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SEM 2 Brain & Behaviour > Neurotransmitters & (basic) Psychopharamcology > Flashcards

Neurotransmitters & (basic) Psychopharamcology Flashcards

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1
Q

The study of the effects of drugs on the nervous system and on behaviour

This is known as…?

A

Psychopharmacology

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2
Q

What is Psychopharmacology?

A

The study of the effects of drugs on the nervous system and on behaviour

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3
Q

Why is it important to study Psychopharmacology?

A
  • Our brain develops a good protective system (blood-brain barrier)
  • BBB does not allow some substances to enter the brain
  • Studying Psychopharmacology tells us that drugs are able to cross the BBB to affect the CNS
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4
Q

Drugs are able to cross the BBB to affect the CNS

How is this possible?

A
  • There are some substances that can cross the BBB through active transport (because they are lipid soluble)
  • The membrane of BBB is made of lipids and if a substance can be dissolved in lipids, it has greater potential of crossing BBB
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5
Q

Define drug effects

A

The changes a drug produces in an animal’s physiological processes and behavior. In the nervous system, most drugs affect synaptic transmission.

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6
Q

The changes a drug produces in an animal’s physiological processes and behaviour. In the nervous system, most drugs affect synaptic transmission.

This is known as…?

A

Drug effects

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7
Q

What are the 2 types of drugs?

A

1) Antagonist
2) Agonist

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8
Q

A drug that opposes or inhibits the effects of a particular neurotransmitter on the postsynaptic cell.

What type of drug is this?

A

Antagonist

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9
Q

A drug that facilitates the effects of a particular neurotransmitter on the postsynaptic cell.

What type of drug is this?

A

Agonist

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10
Q

What is an agonist drug?

A

A drug that facilitates the effects of a particular neurotransmitter on the postsynaptic cell.

Simply - A drug that imitate/pretend to be neurotransmitters that bind with receptors in the brain to increase the effects of neurotransmitters

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11
Q

What is an antagonist drug?

A

A drug that opposes or inhibits the effects of a particular neurotransmitter on the postsynaptic cell.

Simply = A drug that blocks neurotransmitters from doing what they usually do (stop the effect or action of neurotransmitters)

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12
Q

What are sites of action?

A

The locations at which molecules of drugs bind with the molecules located on or in cells of the body

This affects some biochemical processes of the cells

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13
Q

The locations at which molecules of drugs bind with the molecules located on or in cells of the body

This is known as…?

A

Sites of action

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14
Q

What are the 4 main sites of action?

A

1) Production of neurotransmitters in presynaptic cell
2) Storage and release of neurotransmitters
3) Effects on receptors on postsynaptic cell
4) Effects on reuptake

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15
Q

Which drug increases the release of neurotransmitters?

a. Antagonist
b. Agonist

A

b. Agonist

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16
Q

Which drug blocks the storage of neurotransmitters?

a. Antagonist
b. Agonist

A

a. Antagonist

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17
Q

The most important and most complex site of action of drugs in the nervous system is …?

A

On receptors (both presynaptic and postsynaptic)

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18
Q

What happens when drugs are in our system at the same time as when neurotransmitters are supposed to bind with the receptors?

A

Once a neurotransmitter has been released, it must stimulate the postsynaptic receptors.

Some drugs bind with these receptors, just as the neurotransmitter does (they steal the place of neurotransmitters by mimicking their behaviour and binding with the receptors)

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19
Q

Once a drug has bound with the receptor, it can serve as either …… or ………

A

An agonist or an antagonist

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20
Q

Which drug facilitates transmission?

a. Antagonist
b. Agonist

A

b. Agonist

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21
Q

Which drug blocks transmission?

a. Antagonist
b. Agonist

A

a. Antagonist

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22
Q

What are the 2 types of drug binding?

A

1) Competitive binding (or direct agonist/antagonist)

2) Indirect binding (or indirect agonist/antagonist)

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23
Q

What happens in competitive binding (or direct agonist/antagonist)?

A

Drug molecules bind with and activate receptors

This drug mimics the effects of a neurotransmitter

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24
Q

What are the 4 steps to competitive binding (or direct agonist/antagonist)?

