse into the axon
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80
Q

how is the impulse generated along an axn

A
  • action potential triggers a sequence of action potentials along the length of the axon
  • as part of the membrane becomes depolarised due to an influx of sodium ions at the site of the action potential → a local electrical current is created as the charged sodium ions flow between the depolarised part of the membrane and the adjacent resting region
  • the depolarisation spreads to the adjacent region and the nearby Na+ gates will respond to this by opening → triggering another action potential
    • this is repeated along the membrane
    • as a result a wave of depolarisation will pass along the membrane → this is the nerve impulse
  • at the site of the first action potential -> resting potential is restored
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81
Q

what is the refractory period and how long does it last for

A
  • a new action potential can’t be generated in the same section of the membrane for about 5ms→ refractory period
  • it lasts until all the voltage-dependent sodium and potassium ion channels have returned to their normal resting state (closed) and the resting potential is restored
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82
Q

what is the role of the refractory period

A

refractory period ensures that impulses only travel in one direction

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83
Q

what is the all or nothing effect for action potentials

A

all or nothing effect for action potential means that the size of the stimulus (if its above the threshold) has no effect on the size of the action potential

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84
Q

what does the size of the stimulus affect

A
  • the frequency of impulses/ number of impulses
  • the number of neurones in a nerve that are conducting impulses
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85
Q

what is associated with a strong stimulus

A

a high frequency of firing and the firing of many neurones are associated with a strong stimulus

  • this is because there’s only a certain amount of sodium ions
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86
Q

what is the speed of nervous conduction determined by

A
  • speed of nervous conduction is partly determined by the diameter of the axon
  • wider diameter= impulse travels faster
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87
Q

why does a nerve with an axon with a small diameter make it more difficult for an action potential to propogate

A
  • smaller diameter has a larger surface area to volume ratio than axons with a larger diameter
  • this causes a larger amount of ions to leak out of the axon → makes it more difficult for an action potential to propagate
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88
Q

why are the nerve axons of mammals narrower than other species

A

nerve axons of mammals are narrower than other species yet the impulse travels quicker → this can be explained by the presence of the myelin sheath around the mammalian nerve axons

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89
Q

what are the factors that affect speed of conduction

A
  • temperature → increases rate of diffusion
  • myelin sheath
  • diameter of the axon
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90
Q

what is the role of the myelin sheath

A

myelin sheath acts as an electrical insulator, preventing any flow of ions across the membrane
nodes of Ranvier occur in the myelin sheath at regular intervals → these are the only places where depolarisation can occur

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91
Q

why does a myelinated axon have a higher impulse velocity than an unmyelinated axon

A
  • nodes of Ranvier occur in the myelin sheath at regular intervals → 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 an action potential
    • through this, the impulse jumps from one node to the next
    • this is faster than a wave of depolarisation along the whole membrane
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92
Q

describe the first stage of saltatory conduction

A
  • at resting potential there is positive charge on the outside of the membrane and negative charge on the inside
  • high sodium ion conc. on the outside and high potassium ion conc. inside
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93
Q

describe the second stage of saltatory conduction

A
  • 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 (resting) region → causes a change in the electrical charge (potential difference) across this part of the membrane
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94
Q

what is the third stage of saltatory conduction

A
  • a third action potential is initiated by the second
  • in this way local electric currents cause the the nerve impulse to move along the axon
  • at the site of the first action potential, potassium ions diffuse back into the axon → restores the resting potential
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95
Q

why is saltatory conduction beneficial

A
  • saves energy as the whole membrane doesn’t have to be polarised
  • also because the sodium/ potassium pumps uses ATP as they pump the ions via active transport
  • more energy efficient
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96
Q

what is a synapse

A

when two neurones meet, small gap

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97
Q

draw the structure of the synapse

A
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98
Q

what is the synaptic cleft

A

synaptic cleft that separates the presynaptic membrane of the stimulating neurone from the post synaptic membrane of the other cell
gap is 20-50mm → nerve impulse cant jump across it

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99
Q

how does the synapse transmit an impulse

A
  • the arrival of an action potential at the presynaptic membrane causes the release of the neurotransmitter into the synaptic cleft
  • neurotransmitter diffuses across the gap → results in events which cause depolarisation of the postsynaptic membrane and then the impulse goes along the cell
  • the presynaptic cells uses energy to produce the neurotransmitter and package it into vesicles ready for transport out of the cell
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100
Q

what was the first neurotransmitter to be discovered

A

acetylcholine was the first neurotransmitter to be discovered

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101
Q

what is the process of the nerve impulse passing from the pre synaptic neurone to the post synaptic neurone

A
  1. action potential arrives
  2. the membrane depolarises. calcium ion channels open and enter the neurone
  3. calcium ions cause synaptic vesicles containing neurotransmitter to fuse with the presynaptic membrane
  4. neurotransmitter is released into synaptic cleft
  5. neurotransmitter binds with the receptors on postsynaptic membrane. cation channels open and sodium ions flow through the channels
    1. receptors have specific binding site which are complementary to the shape of the neurotransmitter
    2. transmitter changes shape of the protein, causing cation channels to open
  6. membrane depolarises and initiates an action potential (rest of the process for the generation of an action potential occurs → depolarisation, repolarisation, hyperpolarisation, resting state)
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102
Q

what does the extent of depolarisation depend on

A

extent of depolarisation depends on the amount of transmitter reaching the postsynaptic membrane
- this will depend on the frequency of the impulse reaching the postsynaptic membrane
- several impulses required to depolarise the postsynaptic membrane as a single impulse isnt enough
- the number of functioning receptors in the post-synaptic membrane will also influence the degree of depolarising

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103
Q

how are neurotransmitters inactivated

A
  • some neurotransmitters taken up by the presynaptic membrane are used up again
  • others rapidly diffuse away from the synaptic cleft or is taken up by other cells of the nervous system
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104
Q

what happens to acetyl choline after its used

A

acetylcholinesterase breaks down acetylcholine into ethanoic acid and choline so that it can no longer bind to receptors
some breakdown products are then reabsorbed by the presynaptic membrane and reused

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105
Q

what are the 2 roles of synapses in nerve pathways

A
  • control of nerve pathways, allowing flexibility of a response
  • integration of information from different neurones allowing a coordinated response
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106
Q

what are the two main factors that affect the likelihood that the postsynaptic membrane will depolarise

A
  • type of synapse
  • number of impulses received
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107
Q

what do inhibitory synapses do

A

others are inhibitory and make it less likely that the post synaptic membrane will depolarise
- a post synaptic cell can have many inhibitory and excitatory synapses
- whether an action potential results depends on the balance of excitatory and inhibitory synapses acting at a given time

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108
Q

what are the two types of synapses

A

excitatory synapse
inhibitory synapse

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109
Q

what does the excitatory synapse do

A
  • makes the postsynaptic membrane more permeable to sodium ions
  • a single excitatory synapse typically does not depolarise the membrane enough to produce an action potential
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110
Q

what is needed to produce sufficient depolarisation

A

several impulses arriving within a short time produce sufficient depolarisation via the release of neurotransmitters to produce an action potential in the postsynaptic cell

