A level Topic 8 Grey Matter Flashcards

(138 cards)

1
Q

What does the nervous system consist of

A

The central nervous system (CNS) acts as a central coordinating centre for impulses that come in from and are sent out to any part of the body
- Consists of the brain and spinal cord

The peripheral nervous system
- all of the nerves in the body

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2
Q

What is a nerve

A

a bundle of neurones

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3
Q

Structure of a neurone

A

Cell body, shwann cell, dendrites, axon, axon terminal, myelin sheath

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4
Q

What do receptors do

A

Receptors detect stimuli - they can be cells or proteins on cell surface membrane

There are loads of different types of receptors that detect different stimuli

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5
Q

What are effectors and what do they do

A

Effectors are cells that bring about a response to a stimulus to produce an effect

Effectors include muscle cells and cells found in glands e.g. the pancreas

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6
Q

How do receptors communicate with effectors

A

Receptors communicate with effectors via the nervous system or the hormonal system

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7
Q

Sensory neurones

A

Transmit electrical impulses from receptors to the central nervous system - the brain and spinal chords

Cell body branches off in the middle of axon

Dendrites attached to receptor cell

Axon connects cell body with CNS

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8
Q

Relay neurone

A

Within CNS + Connects sensory neurones to motor neurones

Short axons and dendrites compared to other neurone types

Both axons and dendrites are highly branched

Creates an intricate network of connections
Allows complex signal processing and integration within the CNS

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9
Q

Motor neurones

A

transmit electrical impulses between sensory neurones and motor neurones

Large cell body at one end that lies within spinal cord or brain

Many highly branches dendrites extending from the cell body, providing many connections with the axon terminals of other neurones

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10
Q

How does electrical (nerve/action potential) impulses flow

A

A stimulus is detected by receptor cells and an electrical impulse is sent along a sensory neurone

When an electrical impulse reaches the end of neuron chemicals, these neurotransmitters take the information across to the next neurone which then sends an electrical impulse

The CNS processes the information and sends impulses along motor neurones to effectors

Relay neurones transmit electrical impulses between sensory neurones and motor neurones

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11
Q

How eyes respond to dim light

A

Stimulus: dim light

Receptors: Light receptors in your eyes detect the lack of light

CNS: CNS processes the information

Effectors: Radial muscles in the iris are stimulated by the motor neurones

Response: Radial muscles contract to dilate your pupils

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12
Q

How eyes respond to bright light

A

Stimulus: Bright light

Receptors: Light receptors in your eyes detect the bright light

CNS: CNS processes the information

Effectors: Circular muscles in the iris are stimulated by the motor neurones

Response: Circular muscles contract to constrict your pupils

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13
Q

What are glands

A

A gland is a cluster of cells that produces and releases one or more substances through secretion

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14
Q

What are hormones

A

Hormones are ‘chemical messengers’ produced by glands that travel through bloodstream to target cells
Many hormones are proteins or peptides e.g. insulin

Some hormones are steroids e.g. progesterone

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15
Q

How are hormones secreted

A

When glands are stimulated

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16
Q

How are glands stimulated

A

By a change in concentration of a specific substance (sometimes another hormone)

They can also be stimulated by electrical impulses

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17
Q

What happens when hormones are secreted

A

They diffuse directly into the blood, then taken around the body by the circulatory system

They diffuse out of the blood all over the body but each hormone will only bind to specific receptors for that hormone, found on the membrane of some cells (called target cells)

The hormones trigger a response in the target cells (effectors)

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18
Q

Example of hormone process after secretion

A

Stimulus: low blood glucose concentration

Receptors: receptors on pancreas cells detect the low blood glucose concentration

Hormone: the pancreas releases the hormone glucagon into the blood

Effectors: target cells in the liver detect glucagon and convert glycogen into glucose

Response: glucose is released into the blood, so glucose concentration increases

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19
Q

Nervous communication vs hormonal communication

A
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20
Q

Specific receptors

A

Receptors are specific - they only detect one particular stimulus e.g. light, pressure or glucose concentration

There are many different types of receptors that each detect a different type of stimulus

Some receptors are cells e.g. photoreceptor cells that connect to the nervous system

Some receptors are proteins on cell surface membranes e.g. glucose receptors are proteins found in the cell membranes of some pancreatic cells

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21
Q

What happens when a nervous system receptor is in its resting state

A

It is not being stimulated

There is a difference in charge between the inside and the outside of the cell, this means there is voltage across the membrane

The membrane is said to be polarised

The voltage across the membrane is called the potential difference

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22
Q

How is the potential difference generated

A

By ion pumps and ion channels

When a stimulus is detected, the permeability of the cell membrane to ions changes (ions are stopped from moving, or more move in and out of the cell)

This changes potential difference

If the change in potential difference is big enough it’ll trigger an action potential - an electrical impulse along a neurone

An action potential is only triggered if the potential difference reaches a certain level called the threshold level

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23
Q

What happens when you see light

A

Light enters the eye through the pupil, the amount of light that enters is controlled by the muscles of the iris

Light rays are focused by the lens onto the retina, which lines the inside of the eye

The retina contains photoreceptor cells - these detect light

The fovea is an area of the retina where there are lots of photoreceptors

Nerve impulses from the photoreceptor cells are carried from the retina to the brain by the optic nerve (a bundle of neurones)

Where the optic nerve leaves the eye is called the blind spot - there are no photoreceptor cells so it is not sensitive to light

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24
Q

How do photoreceptors convert light into an electrical impulse

A

Light enters the eye, hits the photoreceptors and is absorbed by light-sensitive pigments

