Coordination Flashcards

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1
Q

Describe the neurone cell body.

A

Contains a nucleus and large amounts of rough endoplasmic reticulum. This is associated with the production of proteins and neurotransmitters.

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2
Q

Describe a neurones dendrons.

A

Small extensions of the cell body which subdivide into smaller branched fibres, called dendrites, that carry nerve impulses towards the cell body.

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3
Q

Describe the neurone axon.

A

A single long fibre that carries nerve impulses away from the cell body.

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4
Q

Describe the Schwann cells.

A

Surround the axon, protecting it and providing electrical insulation. They also carry out phagocytosis (removal of cell debris) and play a part in nerve regeneration. Schwann cells wrap themselves around the axon many times, so that layers of their membranes build up around it.

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5
Q

Describe the myelin sheath.

A

Forms a covering to the axon and is made up of the membranes of the Schwann cells. These membranes are rich in a lipid known as myelin. Neurones with a myelin sheath are called myelinated neurones.

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6
Q

Describe the nodes of Ranvier.

A

Gaps between adjacent Schwann cells where there is no myelin sheath. The gaps are 2-3 um long and occur every 2-3 mm in humans.

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7
Q

Describe sensory neurones.

A

Transmit nerve impulses from a receptor to an intermediate or motor neurone. They have on dendron that carries the impulse towards the cell body and one axon that carries it away from the cell body.

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8
Q

Describe motor neurone.

A

Transmit nerve impulses from an intermediate or sensory neurone to an effector, such as a gland or muscle. They have a long axon and many short dendrites.

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9
Q

Describe intermediate neurone.

A

Transmit nerve impulses between neurones, for example, from sensory to motor neurones. They have numerous short processes.

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10
Q

Define a nerve impulse.

A

A self propagating wave of electrical disturbance that travels along the surface of the axon membrane. Temporary reversal of the electrical potential difference across the axon membrane.

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11
Q

How is the movement of ions, such as sodium (Na+) ions and potassium (K+) ions, across the axon membrane controlled?

A
  • The phospholipid bilayer of the axon plasma membrane prevents sodium and potassium ions diffusing across it.
  • Molecules of proteins, known as intrinsic proteins, span phospholipid bilayer. These proteins contain channels, called ion channels, which pass through them. Some of the channels have gates, which can be opened or closed in order to allow Na+ or K+ ions to move through them or stop them from passing through. Some channels stay open all the time, allowing Na+ and K= ions to diffuse through them.
  • Some intrinsic proteins actively transport K+ ions into the axon and sodium ions out of the axon. Called sodium-potassium pump.
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12
Q

What is the resting potential (charge)

A

Ranges from 50 to 90 mV but usually 65 mV. Axon is polarised

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13
Q

What events cause the establishment of the potential difference during the resting potential.

A
  • Na+ ions actively transported OUT of the axon by Na-K pumps.
  • K+ ions actively transported into axon by Na-K pumps.
  • The active transport of Na+ ions is greater than that of K+ ions, so 3 Na+ ions move out for every 2 K+ in.
  • Na+ and K+ ions are positive, however the outward movement of Na+ ions is greater than the inward movement of K+ ions. As a result, there are more Na+ ions in tissue fluid surrounding the axon than in the cytoplasm, and more K+ ions in the cytoplasm than in the tissue fluid, thus creating a chemical gradient.
  • The Na+ ions begin to diffuse back naturally into the axon while the K+ ions begin to diffuse back out.
  • However, most of the K+ gates in the channels are open, while most of Na+ gates are closed.
  • As a result the axon membrane is 100 times more permeable to K+ ions, which therefore diffuse back out of the axon faster than Na+ ions diffuse back in. This further increases potential difference (difference in charge) between -ve inside and +ve outside of axon.
  • There is also an electrical gradient. As more K+ ions diffuse out of the axon, so the outside of the axon becomes more and more +ve. Further outward movement of K+ ions then becomes difficult because, being +ve they are attracted to the overall -ve state inside the axon which compels them to move in and repelled by +ve outside when prevents them moving out.
  • An equilibrium is established in which the chemical and electrical gradients are balanced and there is no net movement of ions.
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14
Q

What is the action potential? (simple)

A

When a stimulus is received by a receptor or nerve ending, its energy causes a temporary reversal of charges on the axon membrane. As a result the -ve charge of -65 mV becomes +40mV. Membrane is said to be depolarised.