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111
Q

what is summation

A

the fact that each impulse adds to the effect of the others

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112
Q

what are the two types of summation

A

spatial summation
temporal summation

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113
Q

what is spacial summation

A

impulses from several different neurones produce an action potential in the post synaptic neurone

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114
Q

what is temporal summation

A

several impulses along one neurone produce an action potential in the post synaptic neurone

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115
Q

how does the inhibitory synapse work

A
  • the neurotransmitter from these synapses opens channels for chloride ions and potassium ions in the postsynaptic membrane
  • these ions will then move through the channels down their diffusion gradients
  • chloride ions will move into the cell carrying a negative charge and potassium ions will move out carrying a positive charge
  • the result will be a greater potential difference across the membrane as the inside becomes more negative than usual (about -90mV) → hyperpolarisation
  • this makes subsequent depolarisation less likely
  • more excitatory synapses will be required to depolarise the membrane
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116
Q

what is the structure of the bipolar neurone

A
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117
Q

how do plants coordinate growth and development

A

plants lack a nervous system so they se chemicals to coordinate growth, development and responses to the environment

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118
Q

which chemicals are used in plants to bring about a response

A

plant hormones, plants regulator/ plant growth substances are chemicals that are produced in the plant in low concentrations and transported to where they cause a response
produced in growing regions of the plant

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119
Q

what are the different types of plant growth factors and what do they do

A
  • gibberellins stimulate flowering and seed germination
  • cytokinins stimulate cell division and cell differentiation
  • ethene stimulates fruit ripening and flowering
  • abscisic acid (ABA) involved in leaf fall
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120
Q

what is positive tropism

A

growth towards the stimulus

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121
Q

what is negative tropism

A

growth away from the stimulus

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122
Q

what is phototropism

A

the growth of a plant in response to light

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123
Q

how do shoots response to light

A

shoots are positively phototropic → grow towards the light

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124
Q

how do roots of plants respond to light

A

roots are negatively phototrophic and grow away from the light

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125
Q

how do shoots respond to gravity

A

shoots are negatively geotropic and grow upwards

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126
Q

how do roots respond to gravity

A

roots are positively geotropic and grow downwards

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127
Q

what did darwins experiment on phototropism show

A
  • the experiments showed an oat coleoptile with its tip cut off stops bending towards the light
  • replacing the tip starts growth towards the light again
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128
Q

what was darwins conclusion from his experiment on phototropism

A

some influence was transmitted from the shoot tip to the lower part of the seedlings, causing them to bend

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129
Q

how did the conclusion of a chemical being made in the tip that is passed down the plant come about

A

this was demonstrated by removing the tip and placing it on a small block of agar and putting the agar on top of the cut end of the coleoptile
the coleoptile started to grow again → a chemical produced by the tip had diffused down through the agar jelly

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130
Q

what investigation did Went carry out to provide further evidence that chemicals are produced in plant shoot

A

by placing the agar blocks on one side of the cut coleoptile tip in the dark → this caused it to curve away from the side receiving the chemical messenger from the agar
the chemical was eventually identified as the auxin, indoleacetic acid (IAA)

131
Q

what is the function of auixns

A
  • one of its major functions is to stimulate growth
  • growth response is a result of cell elongation
    high concentrations of auxins inhibit growth in roots
132
Q

what did Went discover about the amount of auxin in shoots

A

he found that the total amount produced didnt change compared with a shoot illuminated from all sides
- instead more auxin had been passed down the shaded side
- the increased conc. of auxin on the shaded side increased cell elongation
the reduced concentrated on the illuminated side inhibited cell elongation
as a result the shoot grew towards the light stimulus

133
Q

what happens if theres equal concentrations of auxin in the shoot

A

there wil be vertical growth
cell elongation will occur on both sides

134
Q

what is the cholodny-went model

A

explains growth curvature as a result of unequal distribution of auxin due to lateral transport of auxin

135
Q

why was the cholodny-went model critisised

A

criticised due to the small sample sizes and difficulty of measuring the very small concentrations involved

136
Q

what new techniques are being used to study tropisms

A

the use of genetically modified plants which produce fluorescent proteins in the presence of auxin → makes it possible to visualise the location of the auxin

137
Q

how do auxins work in phototropism

A
  • IAA moves to more shaded parts of the shoots and roots so theres uneven growth
  • auxins move to the side where there’s no light / move away from the light
    wherever IAA goes to shoot → elongation occurs
    wherever IAA goes in the root → growth in inhibited
138
Q

why does IAA affect growth

A

because IAA regulates the transcription of genes related to cell elongation and growth

139
Q

how does IAA work in geotropism

A

IAA moves to the underside of shoots and roots so theres uneven growth

140
Q

where is IAA synthesised

A

in actively growing root and shoot tips (meristems) and in developing leaves, seeds and fruits

141
Q

how is IAA transported

A

they are transported long distances in the phloem and shorter distances between cells via specific carrier proteins in the membrane
results in different parts of the plant having different amounts of IAA

142
Q

how do auxins bring about changes in plants

A

the auxins bind to protein receptors in the target cells
- this activates intracellular second messenger signal molecules which activate transcription factors
- these control the transcription of auxin-regulated genes
- the proteins produced bring about metabolic changes which result in a range of responses such as changes in cell expansion, division and differentiation

143
Q

how does cell expansion occur

A

to bring about cell expansion → required loosening of the cell wall
auxin causes the acidification of the cell wall by stimulating activity of proton pumps that move H+ ions out of the cytoplasm and into the cell wall
the low pH activates proteins called expansins which disrupt the bonds that hold cellulose microfibrils and hemicelluloses together→ loosens the wall so it can take up more water by osmosis
there is slippage of the polysaccharides relative to each other, bonds reform in new locations allowing expansion of the cell
- the acidification of the cell wall increases the potential difference across the membrane
- this enhances the uptake of ions into the cell
- the presence of these ions causes water uptake by osmosis → causes cell the swell resulting in cell elongation
- this process happens where the auxins are

144
Q

what does plant growth involve

A
  • plant growth involves cell division and enlargement
  • in the meristem cells are actively dividing and most of these cells enlarge, forming a region of elongation adjacent to the meristem
  • these cells go on to mature and differentiate
145
Q

what is the cortex of the brain

A

outer layer that lies ontop of the cerebrum of the brain
- grey
- highly folded
- composed mainly of nerve cell bodies, synapses and dendrites
- this is known as grey matter

146
Q

where is the cortex

A
  • cortex accounts for two-thirds of the brains mass → largest region of the brain
    • positioned over and around most other brain regions
    • divided into left and right cerebral hemispheres
147
Q

what is each hemisphere of the brain composed of

A
  • composed of four other regions called lobes
    • frontal lobe
    • parietal lobe
    • occipital lobe
    • temporal lobe
148
Q

what is white mater

A
  • composed of axons, lies below the grey matter
  • composed of millions of nerve axons that connect neurones in different parts of the brain
    white colour due to the axons myelin sheath
149
Q

how are the two cerebral hemispheres connected

A
  • the two cerebral hemispheres are connected by a broad band of white matter called the corpus callosum
    • allows communication between the two hemispheres
150
Q

what is the thalamus

A

responsible for routing all the incoming sensory information to the cortex part of the brain via the axons of the white matter