A

1) Drug travels from presynaptic cell
2) Drug binds to receptor on postsynaptic cell
3) If drug is an Agonist, it keeps the postsynaptic site/ion channel open all the time
4) If drug is an Antagonist, it keeps the postsynaptic site/ion channel closed all the time

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25
Q

In competitive binding (or direct agonist/antagonist), what happens if the drug is an antagonist?

A

It keeps the postsynaptic site/ion channel closed all the time

Less ions flow in the cell which stops neurotransmission

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26
Q

In competitive binding (or direct agonist/antagonist), what happens if the drug is an agonist?

A

It keeps the postsynaptic site/ion channel open all the time

More ions flow in the cell which stops neurotransmission

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27
Q

When drug molecules are similar to neurotransmitters, they’re in direct competition to bind with a receptor in the postsynaptic cell

What type of binding is this?

A

Competitive binding (or direct agonist/antagonist)

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28
Q

What happens in indirect binding?

A

A drug that attaches to a binding site on a receptor and facilitates the action of the receptor

It does not interfere with the binding site of the principal neurotransmitter.

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29
Q

What are the 4 steps to indirect binding?

A

1) Drug travels from presynaptic cell
2) Drug binds to a similar neuromodulation binding site as the neurotransmitter but does not take it’s place (happens on postsynaptic cell)
3) If drug is an Agonist, it keeps the postsynaptic site/ion channel open all the time
4) If drug is an Antagonist, it keeps the postsynaptic site/ion channel closed all the time

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30
Q

Drug molecules attach to other sites whilst neurotransmitters attach to their usual site

What type of binding is this?

A

Indirect binding

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31
Q

Some drug molecules do not resemble/imitate neurotransmitters and they find binding site alternatives instead of competing for the same binding site as the neurotransmitters

What type of binding is this?

A

Indirect binding

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32
Q

In indirect binding, what happens if the drug is an agonist?

A

It keeps the postsynaptic site/ion channel open all the time

More ions flow in the cell which stops neurotransmission

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33
Q

In indirect binding, what happens if the drug is an antagonist?

A

It keeps the postsynaptic site/ion channel closed all the time

Less ions flow in the cell which stops neurotransmission

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34
Q

Define reuptake and destruction of neurotransmitters

A

The process of termination of the postsynaptic potential by:

1) Molecules of the neurotransmitter are taken back into the terminal button through the process of reuptake
2) They are destroyed by an enzyme.

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35
Q

What happens in the process of reuptake and destruction of neurotransmitters when drug molecules are present?

A

1) The drug molecules attach to the transporter molecules that are responsible for reuptake and inactivate them, thus blocking reuptake (preventing neurotransmitters from leaving synaptic cleft)

2) In the second case the drug bind with the enzyme that normally destroys the neurotransmitter and prevents the enzymes from working (preventing neurotransmitters from being destroyed)

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36
Q

Both types of drugs prolong the presence of the neurotransmitter in the synaptic cleft (more neurotransmitters remain in the cleft and causes more stimulation of postsynaptic cell by default)

Do they serve as…?

a. Agonist
b. Antagonist

A

a. Agonist

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37
Q

An inert substance given to an organism in lieu of a physiologically active drug; used experimentally to control for the effects of mere administration of a drug

This is known as…?

A

Placebo

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38
Q

Define placebo

A

An inert substance given to an organism in lieu of a physiologically active drug; used experimentally to control for the effects of mere administration of a drug (usually sugar pill)

Simply = A substance that you’re told should produce some kind of effects but in actuality, it is completely harmless/has no specific physiological effect

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39
Q

When experimenters want to investigate the behavioral effects of drugs in humans, they must use control groups whose members receive placebos, or they cannot be sure that the behavioral effects they observe were caused by specific effects of the drug.

This is known as…?

A

Placebo effects

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40
Q

Where people can feel worse after an intervention that should have no ill effects

This is known as…?

A

Nocebo effect

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41
Q

For example:

Doctors say a red pill reduces migraines. So when you consume the red pill, you report that your migraine has been reduced, even though there’s no actual drug in the red pill

What effect is this?

A

Placebo effect

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42
Q

For example:

Doctors say a red pill reduces migraines but it also has nausea side effects. So when you consume the red pill, you report feeling sick and wanting to vomit

What effect is this?