Light bleaches the pigments, causing 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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25
What are the two types of photoreceptors in the human eye
Rods and cones
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Where are rods mainly found and where are cones mainly found
Rods are mainly found in the peripheral parts of the retina Cones are mainly found packed together in the fovea
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What colour do rods and cones give information
Rods only give information in black and white (monochromatic vision) but cones only give information in colour (trichromatic vision)
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What are the three types of cones
Red sensitive, green sensitive and blue sensitive They're stimulated in different proportions so you see different colours
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What pigments/chemicals do rods contain
Rods contain a light sensitive pigment called rhodopsin Rhodopsin is made of two chemicals joined together - retinal and opsin
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What happens when its dark and rods are not stimulated
Sodium ions are pumped out of the cell using active transport But sodium ions diffuse back in to the cell through open sodium channels This makes the inside of the cell only slightly negative compared to the outside (cell membrane is depolarised) This triggers the release of neurotransmitters But the neurotransmitters inhibit the bipolar neurone - the bipolar neurone can't fire an action potential so no information goes to the brain
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What happens when its light and the rods are stimulated
Light energy causes the rhodopsin to break apart into the retinal and opsin - this process is called bleaching The bleaching of rhodopsin causes the sodium ion channels to close So sodium ions are actively transported out of the cell but they can't diffuse back in This means that sodium ions build up on the outside of the cell, making the inside of the membrane much more negative than the outside - the cell membrane is hyperpolarised When the rod cell is hyper polarised it stops releasing neurotransmitters - this means there is no inhibition of the bipolar neurone Because the bipolar neurone is no longer inhibited, it depolarises. If the change in potential difference reaches the threshold, an action potential is transmitted to the brain via the optic nerve
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Neurones in resting state Resting potential
In a neurons resting state, the outside of the membrane is positively charged compared to the inside This is because there are more positive ions outside the cell than inside So the membrane is polarised - there is a difference in charge The voltage across the membrane when its at rest is called the resting potential which is -70mV
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How is resting potential created and maintained
The resting potential is created and maintained by sodium-potassium pumps and potassium ion channels in a neurones membrane
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Sodium-potassium pump and Potassium ion channel
The sodium-potassium pump uses active transport to move three sodium ions out of the neurone for every two potassium ions (K+) moved in - ATP is needed to do this The potassium ion channel allows facilitated diffusion of potassium ions out of the neurone, down their concentration gradient
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The sodium-potassium pump
the membrane is not permeable to sodium ions, so they can't diffuse back in, creating a sodium ion electrochemical gradient because there are more positive sodium ions outside the cell than inside The sodium-potassium pump also moves potassium ions in to the neurone but the membrane is permeable to potassium ions so they diffuse back out through potassium ion channels - this makes the outside of the cell positively charged compared to the inside
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Action potential: 1. stimulus
A stimulus excites the neurone cell membrane, causing a small number of sodium ion channels to open Sodium ions begin to move into the axon down their concentration gradient The membrane becomes more permeable to sodium, so sodium ions diffuse into the neurone down the sodium ion electrochemical gradient - This makes the inside of the neurone less negative
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2. depolarisation
This reduces the potential difference across the axon membrane as the inside of the axon becomes less negative If the potential difference reaches around -55 mV, known as the threshold potential, more sodium ion channels open, leading to a further influx of sodium ions - This second set of sodium ion channels are voltage gated channels Note that an action potential is only initiated if the threshold potential is reached Once the charge has been reversed from -70 mV to around +30 mV the membrane is said to be depolarised and an action potential has been generated
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3. Repolarisation
At a potential difference of around +30mV/after 1 millisecond after action potential is generated: the voltage gated sodium ion channels close and the voltage gated potassium ion channels open, allowing the diffusion of potassium ions out of the axon down their concentration gradient This starts to get the membrane back to its resting potential This movement of potassium ions causes the inside of the axon to become negatively charged again, a process known as repolarisation
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4. Hyperpolarisation
Short period during which the membrane potential is more negative than resting potential Potassium ion channels are slow to close so there is a slight 'overshoot' where too many potassium ions diffuse out of the neurone The potential difference becomes more negative than the resting potential (i.e. less than -70mV)
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What happens to a neurone cell membrane after action potential The refractory period
The period during which the membrane is hyperpolarised The membrane is unresponsive to stimulation during the refractory period, so a new action potential cannot be generated at this time This is because the ion channels are recovering and they can't be made to open - sodium ion channels are closed during repolarisation and potassium ion channels are closed during hyperpolarisation This makes the action potentials discrete events and means the impulse can only travel in one direction This is essential for the successful and efficient transmission of nerve impulses along neurones
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Are neurone cell membranes polarised or depolarised at resting potential
Polarised So they are depolarised during action potential
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How to initiate a nerve impulse in a neurone membrane
It must be depolarised Depolarisation is the reversal of the electrical potential difference across the membrane The depolarisation of the membrane occurs when an action potential is generated Action potentials lead to the reversal of resting potential from around -70 mV to around +30 mV
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What do action potentials involve
Action potentials involve the rapid movement of sodium ions and potassium ions across the membrane of the axon
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So what is an axon potential
An action potential is the potential electrical difference produced across the axon membrane when a neurone is stimulated e.g. when an environmental stimulus is detected by a receptor cell
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Diagram of action potential
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Another diagram
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Transmission of action potential