151
Q

what is the role of the frontal lobe

A

controls higher brain functions such as decision making, reasoning, planning and consciousness of emotion
also concerned with forming associations by combining information from the rest of the cortex and with ideas
it includes the primary motor cortex

152
Q

what is the primary motor cortex

A

has neurones which directly connect to the spinal cord and brain stem and from there to the muscles
- sends info to the body via motor neurones to carry out movements
stores information about how to carry out different movements

153
Q

what does the parietal lobe do

A

concerned with orientation, movement, sensation, calculation, some types of recognition and memory

154
Q

what does the occipital lobe do

A

(visual cortex)→ concerned with processing information from the eyes including vision, colour, shape recognition and perception

155
Q

what does the temporal lobe do

A

concerned with processing auditory information (hearing, sound recognition and speech (left temporal lobe). also involved in memory

156
Q

where are the different lobes on a diagram of the brain

A
157
Q

what is the hypothalamus and what does it do

A
  • contains the thermoregulatory centre
  • monitors core body temp, skin temp and initiates corrective action to restore the body to optimum temp
    other centres are located in the hypothalamus that control sleep, thirst and hunger
    secretes hormones
    connects directly to the pituitary gland which secretes other hormones
158
Q

what does the hippocampus do

A

involved in laying down long term memory

159
Q

what is the basal ganglia

A

a collection of neurones that lie deep within each hemisphere and are responsible for selecting and initiating stored programmed for movement

160
Q

what is the brain stem

A
  • brain stem → oldest part of the brain
    • lies at the top of the spinal column
    • brain stem extends from the midbrain to the medulla oblongata
161
Q

label this diagram of the brain

A
162
Q

what environmental cues do plants respond to

A

light is the most important environmental cue for plants and influences growth and development
- plants detect quantity, direction and wavelength of light using photoreceptors
- they respond to changes in light conditions

163
Q

what are phytochromes

A
  • plants contain a photoreceptor called phytochromes
  • these absorb red and far-red light
164
Q

what is a phytochrome molecule made up of

A

consists of a protein component bonded to a non protein light-absorbing pigment molecule

165
Q

what are the two isomers of the non protein component of phytochrome

A

Pr -> absorbs red light
Pfr -> absorbs far red light

  • these two isomers are photoreversible
  • plants synthesise phytochromes in the Pr form
  • absorption of red light converts Pr into Pfr
166
Q

what happens to the two phytochromes in sunlight

A

in sunlight, Pr is converted into Pfr| and Pfr is converted into Pr
this reaction dominates in sunlight because more red than far-red light is absorbed
so Pfr accumulates in the light

167
Q

what happens to the phytochromes in the dark

A

in the dark, any Pfr present is slowly converted to Pr

168
Q

what is the role of phytochromtes

A

trigger germination

169
Q

how were phytochromes discovered

A

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
- a further flash of red light will promote germination while a second flash of far red inhibits germination
- suggests that the effects of red and far red light are reversible
- the final flash of light determines whether or not gemination occurs

170
Q

how does red and far red light affect germination

A
  • red light → triggers germination as Pr is converted into Pfr whch triggers germination
  • far-red - inhibits germination as Pfr is converted back to Pr which inhibits germination
171
Q

what happens when lettuce seeds are exposed to red light

A

Pr is converted into Pfr → germination

172
Q

what happens when lettuce seeds are in the dark

A

Pr not converted into Pfr → no germination because the appearance of Pfr triggers germination

173
Q

what happens when lettuce seeds are exposed to far-red light

A

when exposed to far-red light Pfr is converted back into Pfr → inhibits germination

174
Q

what factors determine the time of flowering

A

the photoperiod, the relative of day and night
the ratio of Pr to Pfr in a plant enables it to determine the length of day and night

175
Q

what happens to phytochromes during long winter night

A

give a lot of time for Pfr to covert to Pr so that by sunrise all phytochrome will be Pr

176
Q

what happens to phytochromes during the summer

A

summer nights may not be long enough to do so, so some Pfr may still be present in the morning

177
Q

what affects whether a long day plant flowers

A

only flower when the period of uninterrupted darkness if less then 12 hours → they need Pfr to stimulate flowering

178
Q

what affects whether a short day plant flowers

A
  • short day plants tend to flower in the spring or autumn when the period of uninterrupted darkness is greater than 12 hours
    • they need long hours of darkness in order to convert all Pfr present at sundown back to Pr
179
Q

what does Pfr do in terms of flowering in short day plants

A
  • 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 as it causes for some of the converted Pr to convert back to Pfr
    Pr needed for flowering
180
Q

what is greening in plants

A

once a shoot has broken down through oil into sunlight → the plant undergoes profound changes in both its biochemistry

181
Q

how do phytochromes cause greening

A
  • once in the light, phytochromes promote the development of primary leaves, leaf unrolling and the production of pigments
  • they can also inhibit certain processes such as elongation of internodes
182
Q

how do phytochromes switch processes on or off

A

exposure to light causes phytochrome molecules to change from one form to another → brings about a change in shape
phytochrome 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 → allow transcription of light-regulated genes
the transcription and translation of proteins result in the plants response to light
e.g in seedlings, synthesis of the enzymes that control chlorophyll production will result in greening of the shoot

183
Q

what other environmental cues affect the growth of plants

A

gravity
touch and mechanical stress

184
Q

how does gravity act as an environmental cue for plants

A
  • stimulus for a shoot to grow upwards and root to grow downwards after a short distance under the soil is gravity and not light
  • response ensures that developing shoots reach the light while the root grows in the soil
185
Q

how does touch and mechanical stress act as an environmental cue

A
  • some plants are sensitive to touch and mechanical stress
  • rubbing plant stems can result in shorter stems than in controls
  • mechanical stimulus activates signal molecules whose end result is the activation of genes that control growth
  • some plants have leaves that move rapidly in response to mechanical stimulation
186
Q

what is the mechanism that occurs when a plant is touched

A
  • mechanism when its touched → specialised cells lose K+ ions
  • water follows by osmosis and the cells become flaccid → no longer supports the leaf and keep it upright
  • the movement of the leaves is thought to be an adaptation and helps prevent grazing by herbivores
187
Q

how can scientists determine the function of different regions of the brain

A

by studying the consequences of accidental brain damage → can determine the functions of certain regions of the brain
researchers have studied the consequences of injuring or destroying neurones to produce lesions

188
Q

what are lesions

A

lesions are areas of tissue destruction in non-human animal models and the consequences of removal of brain tissue

189
Q

describe the case of phineas gage

A
  • a dynamite explosion propelled a long iron bar through his head
  • he didn’t die and although most of the left hand side of his brain was destroyed he could still walk and talk
  • however after the accident his personality changed
  • highly likely that the accident severed connections between his midbrain and frontal lobes
    • gages reduced ability to control his emotional behaviour after the accident was related to the damage here
190
Q

how can strokes affect the brain

A

brain damage caused by a stroke can cause problems with speaking, understanding speech and writing
paul broca concluded that the lesions in a small cortical area in the left frontal lobe were responsible for deficits in language production which is why some patients cant speak after a stroke