A

Nocebo effect

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43
Q

Define the nocebo effect

A

Where people can feel worse after being told an intervention (that should have no ill effects) has negative sideeffects

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44
Q

What do including placebo and nocebo substances tell us about the way people behave?

A

Tells us that telling people different things can change the results of the experiment

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45
Q

In the brain, most synaptic communication is accomplished by two neurotransmitters

What are they?

A

1) With excitatory effects(glutamate)
2) With inhibitory effects (GABA in the CNS or glycine-spinal cord)

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46
Q

Neurons receive excitatory input from …?

A

Glutamate-secreting terminal buttons

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47
Q

Neurons receive inhibitory input from…?

A

Neurons that secrete either GABA or glycine

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48
Q

Neurons that secrete either GABA or glycine give out…?

a. Excitatory input
b. Inhibitory input

A

b. Inhibitory input

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49
Q

Glutamate-secreting terminal buttons give out…?

a. Excitatory input
b. Inhibitory input

A

a. Excitatory input

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50
Q

Other than glutamate and GABA, what do other neurotransmitters do?

A

They have modulating effects rather than information-transmitting effects.

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51
Q

The release of neurotransmitters other than glutamate and GABA tends to activate or inhibit ….?

A

Entire circuits of neurons that are involved in particular brain functions.

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52
Q

Is acetylcholine excitatory or inhibitory or both?

A

Both

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53
Q

Is norepinephrine excitatory or inhibitory or both?

A

Excitatory

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54
Q

Is dopamine excitatory or inhibitory or both?

A

Both

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55
Q

Is glutamate excitatory or inhibitory or both?

A

Excitatory

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56
Q

Is serotonin excitatory or inhibitory or both?

A

Both

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57
Q

Is GABA excitatory or inhibitory or both?

A

Inhibitory

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58
Q

Is opioid excitatory or inhibitory or both?

A

Inhibitory

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59
Q

What are the 2 receptors of acetylcholine neurotransmitters?

A

Nicotine and Muscarinic

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60
Q

The primary neurotransmitter secreted by the efferent axons of the CNS

This is known as…?

A

Acetylcholine

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61
Q

What does the release of acetylcholine lead to?

A

The control of muscle contractions and muscle movements

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62
Q

The effects of acetylcholine are generally…?

a. Agonist
b. Antagonist

A

a. Agonist (facilitatory)

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63
Q

ACh is involved in regulating what type of sleep?

A

REM

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64
Q

Apart from REM sleep, what else does the release of ACh help with? List 3 more

A
  • Dreaming (doroslateral pons)
  • Perceptual learning (forebrain)
  • Memory (hippocampus)
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65
Q

Where was ACh first found?

A

At the target of the parasympathetic branch of the ANS – outside of the CNS

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66
Q

Who first discovered ACh?

A

Otto Loewi

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67
Q

What did Otto Loewi do in his experiment involving frog hearts?

A

1) Otto Loewi stimulated the heart of a frog (vagus nerve) with electrical impulses and slowed the heartbeat

2) Loewi had the heart pump a small amount of nutrient solution (extracellular fluid around the heart)

3) When the fluid was transferred to another heart, it operated in a similar way (fluid caused the rate of the heart to slow down without it being stimulated)

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68
Q

What did Otto Loewi discover about the relationship between the chemical substance in our body and our organs?

A

Chemical substances convey nerve signals to organs

Believed = There was some chemical substance released by the vagus nerve that caused the first heart rate to slow down. The substance was acetylcholine.

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69
Q

Define Cholinergic Synapses

A

Synapses that have acetylcholine transmitters

Usually happens in any transsynaptic transmission

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70
Q

Synapses that have acetylcholine transmitters are called?

A

Cholinergic Synapses

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71
Q

What happens in stage 1 of a cholinergic synapse?

A

An action potential arrives at the presynaptic membrane.

Voltage-gated calcium channels in the presynaptic membrane open

Calcium ions enter the presynaptic neuron

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72
Q

What happens in stage 2 of a cholinergic synapse?

A

Calcium ions cause synaptic vesicles to fuse with the presynaptic membrane

This releases acetylcholine into the synaptic cleft

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73
Q

What happens in stage 3 of a cholinergic synapse?