When action potential occurs, it can be transmitted along the length of the axon The depolarisation of the membrane at the site of the first action potential causes sodium ions to diffuse sideways along the cytoplasm into the next section of the axon, causing a wave of depolarisation to travel along the neurone, depolarising the membrane in this new section, and causing voltage gated sodium channels to open the wave moves away from the parts of the membrane in the refractory period because these parts can't fire an action potential This triggers another action potential in this section of the axon membrane This process then repeats along the length of the axon This causes a wave of depolarisation to travel along the neurone
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What happens to sodium ions that diffuse backwards
Any sodium ions that diffuse backwards along the membrane are unable to initiate a new action potential due to the hyperpolarised nature of the membrane in the moments following an action potential
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Direction of travel of action potential
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What does the refractory period do
During the refractory period, ion channels are recovering and can't be opened So the refractory period acts as a time delay between one action potential and the next This makes sure that the action potentials don't overlap but pass along as discrete impulses The refractory period also make sure action potentials are unidirectional
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The all or nothing principle
Action potentials are either generated or not generated depending on whether the threshold potential is reached; there is no such thing as a small or large action potential If a stimulus is weak only a few sodium ion channels will open and the membrane won’t be sufficiently depolarised to reach the threshold potential; an action potential will not be generated If a stimulus is strong enough to raise the membrane potential above the threshold potential then an action potential will be generated An impulse is only transmitted if the initial stimulus is sufficient to increase the membrane potential above a threshold potential
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How can stimulus size be detected by the brain
Stimulus size can be detected by the brain because as the intensity of a stimulus increases, the frequency of action potentials transmitted along the neurone increases This means that a small stimulus may only lead to one action potential, while a large stimulus may lead to several action potentials in a row
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How to prevent impulse transmission
Local anaesthetics are drugs that stop you from feeling pain in a localised area of your body They work by binding to sodium ion channels in the membrane of neurones This stops sodium ions from moving into the neurones, so their membranes will NOT depolarise This prevents action potentials from being conducted along neurones and stops information about pain reaching the brain
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Myelin sheath
Some neurones are myelinated - they have a myelin sheath Myelin sheaths are made up of Schwann cells Between the Schwann cells are tiny patches of bare membrane called the nodes of Ranvier Sodium ion channels are concentrated at the nodes
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Saltatory conduction
In sections of the axon that are surrounded by a myelin sheath membrane depolarisation cannot occur, as the myelin sheath stops the diffusion of sodium and potassium ions Action potentials can only occur at the nodes of Ranvier (gaps between the Schwann cells that make up the myelin sheath) Sodium ions diffuse along the axon within the Schwann cells and the membrane at the nodes of Ranvier depolarises when the sodium ions arrive The neurones cytoplasm conducts enough electrical charge to depolarise the next node The action potential therefore appears to ‘jump’ from one node to the next; this is known as saltatory conduction By insulating the axon membrane myelin increases the speed at which action potentials can travel along the neurone Saltatory conduction allows the impulse to travel much faster than in an unmyelinated axon of the same diameter
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Non myelinated neurones
In a non myelinated neurone, the impulse travels as a wave along the whole length of the axon membrane In unmyelinated neurones the speed of conduction is relatively slow because depolarisation must occur along the whole membrane of the axon 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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What is a synapse
Structures known as synapses are found at the junctions between cells in the nervous system e.g. In the sense organs there are synapses between sensory receptor cells and sensory neurones In muscles there are synapses between motor neurones and muscle fibres
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Structure of a synapse
A gap between the neurones known as the synaptic cleft The neurone before the synapse is known as the presynaptic neurone and has a rounded end known as the synaptic knob The neurone after the synapse is known as the postsynaptic neurone Nerve impulses are passed across the synaptic cleft by the diffusion of chemicals known as neurotransmitters e.g. acetylcholine Neurotransmitters are contained within vesicles in the synaptic knob
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Synaptic transmission
Electrical impulses cannot ‘jump’ across the synaptic cleft When an action potential arrives at the end of the axon of the presynaptic neurone the membrane becomes depolarised, causing voltage gated calcium ion channels to open Calcium ions diffuse into the synaptic knob via calcium ion channels in the membrane The calcium ions cause vesicles in the synaptic knob to move towards the presynaptic membrane where they fuse with it and release chemical messengers called neurotransmitters into the synaptic cleft by exocytosis The neurotransmitters diffuse across the synaptic cleft and bind with receptor molecules on the postsynaptic membrane; this causes associated sodium ion channels on the postsynaptic membrane to open, allowing sodium ions to diffuse into the postsynaptic cell If enough neurotransmitter molecules bind with receptors on the postsynaptic membrane then an action potential is generated, which then travels down the axon of the postsynaptic neurone The neurotransmitters are then broken down to prevent continued stimulation of the postsynaptic neurone The enzyme that breaks down acetylcholine is acetylcholinesterase
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Common neurotransmitters
A common neurotransmitter is acetylcholine, or ACh which is involved in muscle contraction and the control of heart rate Dopamine, seratonin
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Threshold potential
Whether or not an action potential is generated depends on whether or not threshold potential is reached, which in turn depends on the number of action potentials arriving at the presynaptic knob Many action potentials will cause more neurotransmitter to be released by exocytosis A large amount of neurotransmitter will cause many sodium ion channels to open Many sodium ion channels opening will allow a large influx of sodium ions, increasing the likelihood of threshold being reached
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Additional roles of the synapse
1. Unidirectionality of impulse transmission Synapses ensure the one-way transmission of impulses Impulses can only pass in one direction at synapses because neurotransmitter is released on one side and its receptors are on the other; chemical transmission cannot occur in the opposite direction 2. Divergence of nerve impulses One neurone can connect to several other neurones at a synapse, allowing nerve signals to be sent in several directions from a single presynaptic neurone 3. Amplification of nerve signals by summation - When an impulse arrives at a synapse it does not always cause an impulse to be generated in the next neurone; a single impulse that arrives at a synaptic knob may be insufficient to generate an action potential in the post-synaptic neurone
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Cerebrum