191
Q

what is neural plasticity

A

some patients can recover some abilities after a stroke which shows the potential of neurones to change in structure and function
- structure of the brain remains flexible even later in life and can respond to changes in the environment
- brain structure and function is affected by both nature and nurture

192
Q

how do CT scans work

A
  • CT scans are thousands of narrow beam X-says rotated around the patient to pass through the tissue from different angles
  • each narrow beam is reduced in strength according to the density of the tissue in its path
  • the X rays are detected and are used to produce an image of a think slice of the brain on a computer screen in which the different soft tissues within the brain can be distinguished
193
Q

what are the limitations of CT scans

A

they only have limited resolution so small structures of the brain cant be distinguished
- CT scans can only give frozen-moment pictures
- they look at structures in the brain rather than function
cant be used for imaging soft tissue -> can only be absorbed by denser material such as bone

194
Q

what can CT scans be used for

A

are used to detect brain disease and to monitor the tissues of the brain over the course of an illness

195
Q

what are the advantages of magnetic resonance imaging

A
  • don’t rely on harmful X-rays
  • can be used more frequently
  • uses a magnetic field and radio waves to detect soft tissue- higher resolution images produced
196
Q

how do MRIs work

A
  • when placed in a magnetic field, the nuclei of atoms line up with the direction of the magnetic field in the way that compass needles aligns itself to the earths magnetic field
  • hydrogen atoms in water are monitored in MRI as there is a high water content in tissues under investigation and hydrogen has a strong tendency to line up with the magnetic field
  • exposed to radiowaves
  • the combined fields cause the direction and frequency of spin of the hydrogen nuclei to change, taking in energy from radiowaves to do so
  • when the radio waves are the hydrogen nuclei returns to their original alignment and release the energy they absorbed
  • this energy is detected and a signal is sent to a computer which analyses it to produce an image on the screen
197
Q

how does an MRI produce an image

A
  • different tissues respond differently to the magnetic field from the radio waves and so produce contrasting signals and distinct regions in the image
  • MRI examines tissues in small sections/ thin slices which when put together give 3D images
198
Q

what are MRIs used for

A
  • MRI is widely used in the diagnosis of tumours, strokes, brain injuries and infections of the brain and spine
  • MRI can be used to produce finely detailed images of the brain structures such as soft tissues, vessels, sinuses, tumours with better resolution than CT scans for the brain stem and spinal cord
199
Q

how does fMRI’s work

A

look at functions of different areas of the brain by following the uptake of oxygen in the active brain areas
deoxyhaemoglobin absorbs the radio wave signal, whereas oxyhaemoglobin doesnt (oxyhaemoglobin present when brain is active)
more deoxyhaemoglobin= more radiowaves absorbed
inc activity-> inc bloodflow to that area
the less radio signals absorbed the higher the level of activity in a particular area → so different areas of the brain will light up according to when they are active
imaged are collected continually while the subject alternates between resting and carrying out a task

200
Q

what are the limitations of MRIs

A

expensive
noisy
cant be used if you have a pacemaker

201
Q

what is the disadv of using fMRI

A

poor temporal resolution

202
Q

what are the uses of PET scans

A
  • used to produce detailed images that allow the structure and functioning of tissues and organs to be evaluated
  • used to help diagnose cancers, heart disease and brain disorders
  • also used to help plan heart surgery, monitor the spread of cancers and observe the effect of treatment
    useful in the diagnosis and monitoring of Alzheimers disease
203
Q

how do PET scans work

A

uses isotopes with short half lives such as carbon-11, nitrogen-13 or oxygen-15 that are incorporated into compounds such as glucose or water or into molecules that bind to receptors- radiotracers
- the patient is first injected with the radiotracer
- as the radiotracer decays, it emits positrons
- when a tissue or organ is active, there will be increased energy use in that area
- an increase in blood flow will show up on a PET image as more radiotracer atoms will be present in that area
- in the tissue when a positron collides with an electron, 2 gamma rays are emitted and these can be picked up by detectors → converted into a signal and then displayed as an image by the computer
- bright spots on the image indicate high levels of neurone activity
- dark spots → low levels of neurone activity
- by running a video sequence of PET images, changes in activity can be followed

204
Q

what are the limitations of PET scans

A
  • however PET scans can only be done once or twice a year due to safety
  • they’re also expensive and so arent used for routine screening
205
Q

what are the symptoms of Alzheimer’s

A
  • memory loss, problems with thinking, problem solving or language
  • symptoms occur when the brain experiences neurone loss
206
Q

how can PET scans be used to detect alzheimers

A
  • as neurones die, pieces of beta-amyloid protein found in the myelin sheath clump together to form clusters of sticky plaque which can block signalling at synapses
  • plaques can also activate immune cells which trigger an inflammatory response
  • the accumulation of beta-amyloid in the brain is an early sign of alzheimers disease and patients can undergo a PET scan with an amyloid tracer to visualise fibres of beta-amyloid in the brain
  • as the condition progress more beta-amyloid plaques accumulate, and synapses and acetylcholine receptors are destroyed in the brain
  • PET thus allow the monitoring of the disease’s clinical progression
207
Q

what is the pathway of an impulse from the eye to the brain

A
  • the axon of the ganglion cells that make up the optic nerve pass out of the eye and extend to several areas of the brain, including a part of the thalamus
  • the impulses are then sent to the primary visual cortex where the information is processed further
  • before reaching the thalamus, some of the neurones in each optic nerve branch off to the midbrain, where they connect to motor neurones involved in controlling the pupil reflex and movement of the eye
208
Q

how does the nervous system develop at conception

A
  • human nervous system begins to develop soon after conception
  • by the 21st day, a neural tube has formed
  • the front part of the neural tube goes onto develop into the brain, while the rest of the neural tube develops into the spinal cord
209
Q

what factors affect postnatal increase in brain size

A
  • the elongation of axons
  • myelination
  • the development of synapses
210
Q

what happens when neurones stop dividing in the brain

A
  • once the neurones have stopped dividing the immature neurones migrate to their final position and start to wire themselves
  • axons lengthen and synapse with the cell bodies of other neurones
  • neurones must make the correct connections in order for a function such as vision to work properly
211
Q

how do axons of neurones from the retina grow

A

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

212
Q

how do axons from thalamus neurones grow

A

axons from these thalamus neurones grow towards the visual cortex in the occipital lobe

213
Q

how is the brain able to create a 3D image of what the eyes see

A
  • one column of the cells receives stimuli from the left eye, the next column from the right eye in an alternating pattern
  • the information from the same area of the retina in the right eye and left eye synapse next to each other
  • this gives the brain the ability to create one 3D image of what the eyes see
214
Q

when was it thought that the column of cells in the visual cortex were formed

A

it used to be thought that these columns of cells in the visual cortex were formed during a critical period for visual development after birth → this is now known to not be the case

215
Q

when is the column of cells in the visual cortex formed and how was this shown

A

Crowley and Katz showed by injecting labelled tracers that the column in the visual cortex are formed before the critical period for the development of vision

216
Q

what is the formation of columns determined by

A

the formation of columns is genetically determined and not the result of environmental stimulus

217
Q

what is the critical period for the development of vision

A
  • There is a window of time during which the brain is particularly sensitive to certain types of stimuli.
  • If these stimuli are not received during this time, normal development may be disrupted
218
Q

what medical observations are there that is evidence for a critical period in visual development