A

Acetylcholine diffuses across the synaptic cleft and binds to specific neuroreceptor sites (either nicotinic or muscarinic) in the post-synaptic membrane

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74
Q

What happens in stage 4 of a cholinergic synapse?

A

Once acetylcholine binds with the receptors, sodium channels open

Sodium (excitatory) ions diffuse into the postsynaptic membrane

This causes depolarisation, which may initiate an action potential.

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75
Q

What happens in stage 5 of a cholinergic synapse?

A

Acetylcholinesterase (enzyme) breaks down acetylcholine in the synaptic cleft

The products diffuse back into the presynaptic neuron where acetylcholine is resynthesised using energy (ATP) from the mitochondria.

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76
Q

What stage of a cholinergic synapse does this occur in?

Calcium ions cause synaptic vesicles to fuse with the presynaptic membrane

This releases acetylcholine into the synaptic cleft

A

Stage 2

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77
Q

What stage of a cholinergic synapse does this occur in?

Once acetylcholine binds with the receptors, sodium channels open

Sodium (excitatory) ions diffuse into the postsynaptic membrane

This causes depolarisation, which may initiate an action potential.

A

Stage 4

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78
Q

What stage of a cholinergic synapse does this occur in?

Acetylcholine diffuses across the synaptic cleft and binds to specific neuroreceptor sites (either nicotinic or muscarinic) in the post-synaptic membrane

A

Stage 3

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79
Q

What stage of a cholinergic synapse does this occur in?

Acetylcholinesterase (enzyme) breaks down acetylcholine in the synaptic cleft

The products diffuse back into the presynaptic neuron where acetylcholine is resynthesised using energy (ATP) from the mitochondria.

A

Stage 5

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80
Q

What stage of a cholinergic synapse does this occur in?

An action potential arrives at the presynaptic membrane.

Voltage-gated calcium channels in the presynaptic membrane open

Calcium ions enter the presynaptic neuron

A

Stage 1

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81
Q

What are Neuromuscular Junctions?

A

A specialized synapse that bridges the motor neuron and the skeletal muscle fibre

It is crucial for the conversion of electrical impulses originating in the motor neuron to action potentials in the muscle fibre

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82
Q

What is the main effect of ACh outside of the CNS?

A

Muscle contraction

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83
Q

What is the process of muscular contractions due to ACh?

A

Same stages as cholinergic synapses, but the postsynaptic membrane is the muscle fibre membrane (Sarcolemma)

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84
Q

Depolarisation of the sarcolemma leads to …?

A

Contraction of muscle fibre

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85
Q

An ionotropic acetylcholine receptor stimulated by nicotine

This is known as…?

A

Nicotine receptor

86
Q

Define a nicotine receptor

A

An ionotropic acetylcholine receptor stimulated by nicotine

87
Q

Where are nicotine receptors found?

A

The autonomic nervous system and neuromuscular junction

88
Q

Nicotine ACh receptors are postsynaptic membrane of…?

A
  • All automatic ganglia
  • All neuromuscular junctions
  • SOme CNS pathways
89
Q

What happens when ACh molecules bind with nicotinic receptors?

A

The sodium ion channels open and sodium ions rush in causing depolarisation (excitatory; action potential occurs)

90
Q

A metabotropic acetylcholine receptor

This is known as…?

A

Muscarinic receptor

91
Q

Define a muscarinic receptor

A

A metabotropic acetylcholine receptor

92
Q

What do muscarinic receptor do?

A
  • Produces parasympathetic nerve effects in the heart, smooth muscles and glands
  • G-protein-couples receptors (receptors influence ion channels by the means of G-protein)
93
Q

What happens when ACh binds with muscarinic receptors?

A

The sodium ion channels open and sodium ions rush in causing depolarisation (excitatory; action potential occurs)

94
Q

Are nicotinic receptors …?

a. Antagonist
b. Agonist

A

b. Agonist

95
Q

Nicotinic receptors are stimulated by (………) and are blocked by (………..)

A

1) Nicotine
2) Curare (paralysis) = Stops ACh from opening ion channels

96
Q

True or False?

Curare acts at the junction between nerve cells and muscles causing paralysis.

A

True

97
Q

Muscarinic receptors are stimulated by (………) and are blocked by (………..)