The largest part of the brain Divided into two halves called cerebral hemispheres The cerebrum has a thin outer layer called the cerebral cortex or 'grey matter'. The cortex has a large surface area so its highly folded to fit into the skull The cerebral cortex consists of the cell bodies of neurones It is highly folded, which increases its surface area and allows it to contain a greater number of neurones With more neurones in the brain, more neurone connections can be made The cerebrum is involved in vision, learning, thinking, emotions and movement Different parts of the cerebrum are involved in different functions e.g. the back of the cortex is involved in vision and the front is involved in thinking
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The hypothalamus
The hypothalamus is found just beneath the middle part of the brain The hypothalamus automatically maintains body temperature at the normal level The hypothalamus produces hormones that control the pituitary gland - a 'master gland' responsible for regulating many body functions, controlling the activity of other glands
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The medulla oblongata
Medulla oblongata is at the base of the brain, at the top of the spinal cord also known as the medulla It automatically controls breathing rate and heart rate The medulla contains co-ordination centres that control different functions e.g. The cardiac centre controls heart rate The respiratory centre controls breathing rate
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The cerebellum
The cerebellum is underneath the cerebrum and it also has a folded cortex Its important for coordinating movement and balance
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What is white matter
myelinated axons of neurones
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What is a tropism
A tropism is the response of a plant to a directional stimulus A plants growth response to an external stimulus
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A positive tropism
Is growth towards the stimulus
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A negative tropism
Growth away from the stimulus
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What is phototropism
The growth of a plant in response to light Shoots are positively phototropic and grow towards light Roots are negatively phototropic and grow away from light
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Geotropism
The growth of a plant in response to gravity Shoots are negatively geotropic and grow upwards Roots are positively geotropic and grow downwards
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Plant growth factors
The growth responses of plants rely on chemical substances that are released in response to a stimulus They don't have nervous systems so cant respond using neurones, and don't have circulatory systems so cant respond using hormones either
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Where are growth factors produced
Growth factors are produced in the growing regions of the plant e.g. shoot tips, leaves and they move to where they're needed in the other parts of the plant
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Auxins
Growth factors called auxins stimulate the growth of shoots by cell elongation - this is where cell walls become loose and stretchy, so the cells get longer Auxins are a group of plant growth factors that influence many aspects of plant growth
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What does high concentration of auxin do
Inhibit growth in plants
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Other plant growth factors
Gibberellins - stimulate flowering and seed germination Cytokinins - stimulate cell growth and division and cell differentiation Ethene - stimulates fruit ripening and flowering Abscisic acid (ABA) - involved in leaf loss and seed dormancy
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what responses does indoleacetic acid (IAA) bring about
Phototropism by altering the transcription of genes inside Altering the expression of genes that code for proteins involved with cell growth can affect the growth of a plant IAA moves to the more shaded part of the shoots and roots, so there's uneven growth
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Where is IAA produced and how is it transported
IAA is produced by cells in the growing parts of a plant before it is redistributed to other plant tissues IAA can be transported from cell to cell by diffusion and active transport Transport of IAA over longer distances occurs in the phloem
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What determines the rate of cell elongation
Concentration of IAA A higher concentration of IAA causes an increase in the rate of cell elongation If the concentration of IAA is not uniform across the stem then uneven cell growth can occur
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How does IAA cause phototropism
When light shines on a stem from one side, IAA is transported from the illuminated side of a shoot to the shaded side An IAA gradient is established, with more on the shaded side and less on the illuminated side The higher concentration of auxin on the shaded side of the shoot causes a faster rate of cell elongation, and the shoot bends towards the source of light
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IAA in roots - geotropism
In roots, IAA concentration also affects cell elongation, but higher concentrations result in a lower rate of cell elongation This is the opposite effect to that of IAA on shoot cells IAA is transported towards the lower side of plant roots The resulting high concentration of auxin at the lower side of the root inhibits cell elongation As a result, the lower side grows at a slower rate than the upper side of the root, causing the root to bend downwards
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How do plants detect light
Using photoreceptors called phytochromes Phytochromes are molecules that absorb light Phytochromes are found in leaves, seeds, roots and stem
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What is flowering in plants controlled by
stimulus of night length When the nights reach a certain length, genes that control flowering may be switched on or off, leading to the activation or inhibition of flowering Genes that are switched on are expressed, leading to production of the polypeptides for which they code, while genes that are switched off are not expressed, so the polypeptides for which they code are not produced
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How can the length of night be detected
The length of night can be detected by a plant because it determines the quantities of different forms of a pigment called phytochrome in the leaf
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Two forms of phytochrome pigment
PR is the inactive form of phytochrome, it absorbs light from the red part of the spectrum (wavelength 660 nm) PFR is the active form of phytochrome, it absorbs light from the far red part of the spectrum (wavelength 730 nm)
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How do phytochromes convert state
Absorption of different wavelengths of light causes a reversible conversion between the PR and PFR forms of phytochrome When PR absorbs/is exposed to red light (660 nm) it is quickly converted into PFR When PFR absorbs/is exposed to far red light (730 nm) it is converted back into PR In the absence of red light (darkness), the unstable PFR gradually converts back into PR
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So in terms of day to day
During the day levels of PFR rise Sunlight contains more wavelengths at 660 nm than 730 so the conversion from PR to PFR occurs more rapidly in the daytime than the conversion from PFR to PR As PFR builds up, genes involved in flowering are transcribed and this means plants flower in summer During the night levels of PR rise Red light wavelengths are not available in the darkness and PFR converts slowly back to PR
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why do high levels of PFR activate flowering