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15
Q

Why does depolarisation occur during the action potential.

A

The channels in the axon membrane change shape, and hence open or close, depending on the voltage across the membrane. Therefore called voltage gated channels.

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16
Q

Describe the action potential.

A
  1. At resting potential some K voltage gated channels are open (permanently) but some Na voltage gated channels are closed.
  2. The energy of the stimulus cause some Na voltage gates channels to open and therefore sodium ions diffuse into the axon through these channels along their electrochemical gradient. Being +vely charged they trigger a reversal of potential difference across the membrane.
  3. As the Na+ ions diffuse into the axon, so more Na channels open, causing an even greater influx of Na+ ions by diffusion.
  4. Once the action potential of around +40mV has been established, the voltage gates on Na+ ion channels close (preventing further influx) and voltage gates on K+ ions begin to open.
  5. The electrical gradient that was preventing further outward movement of K+ ions is now reversed, causing more K+ ion channels to open. This means that yet more K+ ions diffuse out, causing repolarisation of the axon.
  6. The outward diffusion of these K+ ions causes a temporary overshoot of the electrical gradient, with the inside of the axon being more -ve (relative to outside) than usual (HYPERPOLARISATION). The gates on the K+ ion channels now close and the activities of the sodium-potassium pumps once again cause Na+ ions to be pumped out and K+ ions in. The resting potential of -65mV is re-established. Axon is repolarised.
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17
Q

Does the size of the action potential change?

A

No, remains the same from one end of an axon to other.

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18
Q

How (simply) does an action potential pass along a membrane?

A

Nothing physically moves but rather the reversal of electrical charge is reproduced at different points along axon.
As one region of the axon produces an action potential and becomes depolarised, it acts as a stimulus for the depolarisation of the next region of the axon. In this manner, action potentials are regenerated along each small region of the axon membrane. In the meantime, the previous region of the membrane returns to resting potential, that is, it undergoes repolarisation.

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19
Q

Describe the process of the passage of an action potential along an unmyelinated axon.

A
  1. At resting potential the concentration of Na+ ions outside the axon membrane is high relative to the inside, whereas that of the K+ ions is high inside the membrane relative to outsied. The overall conc. of +ve ions is, however, greater on the outside, making this +ve compared to inside. Axon membrane is POLARISED.
  2. A stimulus causes a sudden influx of Na+ ions and hence a reversal of charge on the axon membrane. This is the action potential and the membrane is DEPOLARISED.
  3. The localised electrical circuits established by the influx of Na+ ions cause the opening of Na voltage-gated channels a little further along the axon. The resulting influx of Na+ ions in this region causes DEPOLARISATION. Behind the new region of depolarisation, the Na voltage-gated channels close and K ones open, K ions begin to leave the axon along their electrochemical gradient.
  4. The action potential is propagated in the same way further along the axon. The outward movement of the K+ ions has continued to the extent that the axon membrane behind the action potential has returned to its original state (+ve outside, -ve inside). REPOLARISED.
  5. Repolarisation of the axon allows Na+ ions to be actively transported out, once again returning the axon to its resting potential in readiness for new stimulus if it comes.
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20
Q

Describe the passage of an action potential across a myelinated axon.

A

In myelinated axons, the fatty sheath of myelin around the axon act as an electrical insulator, preventing action potentials from forming. At intervals of 1-3 mm there are breaks in this myelin insulation, called nodes of Ranvier. Action potentials occur at these points. the localised circuits therefore arise between adjacent nodes of Ranvier and the action potentials in effect “jump” from nose to node in a process known as saltatory conduction. As a result, an action potential passes along a myelinated neurone faster than along an unmyelinated one.