A

1) Muscarine (mushroom)
2) Atropine (makes heart beat faster again by depolarising postsynaptic membrane)

98
Q

True or False?

Atropine acts by encouraging acetylcholine to depolarise the post-synaptic membrane and increasing heart rate

A

False

Atropine acts by preventing acetylcholine from depolarising the post-synaptic membrane and increases heart rate

99
Q

What are the 2 main drugs that affect acetylcholine?

A

1) Botulinum toxin (Botox)
2) Black widow spider venom

100
Q

Which of these are acetylcholine antagonists?

1) Botulinum toxin (Botox)
2) Black widow spider venom

A

1) Botulinum toxin (Botox)

101
Q

Which of these are acetylcholine agonists?

1) Botulinum toxin (Botox)
2) Black widow spider venom

A

2) Black widow spider venom

102
Q

Why is Botulinum toxin (Botox) an antagonist drug to acetylcholine?

A

Because it prevents the release of acetylcholine neurotransmitters by the terminal buttons to the muscles

103
Q

What happens to our muscles when Botulinum toxin (Botox) meets acetylcholine?

A

Lack of muscle contractions due to the lack of acetylcholine in muscles

104
Q

What is the behaviour effect of botox in humans?

A
  • People are worse at identifying the emotions of others’ correctly
  • The lack of feedback from their frozen facial muscles impairs their ability to read other people
  • People without botox try on the facial expressions of others to understand what they’re feeling but people with botox can’t do that due to their frozen facial muscles
105
Q

Why is black widow spider venom an agonist drug to acetylcholine?

A

Because it causes excessive/too much release of acetylcholine neurotransmitters

106
Q

What happens to our muscles when black widow spider venom meets acetylcholine?

A

Causes convulsions due to too much muscle contractions

107
Q

What are monoamines?

A

A family of compounds

Neuromodulators derived from single amino acids

108
Q

What are the 4 neurotransmitters that belong to a family of compounds called monoamines?

A

1) Dopamine
2) Norepinephrine
3) Epinephrine
4) Serotonin

109
Q

Because the molecular structures of monoamine substances are similar, some drugs affect the activity of all of them to some degree

True or False?

A

True

110
Q

What does dopamine do?

A

Ensure we have alertness and energy

111
Q

What does Norepinephrine
do?

A

Ensure attention, motivation, pleasure and reward

112
Q

What does Serotonin do?

A

Activates obsessions and compulsions

113
Q

The most basic, single amino acid related to dopamine and norepinephrine is…?

A

Tyrosine

114
Q

When Tyrosine meets an enzyme and goes through a chemical reaction, it becomes…?

A

L-DOPA

115
Q

When L-DOPA meets an enzyme and goes through a chemical reaction, it becomes…?

A

Dopamine

116
Q

When Dopamine meets an enzyme and goes through a chemical reaction, it becomes…?

A

Norepinephrine

117
Q

The reward neurotransmitter is known as…?

A

Dopamine

118
Q

What happens when the reward pathway becomes overstimulated?

A

We experience addiction to something

119
Q

Where does the reward pathway start?

A

In ventral tegmental area

120
Q

What things are considered natural rewards?

A

1) Food
2) Water
3) Sex
4) Nurturing

121
Q

A state in which an organism engages in compulsive behaviour, behaviour is reinforcing (rewarding, pleasurable), loss of control for limiting intake

What is this known as…?

A

Addiction

122
Q

Define addiciton?

A

A state in which an organism engages in compulsive behaviour, behaviour is reinforcing (rewarding, pleasurable)

The more you do/consume something, the more reward or pleasure you get and you can never stop

Loss of control for limiting how much substance you intake

123
Q

What are the 3 components of the brain that make up the reward pathway?

A

1) Prefrontal cortex
2) Nucleus accumbens
3) Ventral tegmental area

124
Q

Studies in the 1950s used rats to test for addiction? What did they do in their experiment?

A

1) Rats were given heroin

2) Heroin was given through consumption

3) If the rats liked the heroin, they press the lever to receive more

4) Heroin was also injected directly into the ventral tegmental area (especially in nucleus accumbens) and rats pressed the lever more often

125
Q

Why do animals and human like heroin so much?