High levels of PFR activate flowering PFR activates expression of genes that stimulate flowering The active gene is transcribed and translated The resulting protein causes flowers to be produced rather than stems and leaves
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Computed Tomography (CT scans)
CT scanners use radiation (X rays) to produce cross sections images of the brain A beam of x-rays are aimed at a patient from all angles around the body Digital x-ray detectors are used to pick up the x-rays as they exit the patient's body Denser tissue absorbs more of the x-ray radiation so shows up as a lighter region on a scan A scan produced in this way shows physical structures of the brain and allows visualisation of any tissue damage E.g. blood is less dense than brain tissue so a CT scan can be used to locate damaged blood vessels and areas of bleeding after a patient has had a stroke Blood has a different density from brain tissue so it shows up as a lighter colour on a CT scan. You can then work out which blood vessels have been damaged and what brain functions are likely to be affected by the bleeding
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Who are CT scans not recommended for
T scans are not recommended for pregnant patients or children due to the risks of exposure to the X-ray radiation, which is given at a higher level than in a normal X-ray The risk of damage from such scans is still very low
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Magnetic Resonance Imaging
Magnetic Resonance Imaging, or MRI, uses a combination of a magnetic field and radio waves to generate images through the body The patient being scanned must remain very still while inside a large magnet Soft tissues can be seen clearly using MRI, and images produced are at a higher resolution than those produced from CT scanning As with CT scanning, MRI is useful for identifying areas of abnormal or damaged tissue, but only enables brain function to be analysed by linking damage on a scan with visible symptoms in a patient MRI is especially useful for tumour diagnosis as tumours show up clearly in images generated in this way MRI scans can therefore be used to identify and locate tumours in the brain
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Evaluate magnetic resonance imaging
MRI scans are considerably more expensive to carry out than CT scans but do not carry the risk associated with the use of potentially harmful x-rays MRI scans are often the imaging method of choice during long-term therapies The magnetic field of an MRI scanner can interfere with medical devices such as pacemakers and insulin pumps, so patients with such devices cannot have MRI scans
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Functional Magnetic Resonance Imaging
Functional MRI, or fMRI, functions in a similar way to MRI, making use of a magnetic field and radio waves to generate images of brain structure The difference between MRI and fMRI is that fMRI scans allow brain function to be studied in real time fMRI scans show the location of oxygenated blood in the brain, therefore indicating which brain regions are active at any one time More oxygenated blood flows to active areas of the brain (to supply the neurones with oxygen and glucose) Molecules in oxygenated blood respond differently to a magnetic field than those in deoxygenated blood — the signal returned to the scanner is stronger from the oxygenated blood, which allows more active areas of the brain to be identified. The scanner measures the ratio of oxygenated to deoxygenated haemoglobin
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Using fMRI's
An fMRI scan gives a detailed, high resolution picture of the brain’s structure, similar to an MRI scan — but they can also be used to research the function of the brain. If a function is carried out whilst in the scanner, the part of the brain that’s involved with that function will be more active. E.g. a patient might be asked to move their left hand when in the fMRI scanner. The areas of the brain involved in moving the hand will be highlighted on the fMRI scan. This can be used in medical diagnosis e.g. searching for the cause of seizures, or in psychology research
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fMRIs in medical diagnosis
fMRI scans show damaged or diseased areas of the brain and allow you to study conditions caused by abnormal activity in the brain (some conditions don’t have an obvious structural cause). E.g. an fMRI scan can be taken of a patient’s brain before and during a seizure. This can help to pinpoint which part of the brain’s not working properly and find the cause of the seizure. Then the patient can receive the most effective treatment for the seizures.
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PET scans (Positron Emission Tomography)
Uses radioactive material 1. radioactive tracer is introduced into the body and is absorbed into the tissues. 2. The scanner detects the radioactivity of the tracer — building up a map of radioactivity in the body. Different tracers can be used — e.g. radioactively labelled glucose can be used to look at glucose metabolism. Very detailed and can be used to investigate both the structure and function of the brain in real time
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PET scans in medical diagnosis
PET scans can show if areas in the brain are unusually inactive or active, so they are particularly useful for studying disorders that change the brain’s activity. E.g. in Alzheimer’s disease, metabolism in certain areas of the brain is reduced — PET scans show this reduction when compared to a normal brain.
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Summarised scans
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What is habituation
The reduced response to an unimportant stimulus after repeated exposure over time Habituation means animals don’t waste energy responding to unimportant stimuli. It also means that they can spend more time doing other activities for their survival, such as feeding. E.g. prairie dogs use alarm calls to warn others of a predator but they’ve habituated to humans because we’re not a threat. They no longer make alarm calls when they see humans, so they don’t waste time or energy.
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What happens if a stimulus changes
If a stimulus to which an animal has become habituated changes, then the nervous system will respond to it again E.g. a constant low-level sound that suddenly becomes louder
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What is the process of habituation
Habituation to a stimulus means fewer electrical impulses are sent to the effectors. 1) Repeated exposure to a stimulus decreases the amount of calcium ions that enter the presynaptic neurone. 2) This decrease in the influx of calcium ions means that less neurotransmitter is released from vesicles into the synaptic cleft, so fewer neurotransmitters can bind to receptors in the postsynaptic membrane. 3) Fewer sodium ion channels on the postsynaptic membrane open — so there is a reduced chance of the threshold for an action potential being reached on the postsynaptic membrane. 4) As a result, less neurotransmitter is released and an action potential is less likely to be generated in the postsynaptic neurone The nerve impulse therefore does not reach the effector organ and the animal does not respond to the stimulus
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What is the visual cortex
an area of the cerebral cortex at the back of your brain. The role of the visual cortex is to receive and process visual information.
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How does the visual cortex recieve and process visual information
Neurones in the visual cortex receive information from either your left or right eye. 1) Neurones are grouped together in columns called ocular dominance columns. If they receive information from the right eye they’re called right ocular dominance columns, and if they receive information from the left eye they’re called left ocular dominance columns. 2) The columns are the same size and they’re arranged in an alternating pattern (left, right, left, right) across the visual cortex.
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How does the visual cortex develop from birth