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21
Q

What factors affect the speed at which action potentials travel.

A
  • The myelin sheath. Acts as an electrical insulator, Action potential jumps from one node of Ranvier to another.. Increases speed of conductance from 30ms-1 to 90ms-1.
  • Diameter of axon. Greater the diameter the faster the speed of conductance. Due to less leakage of ions from a large axon (leakage makes membrane potentials harder to maintain).
  • Temperature. Affects the rate of diffusions of ions and therefore the higher the temp. the faster the nerve impulse. the energy for active transport comes from respiration which is controlled by enzymes (as is Na-K pump). Enzymes function faster at higher temps. to a point. Above a certain temp. enzymes and plasma membrane protein denature.
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22
Q

What is the refractory period.

A

Once an action potential has been created in any region of an axon, there is a period afterwards when inward movement of Na+ ions is prevented because the Na voltage gated channels are closed. During this time it is impossible for a further action potential to be generated.

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23
Q

What is the purpose of the refractory period (3).

A
  1. Ensures that an action potential is propagated in one direction only. An action potential can only pass from an active region to a resting region. This is because an action potential cannot be propagated in a region that is refractory, which means it can only move in forwards direction. Prevents action potential spreading in both directions.
  2. Produces discrete impulses. Due to the refractory period, a new action potential cannot be formed immediately behind the first one. This ensures that action potentials are separated from one another.
  3. It limits the number of action potentials. As action potentials are separated from one another this limits the number of action potentials that can pass along an axon in a given time.
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24
Q

Define threshold value.

A

The minimum intensity that a stimulus must reach in order to trigger an action potential in a neurone.

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25
Q

Why are nerve impulses described as all or nothing responses?

A

There is a certain level of stimulus, called the threshold value, which triggers an action potential. Below the threshold value, no action potential, and therefore no impulse, is generated. Any stimulus, of whatever strength, that is below the threshold value will fail to generate an action potential- nothing part. Any stimulus above threshold value will succeed in generating an action potential. It does not matter how much above threshold a stimulus is, it will only generate one action potential- all part.

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26
Q

How can an organism perceive the size of an impulse?`

A
  • By the number of impulses passing in a given time. The larger the stimulus, the more impulses that are generated in a given time.
  • By having different neurones with different threshold values. The brain interprets the number and type of neurones that pass impulses as a result of a given stimulus and thereby determines its size.
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27
Q

Why do cells need to be coordinated?

A

As species have evolved, their cells have become adapted to perform specialist functions. This means cells have lost the ability to perform other functions. This makes cells dependent upon others to carry out the functions they have lost.
These different functional systems must be coordinated if they are to perform efficiently in a coordinated fashion.

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28
Q

What are the two main systems of coordination in mammals?

A
  • The nervous system

- The hormonal system

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29
Q

How does the nervous system pass impulses?

A

Use nerve cells to pass electrical impulses along their length.

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30
Q

How does the nervous system stimulate target cells?

A

They stimulate their target cells by secreting chemicals known as neurotransmitters directly on to them. (quick)

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31
Q

What are the responses of the nervous system like?

A

Rapid communication between specific parts of an organism. The responses produced are often short lived and restricted to a localised region of the body.
Effect is temporary and reversible.

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32
Q

What is an example of nervous coordination?

A

A reflex action, such as the withdrawal of the hand from an unpleasant stimulus.

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33
Q

How does the hormonal system stimulate target cells?

A

Produces chemicals that are transported in the blood plasma to their target cells, which they then stimulate.

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34
Q

What are the responses of the hormonal system like?

A

Transmission and response slower, less specific form of communication between parts of an organism. The responses are often long lasting and widespread. Travel to all parts of the body but only target organs respond.

Effect may be permanent and irreversible.

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35
Q

What is an example of hormonal communication?

A

The control of blood glucose.

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36
Q

What are chemical mediators?

A

These are chemicals that are released from certain mammalian cells and have an effect on cells in their immediate vicinity.