A

Heroin is transformed into morphine in the brain, which stimulates dopamine pathways (especially nucleus accumbens)

This stimulates the reward pathway/system and trigger the release of dopamine (reward neurotransmitter)

126
Q

Define tolerance

A

A state in which organism no longer responds to a drug

A higher dose is required to achieve the same effect

Simply = When you take really high doses of a drug and you no longer respond to lower intakes of the drug

So in order for the drug to have an effect again, you consume an even higher dose of the drug

127
Q

A state in which organism no longer responds to a drug

A higher dose is required to achieve the same effect

This is known as…?

A

Tolerance

128
Q

Define dependence

A

A state in which organism functions normally only in the presence of a drug

Manifested as physical disturbance when the drug is withdrawn

Simply = When you don’t consume the drug, you don’t function properly (withdrawal syndrome)

129
Q

A state in which organism functions normally only in the presence of a drug

Manifested as physical disturbance when the drug is withdrawn

This is known as…?

A

Dependence

130
Q

Is this tolerance or dependence?

Different areas of the brain are affected when the body does not function well when withdrawn from drugs

A

Dependence

131
Q

Is this dependence or tolerance?

There are different circuits in the brain: it is possible to be dependent on the morphine, without being addicted to it.

A

Dependence

132
Q

Apart from being a pleasure chemical, what else does dopamine do?

A

Regulate movement to the control of attention

133
Q

What is the nigrostriatal system?

A

It starts in the substantia nigra and terminates in the basal ganglia

It plays a role in the control of movement.

134
Q

What system plays a role in the control of movement?

A

Nigrostriatal system

135
Q

When the substantia nigra is depleted, what disease do people develop?

A

Parkinson’s disease because of the loss of dopamine (worsened control of movement and attention)

136
Q

What are the functions of dopamine pathways?

A
  • Reward (motivation)
  • Pleasure
  • Motor function
  • Compulsion
  • Perceveration
137
Q

What are the functions of serotonin pathways?

A
  • Mood
  • Memory processing
  • Sleep
  • Cognition
138
Q

Loss of dopamine can lead to what kinds of diseases?

A

Neurological diseases caused by degeneration of the nigrostriatal system:

  • Tremors
  • Rigidity of the limbs
  • Poor balance
  • Difficulty initiating movements
139
Q

People with Parkinson’s disease and loss of dopamine are treated with…?

A

L-DOPA

140
Q

What is L-DOPA?

A

Precursor of dopamine that can cross the blood brain barrier

141
Q

What happens in the process of a dopaminergic synapse?

A

1) Dopamine is released by a neuron (vesicles) into the synaptic cleft

2) Action potential arrives

3) Action potential is released into the synaptic cleft and dopamine molecules binds to dopamine receptors

4) If no heroin or other drugs are present, the transporter removes dopamine from the synaptic cleft back to the vesicles in the presynaptic cell

4b) If heroin is present, heroin binds to the opiate receptors that signal presynaptic cells to release dopamine

142
Q

What is the effect of cocaine?

A

Inhibition of dopamine reuptake

Cocaine molecules bind with dopamine transporters to block the removal of dopamine in the synaptic cleft back to the presynaptic cells

This causes dopamine to accumulate in the synaptic cleft which stimulates reward pathways more= causes the euphoria commonly experienced immediately after taking the drug

143
Q

Where are cocaine binding sites?

A

Caudal nucleus

144
Q

Which drug increases the activation of the reward system?

A

Cocaine

145
Q

Where does Dopaminergic synapse occur in the reward pathway?

A

Nucleus accumbens

146
Q

Drugs increase the activation of the reward system

This is known as…?

A

Addiction

147
Q

One researcher created Disneyland for rats, giving them the best food, friends, mate, entertainment, etc.

The researcher found that the rats were less likely to consume heroin when given to them

What does this suggest?

A

Rats (and possibly people) who live in difficult and rough environments are more likely to be addicted to drugs that those who have busy and content lives

This is because the rats who lived in Disneyland were busy with other things and have better social connections with other rats (they already feel satisfied and pleasure without having to take drugs; have sufficient dopamine)

148
Q

What do PET activations measure?

A

Measures sugar consumption or glucose

149
Q

Someone who is on cocaine will have more glucose/energy in the brain than someone who does not take drugs

True or False?