Soon after birth the neurones in the visual cortex of baby mammals begin to form connections, or synapses, allowing visual information to be transferred through and processed by the visual cortex Both eyes need to be visually stimulated in order for the neurones in the visual cortex to be organised correctly during this period of early development, known as the critical period Synapses that pass on nerve impulses during this critical period are strengthened and become permanent parts of the structure of the visual cortex Synapses that do not receive nerve impulses during this critical period are lost and cannot be re-formed This can result in blindness in one or both eyes if visual stimulation is not provided during the critical period
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Hubel and Wiesal's research on kittens
They stitched shut one eye of each kitten so they could only see out of their other eye. * The kittens were kept like this for several months before their eyes were unstitched. * Hubel and Wiesel found that the kitten’s eye that had been stitched up was blind. * They also found that ocular dominance columns for the stitched up eye were a lot smaller than normal, and the ocular dominance columns for the open eye were a lot larger than normal * The ocular dominance columns for the open eye had expanded to take over the other columns that weren’t being stimulated — when this happens, the neurones in the visual cortex are said to have switched dominance. They repeated the experiments on young and adult monkeys and saw the same results. Hubel and Wiesel’s experiments showed that the visual cortex only develops into normal left and right ocular dominance columns if both eyes are visually stimulated in the very early stages of life.
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What happens when they conducted the same experiment on adult cats
* They stitched shut one eye of each cat, who were kept like this for several months. * When their eyes were unstitched, Hubel and Wiesel found that these eyes hadn’t gone blind. * The cats fully recovered their vision and their ocular dominance columns remained the same.
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Critical period in humans
Hubel and Wiesel’s experiments on cats show there’s a period in early life when it’s critical that a kitten is exposed to visual stimuli for its visual cortex to develop properly. This is called the critical period. The human visual cortex is similar to a cat’s visual cortex (the human visual cortex has ocular dominance columns too) so Hubel and Wiesel’s experiments provide evidence for a critical period in humans.
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Investigation on visual development in humans (cataracts)
Scientists have also investigated visual development in humans, e.g. by looking at cataracts in the eye: A cataract makes the lens in the eye go cloudy, causing blurry vision. * If a baby has a cataract, it’s important to remove the cataract within the first few months of the baby’s life — otherwise their visual system won’t develop properly and their vision will be damaged for life. * If an adult has a cataract then it’s not so serious — when the cataract is removed, normal vision comes back straight away. This is because the visual system is already developed in an adult.
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What happens during the critical period of development
Baby mammals (including humans) are born with lots of neurones in their visual cortex. These neurones need visual stimulation to become properly organised. 2) Proper organisation of the visual cortex involves the elimination of unnecessary synapses to leave behind those that are needed in processing visual information. 1) During the critical period of development, synapses that receive visual stimulation and pass nerve impulses into the visual cortex are retained. 2) Synapses that don’t receive any visual stimulation and don’t pass on any nerve impulses to the visual cortex are removed. 3) This means that if the eyes are not stimulated with visual information during this critical period of development, the visual cortex will not develop properly as many of the synapses will be destroyed.
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Ethical issues with using animals in medical research
AGAINST Animals are different from humans, so drugs tested on animals may have different effects in humans. Experiments can cause pain and distress to animals. There are alternatives to using animals in research, e.g. using cultures of human cells or using computer models to predict the effects of experiments. Some people think that animals have the right to not be experimented on, e.g. animal rights activists. FOR Animals are similar to humans, so research has led to loads of medical breakthroughs, e.g. antibiotics, insulin for diabetics and organ transplants. Animal experiments are only done when it’s absolutely necessary and scientists follow strict rules, e.g. animals must be properly looked after, painkillers and anaesthetics must be used to minimise pain. Using animals is currently the only way to study how a drug affects the whole body — cell cultures and computers aren’t a true representation of how cells may react when surrounded by other body tissues. It’s also the only way to study behaviour. Other people think that humans have a greater right to life than animals because we have more complex brains, e.g. compared to rats, fish, fruit flies (which are commonly used in experiments).
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What does brain development refer to
growth of the brain and the formation of connections between neurones, or neural pathways
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What factors that can be measured to determine brain development
Brain size Number of neurones The level at which the brain is functioning
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Nature-nurture debate
Brain development is influenced by both genetic and environmental factors The impact of genetic factors can be referred to as the impact of 'nature' on development while the impact of environmental factors can be referred to that of 'nurture' It is very difficult to determine which of nature or nurture has the greatest influence on brain development The genes and environment of an organism interact with each other and it is difficult to separate out the impacts of each A scientist would have to completely remove the influence of one of the factors in order to investigate the other
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5 methods for investigating the effects of nature and nurture on brain development
1. Animal Experiments 2. Twin studies 3. Cross cultural studies 4. Newborn studies 5. Brain damage studies
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Animal experiments
1) Scientists study the effects of different environments on the brain development of animals of the same species. Individuals of the same species will be genetically similar, so any differences in their brain development are more likely to be due to nurture than nature. 2) To study the effects of different genes, scientists can genetically engineer mice to lack a particular gene and then raise mice with and without the gene in similar environments. 3) Differences between the brain development of the genetically engineered mice and normal mice are more likely to be due to nature than nurture. For example, animal experiments have shown that: * Rats raised in a stimulating environment have larger brains and get better scores on problem-solving tasks than rats raised in boring environments (e.g. in a bare, dark cage). This suggests nurture plays a big role in brain size and the development of problem-solving skills. * Rats reared in isolation have similar brain abnormalities to those found in schizophrenic patients, suggesting nurture plays a big role in brain development. Mice engineered to lack the Lgl1 gene develop enlarged brain regions and fluid builds up in their brains. This suggests that nature plays a big role in brain development.
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Twin studies