A
  • a young Italian boy has a minor eye infection as a baby
  • as part of his treatment his eyes were bandaged for 2 weeks
  • when the bandage was removed he was left with permanently impaired vision
219
Q

how can studies of people born with cataracts contribute to the understanding in critical periods in develpment

A
  • cataracts is the clouding of the lens of the eye which affects the amount of light getting to the retina
  • if cataracts arent removed before the child is 10 they can result in permanent impairment of the persons ability to perceive shape or form, including difficulties in face recognition
220
Q

what study on new born animals has been carried out to provide evidence for the critical period

A
  • a group of newborn monkeys were raised in the dark for the first 3-6 months of their lives and another was exposed to light but not to patterns
  • when the monkeys were returned to the normal visual world, researchers found that both groups led difficulty with objects discrimination and pattern recognition
221
Q

what is the molecular deprivation investigation

A
  • Hubel and Wiesel raised monkeys from birth to 6 months, depriving them of any light stimulus in one eye
  • after 6 months the eye was exposed to light
  • on exposure to light it was clear that the monkey was blind in the light-deprived eye
    retinal cells in the deprived eye did respond to light stimulus, but the cells of the visual cortex didn’t respond to any input from the formerly deprived eye
222
Q

what conclusions were made from the studies on new born animals on finding evidence for the critical period in visual development

A
  • deprivation for only a single week during a certain period after birth produce the same result, with the deprived eyes visual cortex cells failing to respond to light
  • deprivation in adult monkeys had no effect
  • a visual deprivation of both eyes during this critical period has much less effect than when just one eye is deprived
223
Q

what is the difference between the structures of the visual cortex in new born monkeys and adult monkeys

A
  • at birth in monkeys there is a great deal of overlap between the territories of different axons
  • in adults there is less overlap even though the mass of the brain is greater with more dendrites and synapses
224
Q

what occurs when theres light deprivation in one eye and what does this suggest

A
  • after light deprivation in one eye, columns with axons from the light-deprived eye are narrower than those for the eye receiving light stimulation
  • dendrites and synapses from the light-stimulated eye take up more territory in the visual cortex
  • this suggests that visual stimulation is required for the refinement of the columns and so for full development of the visual cortex
225
Q

how do axons compete for target cells in the visual cortex

A
  • axons compete for target cells in the visual cortex
  • every time a neurone fires onto a target cell, the synapses of another neurone sharing the target cell are weakened and they release less neurotransmitter
    • if this happens repeatedly the synapses that arent firing will be cut back
226
Q

what happens to the synapses in a light deprived eye

A
  • when one eye is deprived of light, the axons from that eye will not be stimulated
  • in the area of the visual cortex, where neurones from both eyes overlap, only the synapses on axons receiving light stimulation will fire
  • the synapses from the light-deprived eye will be weakened and eventually lost
227
Q

what happens if the synapses are made and maintained during the critical period

A
  • if synapses are made and maintained during the critical period, neurones in the visual cortex are able to respond to the information from the retina
  • individual neurones in the columns of cells within the visual cortex respond in different ways to the information from the retina and to different characteristics of the object being viewed
228
Q

what are simple cell neurones

A

respond to bars of light

229
Q

what are complex neurone cells

A

respond to edges, slits or bars of light that move
other neurones respond to the angle of the edge, and others to contours, movement or orientation

230
Q

what does visual perception involve

A

it involves knowledge and experience as the brain interprets the sensory information received from the retina to create our visual experience of the world

231
Q

what is depth perception

A
  • when we look at an object we can make a judgement about how far away the object is
  • the brain does this in different ways for close and distant objects
232
Q

what happens in the visual cortex for close objects which are less than 30m away

A
  • depend on the presence of cells in the visual cortex that obtain information from both eyes at once
  • the visual field is seen from two different angles
    • cells in the visual cortex let us compare the view from one eye with that from the other
    • this is called stereoscopic vision and allows the relative positions of objects to be perceived
233
Q

what happens in the visual cortex for distant objects which are more than 30m away

A
  • the images on our two retinas are very similar so visual cues and past experiences are used when interpreting the images
  • image converges → gives impression of distance
234
Q

what can help determine depth of an image

A
  • smaller image = further away as you know the rough size of the object from experience
  • overlaps of images and changes in colour also help in judging depth
  • even if an object becomes smaller on the retina, we perceive is as moving further away
235
Q

what were cross cultural studies used for

A

can help to answer the question of whether depth perception is innate or learned by studying how different people respond to optical illusions

236
Q

why may kenge have not been able to recognise buffalos from far away

A
  • kenge was unable to recognise buffalo from a distance, but could recognise them from up close
  • he may not have developed depth perception over long distances because he has no experience of seeing long distances on an open plain, having always lived in the enclosed forest
237
Q

what is the carpentered word hyothesis

A

those of us who live in a world dominated by straight lines and right angles tend to perceive depth cues very different from those who live in a ‘circular culture’

238
Q

how do people who live in a carpentered world interpret images

A

in the carpentered world we are surrounded by building with right-angle corners so unconsciously from an early age we tend to interpret images with acute and obtuse angles (as long as they don’t differ too much from 90 degree) as right angles

239
Q

how do people who live in a circular culture interpret images

A
  • people who live in a ‘circular culture’ with few straight lines or right angle corners (such as those with circular houses and no roads) have little experience of interpreting acute and obtuse angles on the retina as representations of right angles
    • studies have shows they are rarely fooled by visual illusions such as the Muller-Lyer illusion
240
Q

what is the muller-lyer illusion

A
  • in the Muller-Lyer illusion, the angles between the line and the arrowheads are interpreted as right angles, providing depth clues to the image
  • we unconsciously perceive X to be shorter because depth clues make us think its further away and Y is closer to us
241
Q

what do some researchers think the lack of susceptibility to the muller-lyer illusion may be due to

A

suggest its not the result of different experience, but due to genetic differences in pigmentation between individuals
- they suggest that individuals who find it harder to detect contours are less susceptible to the Muller-Lyer illusions
- they link poor contour detection to high retinal pigmentation
- in light coloured people, with low retinal pigmentation, contour detection is good so are more easily caught out by the illusion (According to the argument)

242
Q

how were depth cues in pictures investigated

A
  • in another cross cultural study, individuals from a number of different cultures were shown pictures wth depth cues such as object size, overlap of objects and linear perspective
  • it was found that all young children had difficulty perceiving the pictures as 3D
    they wouldve said that the man is pointing to the elephant
    by the age of 11 almost all of the children interpreted the pictures in 3D
  • non literate adults didnt interpret the image as 3D
  • they had less experience of depth cues in pictures
243
Q

what conclusion can be made from the study of depth cues in pictures

A
  • therefore depth cues in pictures arent innate and they have to be learnt
  • this suggests that visual perception is partly learnt
244
Q

what do studies with new born babies show

A

the fact that babies are born with a range of characteristic behaviours suggest that they are determined by genes e.g crying, walking movements and grasping
these types of inborn capacities exhibited by a new born baby are used as evidence for the role of genes in determining the hard wiring of the brain before birth