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37
Q

What types of cells usually release chemical mediators and what does it lead to?

A

Typically released by infected or injured cells and cause small arteries and arterioles to dilate. This leads to a rise in temperature and swelling of the affected area- so called “inflammatory response”.

38
Q

What are two examples of chemical mediators?

A

HISTAMINE

PROSTAGLANDINS

39
Q

Where is histamine stored?

A

certain white blood cells

40
Q

When is histamine released?

A

Following injury or in response to an allergen, such as pollen.

41
Q

What does histamine cause?

A

Dilation of small arteries and arterioles and increased permeability of capillaries, leading to localised swelling, redness and itching.

42
Q

Where are prostaglandins found?

A

In cell membranes

They are not stored but synthesised when needed.

43
Q

What do prostaglandins cause?

A

Dilation of small arteries and arterioles. Their release following injury increases the permeability of capillaries. They also affect blood pressure and neurotransmitters. In doing so they affect pain sensation.

44
Q

Why do prostaglandins not last long at site of formation?

A

rapidly diffuse to other sites or are rapidly metabolised.

45
Q

Where else are prostaglandins used?

A

In the lungs- modify ventilation by constricting or contracting airways.

In newborns- Prostaglandins are instrumental in termination of umbilical blood flow and in the diversion of venous blood to the lungs for aeration.

46
Q

How are prostaglandins made?

A

Not secreted from a gland, instead they are made by a chemical reaction at the site where they are needed and can be made in nearly all organs of the body.

47
Q

What are two types of prostaglandins?

A

Thromboxane- when a blood vessel is injured, thromboxane stimulates the formation of a blood clot to try and heal the damage; it also causes the muscle in the blood vessel wall to contract to try and prevent blood loss.

Prostacylin- Opposite effect of thromboxane. Reduces blood clotting and removes any clots which are no longer needed, also causes muscle in blood vessel wall to relax, so that vessel dilates.

48
Q

What must plants respond to, how and why do they respond?

A
  • Light- Stems grow towards light (+vely phototropic) because light is needed for photosynthesis.
  • Gravity- Plants need to be firmly anchored in the soil. Roots are sensitive to gravity and grow in the direction of its pull. (+vely geotropic).
  • Water- Almost all plant roots grow towards water (+vely hydrotropic) in order to absorb it for use in photosynthesis and other metabolic processes, as well as for support.
49
Q

Why is the term pant growth factor used rather than plant hormone?

A
  • They exert their influences by affecting growth.
  • Unlike animal hormones, they are made by cells located throughout the plant rather than in particular organs.
  • Unlike animal hormones, some plant growth factors affect the tissues that release them rather than acting on a distant target organ.
50
Q

Properties of plant growth factors.

A

Produced in small quantities. They have their effects close to the tissue that produces them.

51
Q

What is an example of a plant growth factor?

A

indoleacetic acid (IAA)

52
Q

What does IAA do?

A

Causes plant cells to elongate.

53
Q

Describe the process of a young shoot bending towards light.

A
  1. Cells at the tip of the shoot produce IAA, which is then transported down the shoot.
  2. The IAA is initially transported to all sides as it begins to move down the shoot.
  3. Light causes the movement of IAA from the light side to the shaded side of the shoot.
  4. A greater concentration of IAA builds up on the shaded side of the shoot than the light side.
  5. As IAA causes elongation of cells there is a greater concentration of IAA on the shaded side of the shoot, the cells on this side elongate more.
  6. The shaded side of the shoot grows faster, causing the shoot to bend towards the light.
54
Q

SYNAPSE

A

Junction between a neurone ans another neurone, or between a neurone and an effector cell, e.g. a muscle or a gland cell.

55
Q

SYNAPTIC CLEFT

A

Tiny gap between the cells at a synapse (between presynaptic knob and postsynaptic membrane.

56
Q

SYNAPTIC KNOB

A

The presynaptic neurone has a swelling, this contains vesicles filled with chemicals called neurotransmitters.
Contains many mitochondria and large amounts of endoplasmic reticulum

57
Q

Synapses transmit impulses from one neurone to another, what does this allow?