A

False

Someone who is on cocaine will have less glucose/energy in the brain than someone who does not take drugs

150
Q

Which monoamine plays a role in the regulation of mood, the control arousal and is also involved in the regulation of pain?

A

Serotonin

151
Q

Define serotonin

A

Play a role in the regulation of mood, the control arousal and is also involved in the regulation of pain

152
Q

Serotonin is also called…?

A

5-HT

153
Q

Serotonin is involved the control of… List 8 things

A
  1. appetite
  2. sleep
  3. memory and learning
  4. temperature regulation
  5. cardiovascular function
  6. muscle contraction
  7. endocrine regulation
  8. depression (as antidepressants)
154
Q

What are the serotonin nerve pathways in the brain?

A

1) Starts in the raphe nuclei in the brain stem

2) Then moves to either the amygdala, hippocampus and prefrontal cortex or go down into the brains stem

155
Q

What happens during a serotonin synapse?

A

1) Serotonin is released from the vesicles into the synaptic cleft and diffuses to activate serotonin receptors

2) Serotonin molecules bind with the receptors on the postsynaptic cells

3) Action potential occurs

156
Q

What do serotonin transporter do?

A

Serotonin transporters transport serotonin from the synaptic cleft back to its vesicles in the presynaptic cell

157
Q

What does the LSD do?

A

LSD stimulates centres of the sympathetic nervous system in the midbrain, which leads to pupillary dilation, increase in body temperature, and rise in the blood-sugar level.

158
Q

Stimulates centres of the sympathetic nervous system in the midbrain, which leads to pupillary dilation, increase in body temperature, and rise in the blood-sugar level.

This is known as…?

A

LSD

159
Q

LSD also has a (…..) blocking effect

A

Serotonin

160
Q

What is LSD?

A

LSD (lysergic acid diethylamide) is a hallucinogenic drug

Hallucinogens change the way people sense the world around them

161
Q

What are hallucinogenic drugs?

A

Drugs that change the way people sense the world around them

162
Q

What is MDMA (ecstasy)?

A

A drug that serves as a noradrenergic and serotonergic agonist

It has excitatory and hallucinogenic effects

163
Q

Does MDMA (ecstasy) have inhibitory or excitatory effects?

A

Excitatory effects (it increases empathy)

164
Q

When people take MDMA (ecstasy) what do they claim to feel?

A

Warmth around other people and increased empathy

165
Q

What happens during MDMA (ecstasy) intake?

A

Serotonin in the acute stage reduces appetite, improved perception, allow for better memory, elevates mood and the general feeling of warmth. and empathy

166
Q

What happens after MDMA (ecstasy) wears off?

A

The reuptake of serotonin molecules is prevented and serotonin is left in the synaptic cleft

Prolong duration of serotonin in the synaptic cleft produces opposite effects (hypothermia, clouded thinking, disturbed behaviour and muscle twitches)

167
Q

What are the effects of ecstasy on serotonin transporters?

A

1) Prevent reuptake of serotonin molecules

2) Work in reverse mode (bring more serotonin to the synapse rather than transport it back)

168
Q

What are the adverse effects of ecstasy?

A
  • Clouded thinking
  • Hypothermia
  • Disturbed behaviour
  • Jaw clenching and muscle twitching
169
Q

What are the long term effects of consuming MDMA (ecstasy) on serotonin levels?

A

Serotonin levels never return to normal even after you don’t take MDMA for years

170
Q

What happened to the monkeys in the experiment involving MDMA consumption?

A

1) Monkeys were given ecstasy twice a day, for 4 days, for 2 weeks

2) After stopping the MDMA consumption, monkeys were sacrificed in order to look at the concentration of serotonin in the prefrontal
cortex

3) Ecstasy monkeys, compared to controlled condition monkeys, had less serotonin levels in the prefrontal cortex, 2 weeks after consuming MDMA

4) Some non-sacrificed ecstasy monkeys lived up to 7 years and the initial serotonin levels never returned

171
Q

What was the study done on animals to test for drug effects in the brain?

A

Neurotoxicity

172
Q

Other than lower serotonin levels, what are the other long term effects of MDMA?

A

Impairments of verbal and visual memory

173
Q

How does MDMA affect verbal and visual memory?