245
Q

what is the visual cliff study with new born babies

A
  • in a classic experiment, babies are encouraged to crawl across a table made of glass or Perspex, below which is a visual cliff
  • patterns placed below the glass create the appearance of a steep drop
246
Q

how does the viual cliff study with new born babies determine whether depth perception is innate or learnt and what was the result

A
  • if the perception of depth is innate, then babies should be aware of the drop even if they havent previously experienced the stimulus themselves
  • the - the experiment is only possible with babies who have learned to crawl
  • its likely that a six-month old baby may have already learned depth perception
  • therefore the experiment was repeated with animal that can walk as soon as theyre born, such as chicks, kids and lambs
  • they too refused to cross the cliff
247
Q

what forms the bases of learning and memory

A
  • memory stores vast amounts of information from sights and sounds to emptions and skills
  • changes to synapses, changes in the network of neurones also forms the basis of learning and memory
    is any relatively permanent change in behaviour or knowledge that comes from experience
248
Q

where are memories stored

A
  • memory is not localised in one part of the brain
  • its distributed throughout the cortex with different sites for short and long-term memory
  • different types of memory are controlled by different parts of the brain
  • this is clearly demonstrated by looking at cases where people lost the use of different parts of their brain
249
Q

explain the study of the patient HM

A
  • HM who suffered from severe epilepsy
  • areas of the brain that was thought to be causing the problem was removed → immediately caused amnesia
  • HMs long term memory from before the operation were unaffected but he could no longer for new long term memories
  • his memories for how to do everyday things was still intact
  • this case shows that making memories is an active process
250
Q

how are memories stored

A
  • in the brain, neurones connect with many other neurones to make up a complex network

memories can be created by:

  • the pattern of connections
  • the strength of synapses
251
Q

why are sea slugs used to study habituation

A
  • neurobiology of a sea slug is simpler than that of a human
  • sea slugs have large accessible neurones → so those involved in behaviours can be identified
252
Q

what is a siphon on a sea slug

A
  • giant sea slug breathes through a gill located in a cavity on the upper side of its body
  • water is expelled through a siphon tube at one end of the cavity
  • if the siphon is touched the gill is withdrawn into the cavity
    • this is a protective reflex action similar to the removal of a hand from a hot plate
253
Q

how is habituation achieved

A
  • with repeated stimulation, Ca2+ channels become less responsive so less Ca2+ crosses the presynaptic membrane
  • less neurotransmitter released
  • less depolarisation of the postsynaptic membrane → no action potential is triggered in the motor neurone
254
Q

why have sea slugs become habituated to waves

A

since the slugs live in the sea and their gills are hit by a wave they’ve learnt not to withdraw their gill every time a wave hits them → have become habituated to waves

255
Q

what is habituation

A
  • habituation is a type of learning
    • gives animals the ability to ignore the unimportant repetitive stimuli so that limited sensory, attention, memory resources can be concentrated on more threatening or rewarding stimuli
256
Q

what is sensitisation

A

happens when an animal develops an enhanced response to a stimulus

e.g notice smaller noises more after hearing a loud noise when home alone

257
Q

how is sensitisation achieved in a sea slug to enhance gill withdrawal response

A
  • impulse due to electric shock to tail
  • serotonin released
  • gradual calcium ion uptake
  • impulse passes along sensory neurone due to the water jet stimulating the siphon
  • more neurotransmitter released
  • greater depolarisation
  • higher frequency of action potentials
  • enhanced gill withdrawal response
258
Q

what does long term memory storage involve

A
  • long term memory storage involves an increase in the number of synaptic connections
    • repeated use of a synapse leads to the creation of additional synapses between the neurones
259
Q

what does it mean if you accept t hat animals have rights

A
  • accepting that animals have rights means that you can only use animals which have consented to participate in medical experiments
  • this would bring an end to the use of animals in medical research
260
Q

what is the animal welfare approach for ethics of using animals is research

A
  • cant use vertebrates in medical experiments if there are non animal alternatives in the EU
  • strict guidelines followed if there’s no non animal alternatives for animals being used in research → as long as its necessary
261
Q

what is the animal suffering and experiencing pleasure argument for ethics of using animals in research

A
  • animal rights and welfare approach assumes the animals can suffer and experience pleasure
  • most experts reckon fish, spiders, insects cant suffer
262
Q

what is the utilitarianism approach to the use of animals

A
  • utilitarianism - the belief that the right course of action is the one that maximises the amount of overall happiness or pleasure in the world
  • this allows certain animals to be used in medical experiments as long as the overall expected benefits are greater than the overall expected harms
    e.g finding a cure for cancer using 250 000 mice but only 50 000 suffer for half of their life
263
Q

what is the blood brain barrier

A
  • the endothelial cells forming the capillary cells in the brain are more tightly joined together than those in capillaries elsewhere in the body
    • they form a barrier to control the movement of substances into the brain
    • protect the brain from the effects of changes in blood ionic composition
    • protect brain from toxic molecules
264
Q

when can drugs cause issues

A

can cause issues when they cross the blood-brain barrier
imbalances in naturally occurring brain chemicals can cause issues

265
Q

what is dopamine

A
  • dopamine is a neurotransmitter secreted by neurones in the midbrain especially
  • the axons of the neurones in this mid brain extend throughout the frontal cortex, brain stem and spinal cord
266
Q

what happens in people with parkinsons disease

A
  • in people with parkinsons, dopamine secreting neurones in the basal ganglia die
    • these neurones normally release dopamine in the motor cortex
  • the motor cortex in people with parkinsons disease receive little dopamine → and theres a loss of control of muscular movement
267
Q

what are the main symptoms of parkinsons

A
  • stiffness of muscles
  • tremour of muscles
  • slowness of movement
  • poor balance
  • walking problems
  • depression and difficulties with speech and breathing may also arise
268
Q

name examples of treatments used for parkinsons

A

selegiline
L-dopa
dopamine agonists
genes for proteins that increase dopamine production being inserted into the brain (being trialled)
deep brain stimulation

269
Q

how does selegiline work to treat parkinsons

A
  • slows the loss of dopamine from the brain
    • this drug is an MAO inhibitor
    • it inhibits monoamine (MAO) oxidase which is the enzyme responsible for breaking down dopamine in the brain
    • increases availability of dopamine
    • two types of monoamine oxidase: MAOB and MAOA
    • MOAB is used in parkinsons treatment
270
Q

why cant dopamine itself be used to treat parkinsons

A

it cant cross into the brain from the blood stream

271
Q

how can L-dopa be used to treat parkinsons

A
  • precursor in the manufacture of dopamine
    • once in the brain L-dopa coverts into dopamine
    • increases conc. of dopamine and controls the symptoms of the disease
272
Q

how can dopamine agonists be used to treat parkinsons

A
  • dopamine agonists → drugs that activate the dopamine receptor directly
    • the rug mimics the role of dopamine in the brain
    • it binds to dopamine receptors at synapses and triggers action potentials
    • can be useful in treating parkinsons as they avoid higher than normal levels of dopamine in the brain
273
Q

how can deep brain stimulation be use to treat parkisnons

A
  • a type of surgery used to treat the symptoms of the disease
    • person can reduce their medication and therefore reduce side effects
274
Q

what happens if theres excess dopamine in the brain

A

believes to be major cause of schizophrenia

275
Q

how can excess dopamine in the brain be treated

A
  • excess dopamine in the brain can be treated with drugs that block the binding of dopamine to its post synaptic receptor sites
  • these drugs are simular to dopamine in structure but unable to stimulate the receptors
276
Q

what are the side effects of the drug used to treat excess dopamine in the brain

A

side effect of the patients taking this drug is that it can induce the symptoms of parkinsons