A
  • A single impulse along one neurone to be transmitted to a number of different neurones at a synapse. This allows a single stimulus to create a number of simultaneous responses.
  • A number of impulses to be combined at a synapse. This allows stimuli from different receptors to interact in order to produce a single response.
58
Q

NEUROTRANSMITTER

A

One of a number of chemicals that are involved in communication between adjacent neurones or between nerve cells and muscles. Two important examples are acetylcholine and noradrenaline.

Only made in presynaptic neurone.

59
Q

When are neurotransmitters released into synaptic cleft?

A

When an action potential reaches the synaptic knob.

60
Q

What do neurotransmitters do once they are released?

A

The neurotransmitter diffuses across the synapse to receptor molecules on the postsynaptic neurone.

61
Q

What happens after the neurotransmitter diffuses across the synapse?

A

Binds with the receptor molecules and sets up a new action potential in the postsynaptic membrane.

62
Q

UNIDIRECTIONALITY

A

Synapses can only pass impulses in one direction from the presynaptic neurone to the postsynaptic neurone. In this way they acts like valves.

63
Q

SUMMATION

A

When action potentials are made to have sufficient amounts of neurotransmitter to trigger a new action potential.

Entails a build up of neurotransmitter in the synapse by one of two ways:
Spatial summation
Temporal summation.

64
Q

What is the problem with low frequency action potentials?

A

Often produce insufficient neurotransmitter to trigger a new action potential in the post synaptic neurone.

65
Q

SPACIAL SUMMATION

A

A number of different presynaptic neurones together release enough neurotransmitter to exceed the threshold value of the postsynaptic neurone. Together they therefore trigger a new action potential.

66
Q

TEMPORAL SUMMATION

A

In which a single presynaptic neurone releases neurotransmitter many times over a short period. If the total amount of neurotransmitter exceeds the threshold value of the postsynaptic neurone, then a new action potential is triggered.

67
Q

INHIBITION

A

On the post-synaptic membrane of some synapses, the protein channels carrying chloride ions (Cl-) can be made to open. This leads to an inwards diffusion of Cl- ions, making the inside of the postsynaptic membrane even more negative than when it is at resting potential. This is called hyperpolarisation and makes it less likely that a new action potential will be created.
THESE SYNAPSES ARE CALLED INHIBITORY SYNAPSES

68
Q

Describe the mechanism of transmission across a cholinergic synapse?

A
  1. The arrival of an action potential at the end of the presynaptic neurone causes calcium ion channels to open and calcium ions (Ca2+) enter the synaptic knob.
  2. The influx of Ca2+ ions into the presynaptic neurone causes synaptic vesicles to fuse with the presynaptic membrane, so releasing acetyl choline into the synaptic cleft.
  3. Acetyl choline molecules fuse with receptor sites on the Na+ ion channel in the membrane of the postsynaptic neurone. This causes the sodium ion channels to open, allowing Na+ ions to diffuse in rapidly along a conc. gradient.
  4. The influx of sodium ions generates a new action potential in the postsynaptic neurone.
  5. Acetylcholinesterase hydrolyses acetylcholine into choline and ethanoic acid (acetyl), which diffuse back across the synaptic cleft into the presynaptic neurone. In addition to recycling the choline and ethanoic acid, the breakdown of acetylcholine also prevents it from continuously generating a new action potential in the postsynaptic neurone.
  6. ATP released by mitochondria is used to recombine choline and ethanoic acid into acetylcholine. This is stored in synaptic vesicles for future use. Sodium ion channels close in the absence of acetylcholine in the receptor sites.
69
Q

Where do cholinergenic synapses most commonly occur?

A

in vertebrates, where they occur in the centrak nervous system and at neuromuscular junctions.

70
Q

EXITATORY NEUROTRANSMITTERS/RECEPTORS

A

They create a new action potential in the postsynaptic neurone.