Identical twins are genetically identical to each other so if they are raised in different environments then any differences in brain development would be due to nurture, while similarities would be due to nature E.g. the IQ scores of identical twins are very similar which implies that nature plays an important role in intelligence When identical twins are raised together their environments will be very similar, so it can be very difficult to distinguish between the impacts of nature and nurture Scientists will often use non-identical twins raised in a similar environment as a control group when studying identical twins raised together in the same environment Non-identical twins are genetically different This cancels out the effect of the environment, meaning any observable difference in brain development between the identical and non-identical twins will be likely due to nature Traits that are more common in identical twins than non-identical twins are likely to be determined by largely genetic factors Traits that show little difference between the pairs of twins are likely to be determined by largely environmental factors Stuttering of both twins is more common in identical twins than in non-identical twins. This suggests nature plays a big role in developing the speech area of the brain. * There’s no difference in reading ability between pairs of identical and non-identical twins. This suggests nurture plays a big role in reading ability.
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Cross cultural studies
Children brought up in different cultures have different environmental influences, e.g. beliefs and education. 2) Scientists can study the effects of a different upbringing on brain development by comparing large groups of children who are the same age but from different cultures. 3) Scientists look for major differences in characteristics. Any differences in brain development are more likely to be due to nurture, whereas any similarities will more likely be due to nature The mapping abilities (e.g. perspective drawing) of young children are well-developed across cultures. This suggests that nature plays a big role in mapping abilities.
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New born studies
The brain of a newborn baby hasn’t been affected by the environment. 2) Scientists study the brains of newborn babies to see what functions they’re born with and how developed different parts of the brain are — what they’re born with is more likely to be due to nature than nurture. For example, newborn studies have shown that: * Babies are born with a number of abilities, e.g. they can cry, feed and recognise a human face. This suggests that nature plays a big role in controlling these abilities. * Newborn babies don’t have the ability to speak, suggesting that nurture plays a big role in the ability to speak.
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Brain damage studies
Damage to an adult’s brain can lead to the loss of brain function, e.g. a stroke may cause loss of vision. 2) If an adult’s brain is damaged, it can’t repair itself so well because it’s already fully developed. But a child’s brain is still developing — so scientists can study the effects of brain damage on their development. 3) Scientists compare the development of a chosen function in children with and without brain damage. 4) If the characteristic still develops in children who have brain damage, then brain development is more likely to be due to nurture than nature for that characteristic. 5) If it doesn’t develop in children who have brain damage, then brain development is more likely to be due to nature than nurture for that characteristic (because nurture isn’t having an effect). For example: Children aged 1-3 who were born with damage to the area of the brain associated with language, show a delay in the major language milestones (e.g. understanding words, producing sentences) when compared to children born without brain damage. * But by age 5, their language skills are the same as children with no brain damage. If a young child’s brain is damaged, they can still develop language — this suggests that nurture plays a big role in language development.
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What are neurotransmitters
Chemicals that transmit nerve impulses across synapses Some disorders are linked to an imbalance of specific, naturally occurring neurotransmitters in the brain.
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Parkinsons disease
Parkinson’s disease is a brain disorder that affects the motor skills (the movement) of people. 1) In Parkinson’s disease the neurones in the parts of the brain that control movement are destroyed. 2) These normally produce the neurotransmitter dopamine, so losing them causes a lack of dopamine. 3) This means that less dopamine is released into the synaptic clefts, so less dopamine is available to bind to the receptors on the postsynaptic membranes. 4) Fewer sodium ion channels on the postsynaptic membrane open, so the postsynaptic cell is less likely to depolarise. 5) This means fewer action potentials are produced, leading to symptoms like tremors (shaking) and slow movement. 6) Scientists know that the symptoms are caused by a lack of dopamine so they’ve developed drugs (e.g. L-dopa, see below) to increase the level of dopamine in the brain.
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Depression
Scientists think there’s a link between a low level of the neurotransmitter serotonin and depression. 1) Serotonin transmits nerve impulses across synapses in the parts of the brain that control mood. 2) Scientists know that depression is linked to a low level of serotonin so they’ve developed drugs (antidepressants) to increase the level of serotonin in the brain. 3) Some drugs that are used to treat depression (called selective serotonin reuptake inhibitors — SSRIs) increase serotonin levels by preventing its reuptake at synapses.
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L-dopa
L-dopa is a drug that’s used to treat the symptoms of Parkinson’s disease. 2) Its structure is very similar to dopamine. 3) When L-dopa is given, it’s absorbed into the brain and converted into dopamine by the enzyme dopa-decarboxylase (dopamine can’t be given to treat Parkinson’s disease because it can’t enter the brain). This increases the level of dopamine in the brain. 4) A higher level of dopamine means that more nerve impulses are transmitted across synapses in the parts of the brain that control movement. 5) This gives sufferers of Parkinson’s disease more control over their movement.
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MDMA (ecstasy)
MDMA increases the level of serotonin in the brain. 2) Usually, serotonin is taken back into a presynaptic neurone after triggering an action potential, to be used again. 3) MDMA increases the level of serotonin by inhibiting the reuptake of serotonin into presynaptic neurones — it binds to and blocks the reuptake proteins on the presynaptic membrane. 4) MDMA also triggers the release of serotonin from presynaptic neurones. 5) This means that serotonin levels stay high in the synapse and cause depolarisation of the postsynaptic neurones in parts of the brain that control mood. 6) So the effect of MDMA is mood elevation. When an individual takes MDMA they may feel extreme euphoria and enhanced touch and bodily sensations
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Drugs for treatment of depression
SSRIs (selective serotonin reuptake inhibitors) are a class of antidepressant that prevent the uptake of serotonin at synapses; this increases the overall levels of serotonin in the brain TCAs (tricyclic antidepressants) increase levels of both serotonin and noradrenaline in the brain MAOB inhibitors inhibit enzymes that would otherwise break down neurotransmitters in the synaptic clefts in the brain
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Drugs for the treatment of Parkinsons