277
Q

what is serotonin

A
  • seratonin → important neurotransmitter in determining a persons mood
  • neurones that secrete serotonin are found in the brains tem
  • their axons extend into the cortex, cerebellum, spinal cord → targets a large area of the brain
278
Q

what is a lack of serotonin linked to

A
  • lack of serotonin linked to depression
    dopamine and noradrenaline also has a role
    its not fully understood whether the lack of serotonin is a cause of depression or a result of it
  • depression→ persistently feeling safe for weeks or months and those feeling interfere with everyday life
    • associated with feelings of sadness, anxiety and hopelessness, loss of interest in pleasurable activities and reduced energy levels, insomnia, restlessness and thoughts of death
279
Q

what is thought to be the cause of depression

A
  • causes of depression not completely understood
  • there may be a genetic element
  • it may be a multifactorial condition → several genes may be involved in being susceptible to depression
    • environmental factors also contribute
280
Q

what gene is known to influence the susceptibility of depression and what does it do

A

gene 5-Htt
it codes for transporter protein that controls serotonin reuptake into presynaptic neurones
people with the short version of 5-HTT gene are more likely to develop depression after a stressful life event
two people who inherit the same susceptibility genes may not both develop depression →it will depend on environmental factors acting as triggers to bring about the symptoms of the disease

281
Q

what happens in someone who is depressed in terms of impulses

A
  • when someones depressed fewer nerve impulses are transmitted around the brain → may be related to low levels of neurotransmitters being produced
  • people with depression have pathways with a number of abnormalities
  • molecules needed for serotonin synthesis are often present in low concentrations but the serotonin binding sites are more numerous than normal → may be to compensate for the low level of the molecule
282
Q

how can twin studies help determine whether a disease or trait has a genetic cause

A

identical twins are produced by the division of the same egg → are almost genetically identical
- if a trait identified in one twin is caused by a gene then its likely to be present in the other twin
- when environment has a greater effect similarity between identical twins fall

283
Q

what do twin studies suggest in terms of depression

A

twin studies suggest that there may be a specific gene that causes clinical depression to develop in certain families but they also indicate that there’s a number of other genetic factors that determine the vulnerability to depression

284
Q

what was the first drug used to treat depression and why arent they used anymore

A

monoamine oxidase inhibitors
- break down neurotransmitters including serotonin
- they’re rarely used nowadays as they have a lot of side effects

285
Q

give an example of an effective drug which is used to treat depression nowadays and what does it do

A
  • one of the most effective types of drugs inhibits the reuptake of serotonin from the synaptic cleft
  • e.g Prozac → maintains higher levels of serotonin and increase the rate of nerve impulse in serotonin pathways
    • reduced some symptoms of depression
286
Q

how can drugs affect synapse transmission

A

may prevent the release of a neurotransmitter, block or open ion channels
may inhibit the a breakdown enzyme which breaks down the neurotransmitter
a chemical with a similar molecular structure to a particular neurotransmitter is likely to bind to the same receptors and stimulate the post synaptic neurone

287
Q

what is MDMA and what does it do

A
  • the drug MDMA is in ecstasy
  • it affects thinking mood and memory
  • it can cause anxiety and altered perception (similar to hallucination
  • most desirable effect of ecstasy → provides feelings of emotional warmth and empathy
288
Q

what are the short and long term effects of MDMA

A
  • short term effects of MDMA → changes in behaviour and brain chemistry
  • long term effects → changes in behaviour and brain structure, insomnia, depression
289
Q

how does MDMA in ecstasy affect synapses

A
  • MDMA increases the conc of serotonin in the synaptic cleft by binding to molecules in the presynaptic membrane that are responsible for transporting serotonin back into the cytoplasm
  • prevents removal of serotonin from synaptic cleft
  • the drug may also cause further increasing amount of serotonin outside the cell
  • these higher levels of serotonin bring about the mood changes seen in a user of ecstasy
  • may be possible that MDMA has a similar effect on molecules that transport dopamine
290
Q

what are the effects of using MDMA

A
  • users report feelings of euphoria, wellbeing and enhanced senses
    • these are side effects and unpredictable consequences of using the drug
  • some experience clouded thinking, agitation and disturbed behaviour
  • can also cause sweating, dry mouth, increased heart rate, fatigue, muscle spasms and hyperthermia
    • as MDMA an disrupt the ability of the brain to regulate body temp
291
Q

what can a single high dose or repeated doses of MDMA cause

A

repeated doses or a single high dose of MDMA can cause hyperthermia, high BP, irregular heartbeat, muscle breakdown and kidney failure → can be fatal

292
Q

why cay MDMA have an effect on normal brain activity even when the drug isnt being taken

A

this is because the drug has stimulated so much serotonin release that cells cant synthesise enough to meet demand when its gone → results in the feeling of depression

293
Q

what can the human genome project be used to do

A
  • human genome project helping us to gain a better understanding of the way genes control phenotype
  • this is leading to major advances in understanding of diseases which are genetic and help improve treatments
  • hoped that it will also help put us in a better position to avoid risk factors to out own genetic make up
    can be used to make personalisaed medicien
294
Q

what is the genome

A
  • genome → all of the DNA of an organism
    • includes the genes that carry all the info for making proteins needed by the organism
295
Q

how can the sequence of bases in DNA be found

A
  • DNA is used as a template to replicate a set of DNA fragments each differing in length by one base
  • the fragments are separated according to size using gel electrophoresis → the base at the end of each fragment is identified
  • this allows the sequence of bases in the whole DNA chain to be determined
296
Q

what can DNA base sequencing be used for

A

from this it became possible to work out the entire sequence of bases in the human genome and determine the location of all our genes
using the sequence biologists are gaining a better understanding of the genome itself, identifying new genes, working out how theyre controlled and discovering what they code for
- plays a major part in research into the role of genes in disease and the development of new diagnostic techniques and treatments
- can be used to find genetic variants that are shared by atleast 1% of the populations studied

297
Q

how many genes does the human genome have roughly

A
  • estimated that our genome has 20 000 to 25 000 genes → gives rise to complex proteins
  • average gene consists of 3000 bases
298
Q

what has the role of non coding regions of DNA thought to be

A
  • comparative genomics studies suggest that some of this non coding DNA has been conserved for a long time
  • this suggests that they confer a selective advantage in preserving useful biological traits or minimising traits that arent useful
299
Q

what are SNPs

A

single nucleotide polymorphism (SNP)→ DNA sequence variation that occurs when a single nucleotide in the genome sequence is altered in at least 1% of the population, with one base substituted for another