71
Q

INHIBITORY NEUROTRANSMITTERS/RECEPTORS

A

They make it less likely that a new action potential will be created by the postsynaptic neurone.

72
Q

What are the two main ways that drugs act on synapses?

A
  • They stimulate the nervous system by creating more action potentials in postsynaptic neurones.
  • They inhibit the nervous system by creating fewer action potentials in postsynaptic neurones.
73
Q

How can a drug stimulate the nervous system?

A

Mimics neurotransmitter, stimulating the release of more neurotransmitter or inhibiting the enzyme which breaks down the neurotransmitter.

74
Q

What is the outcome of a drug which stimulates the nervous system?

A

To enhance the body’s responses to impulses passed along the postsynaptic neurone.

75
Q

How can a drug inhibit the nervous system?

A

By inhibiting the release of neurotransmitter or blocking the receptors on sodium/potassium ion channels on the postsynaptic neurone.

76
Q

What is the outcome of a drug which inhibits the nervous system?

A

To reduce the body’s responses to impulses passed along the postsynaptic neurone.

77
Q

What does the effect of a drug on a neurotransmitter depend on?

A

The type of transmitter.
e.g. a drug that inhibits a n exitatory neurotransmitter will reduce a particular effect, but a drug that inhibits an inhibitory neurotransmitter will enhance a particular effect.

78
Q

ENDORPHINS

A

Neurotransmitters used by certain sensory nerve pathways, especially pain pathways.
Endorphins block the sensation of pain by binding to pain receptor sites.

79
Q

What drugs bind to the specific receptor sites used by endorphins?

A

Morphine, codeine and heroin.

80
Q

SEROTONIN

A

A neurotransmitter involved in the regulation of sleep and certain emotional states (ACTS TO LIGHTEN MOOD). Reduced activity of the neurones that release serotonins is thought to be one cause of clinical depression.
When depression occurs, there may be a reduced amount of serotonin released from nerve cells in the brain.

81
Q

What drug affects serotonin within synaptic clefts?

A

Prozac

82
Q

How does prozac work?

A

prevent serotonin being reabsorbed back into the nerve cells in the brain so more builds up.

83
Q

GABA

A

A neurotransmitter that inhibits the formation of action potentials when it binds to postsynaptic neurones.

84
Q

What does valium do?

A

A drug that enhances the binding of GABA to its receptors.

85
Q

AGONSITIC DRUGS

A

Are the same shape as neurotransmitters so they mimic their action at receptors. This means more receptors are activated.

86
Q

Give an example of an agonistic drug and explain how it works.

A

NICOTINE mimics acetylcholine so binds to nicotinic cholinergic receptors in the brain.

87
Q

ANTAGONISTIC DRUGS

A

Block receptors so they can’t be activated by neurotransmitters. This means fewer receptors can be activated.

88
Q

What is an example of an antagonistic drug and how does it work?

A

CURARE blocks the effects of acetylcholine by blocking nicotinic cholinergic receptors at neuromuscular junctions, so muscle cells can’t be stimulated. This results in the muscles being paralysed.

89
Q

What does it mean if a drug inhibits the enzyme that breaks down neurotransmitters?

A

More neurotransmitters in the synaptic cleft to bind to receptors and they’re there for longer.

90
Q

How do nerve gases work?

A

Stop acetylcholine from being broken down in the synaptic cleft. Can lead to loss of muscle control.

91
Q

What is an example of a drug that stimulates the release of neurotransmitter and one that inhibits the release?

A

AMPHETAMINES: Stimulate the release of neurotransmitter from the presynaptic neurone so more receptors are activated.

ALCOHOL: Inhibit the release of neurotransmitters from the presynaptic neurone so fewer receptors are activated.

92
Q

How do amphetamines increase the amount of dopamine in the synaptic cleft?

A
  1. They invade the nerve cell preceding the synapse (or gap) and push out extra dopamine into the synapse
  2. They then block the transporter molecules to prevent the re-uptake of dopamine, artificially holding the dopamine at high levels