Dopamine agonists Produce the same effect as dopamine by binding to and activating the dopamine receptors on the postsynaptic membrane Dopamine precursors These are chemicals that can be converted into dopamine in the neurones E.g. L-dopa Enzyme inhibitors Monoamine oxidase B (MAOB) inhibitors inhibit the activity of enzymes that would normally break down dopamine in the synaptic cleft, raising levels of dopamine present in the brain Gene therapy This would involve the addition of genes to the affected cells in the brain to either increase dopamine production or prevent the destruction of dopamine-producing cells Stem cell therapy Stem cells could be used to replace the lost dopamine-producing cells in the brain
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What is personalised medicine
involves the development of targeted drugs to treat a variety of human diseases in individuals with different genotypes Such drugs can be tested on synthetic tissues; groups of cells cultured in a lab that are genetically identical to certain groups of patients
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What is HGP
The Human Genome Project (HGP) was a 13 year long project that identified all of the genes found in human DNA (the human genome). 2) The information obtained from the HGP is stored in databases. 3) Scientists use the databases to identify genes, and so proteins, that are involved in disease. 4) Scientists are using this information to create new drugs that target the identified proteins, e.g. scientists have identified an enzyme that helps cancer cells to spread around the body — a drug that inhibits this enzyme is being developed. 5) The HGP has also highlighted common genetic variations between people. 6) It’s known that some of these variations make some drugs less effective, e.g. some asthma drugs are less effective for people with a particular mutation. 7) Drug companies can use this knowledge to design new drugs that are tailored to people with these variations — these are called personalised medicines. 8) Doctors can also personalise a patient’s treatment by using their genetic information to predict how well they will respond to different drugs and only prescribe the ones that will be most effective.
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Genetic screening
Genetic screening allows individuals with a high chance of developing specific diseases to be identified and means that preventative measures can be taken e.g. Certain genetic mutations are known to increase the risk of an individual developing breast cancer, so those who know that they have such a mutation can have surgery in advance to reduce their risk An individual may be able to make certain life choices regarding diet and lifestyle based on knowledge of their genetic risk of cancers and heart disease Doctors can also use an individual's genome to work out how well they might respond to specific treatments, allowing treatments to be selected on the basis of an individual's genotype
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Social, moral and ethical issues
Increased research costs for drug companies could increase the price of new medicines and mean that only wealthier people have access to personalised medicine There is fear that insurance companies and employers may use personalised medical data against individuals to unfairly discriminate against them e.g. insurance costs might increase for people with certain genetic variants Some patients may be refused personalised medicine if it is not predicted to be that effective for them, even if there are no other treatment options Knowing that the only medication available may not work could be very distressing for the individual being treated and their families as it could be their only hope to treat a disease
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What are GMO's
Genetically modified organisms (GMOs) are organisms that have had their DNA altered. Microorganisms, plants and animals can all be genetically modified to produce proteins which are used as drugs
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How are microorganisms genetically engineered to produce drugs
1) The gene for the protein (drug) is isolated using enzymes called restriction enzymes. 2) The gene is copied using PCR 3) Copies are inserted into plasmids (small circular molecules of DNA). - plasmids are a type of vector, vectors carry genes into an organism 4) The plasmids are transferred into microorganisms. 5)The genetically modified micro-organisms are grown in large fermenters containing nutrients, enabling them to multiply and produce large quantities of the new protein 6) The protein can then be purified and used as a drug. Lots of drugs are produced from genetically modified bacteria, for example human insulin (used to treat Type 1 diabetes) and human blood clotting factors (used to treat haemophilia).
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How are plants genetically engineered to produce drugs
1) After the gene for the protein is inserted into a plasmid and then transferred to a bacterial cell 2) The bacterium infects a plant cell. - bacterium is used as a vector to carry the gene into the plant 3) The bacterium inserts the gene into the plant cell DNA — the plant cell is now genetically modified. 4) The plant cell is grown into an adult plant — the whole plant contains a copy of the gene in every cell. 5) The protein produced from the gene can be purified from the plant tissues, or the protein (drug) could be delivered by eating the plant. Some drugs have been produced from genetically modified plants, for example human insulin and a cholera vaccine.
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How are animals genetically engineered to produce drugs
1. The gene for the protein (drug) is injected into the nucleus of a fertilised animal egg cell (zygote) 2) The egg cell is then implanted into the uterus of a surrogate adult animal — it grows into an aadult animal that contains a copy of the gene in every cell. 3) The protein produced from the gene is normally purified from the milk of the animal. Various animals have been modified with human genes to produce drugs, for example human antithrombin (used to treat people with a blood clotting disorder) has been produced from genetically modified goats.
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Benefits associated with using GMO's
1. Agricultural crops can be modified so that they give higher yields or are more nutritious. This means these plants can be used to reduce the risk of famine and malnutrition. 2) Crops can also be modified to have pest resistance, so that fewer pesticides are needed. This reduces costs (making food cheaper) and reduces any environmental problems associated with using pesticides. 3) Industrial processes often use enzymes. These enzymes can be produced from genetically modified organisms in large quantities for less money, which reduces costs. 4) Some disorders can now be treated with human proteins from genetically engineered organisms instead of with animal proteins. Human proteins are safer and more effective. For example, Type 1 diabetes used to be treated with cow insulin but some people had an allergic reaction to it. Human insulin, produced from genetically modified bacteria, is more effective and doesn’t cause an allergic reaction in humans. 5) Vaccines produced in plant tissues don’t need to be refrigerated. This could make vaccines available to more people, e.g. in areas where refrigeration (usually needed for storing vaccines) isn’t available. 6) Producing drugs using plants and animals would be very cheap because once the plants or animals are genetically modified they can be reproduced using conventional farming methods. This could make some drugs affordable for more people, especially those in poor countries.
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Risks associated with using GMO's
1) Some people are concerned about the transmission of genetic material. For example, if herbicide-resistant crops interbreed with wild plants it could create ‘superweeds’ — weeds that are resistant to herbicides, and if drug crops interbreed with other crops people might end up eating drugs they don’t need (which could be harmful). 2) Some people are worried about the long-term impacts of using GMOs. There may be unforeseen consequences. 3) Some people think it’s wrong to genetically modify animals purely for human benefit.
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Risks and benefits (table)