300
Q

what may SNPs do

A
  • SNPs may alter the protein formed or may have no effect on cell function
  • scientists believe that possession of particular SNPs could predispose people to a disease or influence their response to a drug
301
Q

how can genes be identified aswell as their function

A
  • its now possible to locate a candidate gene (this is a gene which may cause a particular disease) on our DNA and then screen the gene for mutations in affected individuals
  • analysing DNA sequence patterns in humans side by side with those in well studied model organisms e.g yeast has become a good strategy in identifying human genes and interpreting their function
302
Q

which genes have been identified for parkinsons

A

several genes associated with Parkinson’s have been identified including parkin, DJ1 and PINK1

303
Q

what kind of disease is alzheimers and what is its symptoms

A
  • alzheimers is a multifactorial disease → age, genes, environment are all factors which can inc risk

symptoms:

  • confusion
  • progressive severe memory loss
304
Q

what is a drug target

A

a drug target is a specific molecule that a drug interacts with to bring about its effect

305
Q

how can new target drugs be found

A

identification of disease genes and their products allowed biologsits to find new target drugs

306
Q

how can sequencing a persons genome be used to produce personalised medicine

A
  • differences in response to a drug may be due to slight variations in the genome, depending on the SNPs they have
  • prescribing the best drug for a patient is usually trial and error
  • info about a persons genome is hoped to enable doctors to prescribe the right drug and correct dose
  • some SNPs have been associated with differences in target drugs and the effects of drugs
    if a person knew they carried mutations associated with a particular disease they may make changes to their lifestyle to reduce the risk of the disease or opt for preventative treatment
307
Q

what can advances in genome sequencing be used to do

A
  • advances in genome sequencing allow accurate, quick and inexpensive DNA sequencing → improve diagnosis, treatment and preventions of diseases with gene based personalised medicine
  • pharmacogenomics→ sequencing a patients DNA to determine if they possess a specific SNP which is associated with a severe side effect to a particular drug enables it to be modified to suit the individual
308
Q

what ethical implications are there involved with the human genome sequencing

A
  • who should decide about the use of genetic predisposition tests and when they should be used
  • confidentiality problems with making and keeping record of an individuals genotype
  • personalised medicine is expensive so theres restricted availability → problem with deciding who is eligible for such treatments
  • individuals identified for possesing genes associated with inherited diseases may face discrimination in employment or when applying for insurance→ may not be able to get certain types of cover
    • possession of gene doesnt mean the person will develop the disease
309
Q

how can modifying organisms be used to produce drugs

A
  • plasmid cut using restriction enzymes
  • using the same restriction enzyme cut a piece of DNA from another species
  • DNA from the other species can be inserted/spliced into the plasmid → theyll have the same sticky ends as same restriction enzyme used
  • plasmid inserted back into bacteria
  • bacteria allowed to multiply in fermenter
  • protein produced extracted from the culture
  • can be used to produce vaccines, insulin etc
310
Q

how can genetically modofied plants be produced

A
  • artificial selection
    foreign genes being inserted into plants
311
Q

what is artificial selectio

A
  • artificial selection - choosing alleles for characteristics that are valuable
  • in this way crops have steadily improved
  • plant breeding is a slow process
  • when genetic engineers introduce new genes with alleles for desired characteristics into a plants DNA → genetically modified plants can be produced quicker
312
Q

what can genetically modified crops be used for

A

can be used to mass produce medicines or other chemicals cheaply and efficiently

313
Q

what are the different ways foreign genes be inserted into plants to produce GMOs

A
  • in each case a length of DNA that carries the gene to be used is known as a vector:
  • a bacterium which infects many species of plant can be used
    • when the bacteria invades plant cells, genes from the plasmid DNA become incorporated into the chromosomes of plant cell
    • insert gene into plasmid and carries the genes into plant DNA
  • minute pellets covered in DNA carrying the desired genes are shot into plant cells using a particle gun
  • viruses → infect cells by inserting their DNA or RNA → can be used to transfer new genes into cell
314
Q

how can gene insertion be screened to ensure its successful

A
  • this is done by incorporating a gene for antibiotic resistance, called a marker gene along with the new desired gene
  • the antibiotic is toxic to plant cells at a high conc
  • the plant cells are incubated with the antibiotic → kills off any cells that havent been taken up by the new genes
  • the only cells that survive are the ones that have successfully incorporated the new genes and are resistant
  • the GM plant cells can be cultured in agar with nutrients and plant growth substance to produce new plants
  • this micropropagation can multiple a single cell to form a callus which then differentiates to form plantlets and then novel plants
315
Q

how can genetically modified animals be produced

A
  • inject DNA into nucleus of fertilised egg
  • egg implanted into surrogate
  • DNA is only successfully incorportated into genome of 1% of treated embryos
  • retrovirus also been used to introduce new genes into fertilised egg→ virus incorporates its DNA into host
316
Q

recall the issues with genetic modification

A

health issues
antibiotic resistance
harmful products from new genes
environmental
who owns these new organisms

317
Q

why may health issues arise from genetic modification

A
  • transfer of antibiotic resistance genes to microbes
  • formation of harmful products by new genes
  • transfer of viruses from animals to humans
318
Q

why may antibiotic resistance occur as from genetic modification

A
    • GM contains marker gene as well as gene with codes for desired protein
  • the gene could be passed onto pathogenic microbes in the gut when the plant is eaten
  • the microbes could build up antibiotic resistance
  • however → no evidence that dietary DNA can be integrated into genome of a gut bacterium of into the genome of an animal
319
Q

why may environmental issues occur from genetic modification

A
  • GM has increased crop production and prevented use of pesticide issues such as the following still remain:
    • transfer of genes to non target species
    • the possible breeding of superweeds
    • GM could lead to inc use of chemicals in agriculture
    • cross pollination can occur over long distances and some crops grown are related to wind plants and can cross with them → so genes used in GM crops may spread to conventional crops or to wild plants
320
Q

how can environmental issues from genetic modification be evaluated

A
  • most of our crops cant survive in the wild
  • wild species would overrun our crops without the use of pesticide, fertilisers etc
  • therefore any escaped transgenic crop may disappear quickly
  • however if this gene makes any plant its transferred to fitter then it could produce super weeds which could have an advantage over others in the wind
  • invasive species → superweeds
321
Q

what solution is there to GM superweeds

A
  • one solution to GM superweeds would be to ensure that outcrosses (crosses between GM and other plants of a different variety) arent fertile
  • or development of tech to ensure pollen deosnt contain the modified gene so it cant spread
322
Q

what is the ownership issue when it comes to GMOs

A
  • many farmers may keep GM seeds to save money so they dont have to buy more
  • however these seeds may not be as good as the original
  • biotech companies now have patents on new tech used in GM
  • developing countries unlikely to be able to afford expensive licences to new tech to grow GM crops and they may need them more as they may find it difficult to compete with GM crops in affluent countries → these farmers may become poorer
  • difficult to predict social consequences of scientific development
323
Q

how do you carry out a spearmans rank test

A

ranks all of the values from lowest to highest
calculate the difference between ranks-> d
then square the d values
sum of d squared values
insert values into the formula
n= number of the amount of data collected

324
Q

why is it difficult to treat parksinsons

A

dopamine cant cross blood brain barrier
excess dopamine could lead to schizophrenia