A

MDMA depletes presynaptic neurons of serotonin and causes degeneration of serotonin nerve terminals

This affects the hippocampus and prefrontal areas which are important for memory

This leads to memory impairment (alzheimer’s disease)

174
Q

What is believed to cause mild-severe depression?

A

Low serotonin levels

175
Q

What are the symptoms of depression supposedly caused by low serotonin levels?

A
  • Anxiety
  • Apathy
  • Fear
  • Feelings of worthlessness
  • Insomnia and fatigue.
176
Q

True or False?

If depression arises as a result of a serotonin deficiency then pharmaceutical agents that increase the amount of serotonin in the brain should not be helpful in treating depressed patients.

A

False

If depression arises as a result of a serotonin deficiency then pharmaceutical agents that increase the amount of serotonin in the brain should be helpful in treating depressed patients.

177
Q

What do Anti-depressant medications do?

A

Increase serotonin levels at the synapse by blocking the reuptake of serotonin into the presynaptic cell

178
Q

What is the most well known medication to help with depression?

A

SSRIs (selective serotonin reuptake inhibitors)

179
Q

How do SSRIs help with depression?

A

SSRIs bind to the presynaptic receptors to prevent serotonin from returning to the presynaptic cell (prevent reuptake)

Ensures more serotonin is left in the synaptic cleft; affects postsynaptic transmission

180
Q

How many consumers of SSRIs actually benefit from the drug?

A

43%

181
Q

How long does it take for SSRIs to kick in?

A

At least 3-4 months

182
Q

True or False?

Norepinephrine (NE) or noradrenaline is both a hormone and a neurotransmitter

A

True

183
Q

As a hormone, secreted by the adrenal gland, norepinephrine works alongside (…………) to give the body (…………) in times of (……)

A

1) Epinephrine / adrenaline 2) Sudden energy
3) Stress (known as the “fight or flight” response)

184
Q

Medications that inhibit the reuptake of Norepinephrine can be effective to treat (……)?

A

Depression

185
Q

Elevated norepinephrine are found in patients experiencing ….?

A

Mania

186
Q

Epinephrine (adrenaline) is a hormone secreted by the (………..) and serves as a (……..)

A

1) Adrenal medulla/gland
2) Neurotransmitter in the brain

187
Q

There are 2 neurotransmitters that have only excitatory and only inhibitory effect

These are…?

A

1) Glutamate (only excitatory)
2) GABA (only inhibitory)

188
Q

The most common neurotransmitters in the CNS are…?

A
  • Glutamate
  • Gamma- aminobutyric acid (GABA)
  • Glycine
189
Q

Where is glutamate found?

A

Everywhere in the CNS

190
Q

What do glutamate molecules release when they bind with receptors?

A

Magnesium (important in learning)

191
Q

Why is glutamate an excitatory neurotransmitter in the brain?

A

It induces excitatory postsynaptic potentials

192
Q

What do glutamate molecules bind to?

A

NMDA receptors in the postsynaptic cells

193
Q

A specialized ionotropic glutamate receptor

This is known as…?

A

NMDA receptor

194
Q

NMDA receptors have many binding sites. What happens when glutamate binds to it?

A

Releases magnesium for ion channels to open (excitatory)

195
Q

What does PCP or angel dust synthetic drug do?

A

PCP is an indirect NMDA receptor antagonist

It blocks the action of NMDA receptors

They are commonly used as anesthetics for animals and humans

196
Q

What is GABA?

A

Gamma-aminobutyric acid is an amino acid

197
Q

Where is GABA found?

A

Everywhere

198
Q

What is the the most important inhibitory neurotransmitter in the brain and glycine in the spinal cord?

A

GABA

199
Q

True or False?

The GABA neurotransmitter and its receptors are critical to how humans think and act

A

True

200
Q

GABA is part of the brain system that allows us to…?

A

Fine-tune our moods, thoughts, and actions with an incredible level of detail

201
Q

Imbalances in GABA also related to…?

A
  • Bipolar disorder
  • Schizophrenia
  • Anxiety disorder.
202
Q

GABA is like driving a car. You need the accelerator, but at every stage you need the brakes to work

What does this mean?

A

Some of our other neurotransmitters apply the spark and the “gas” to the engine

But GABA supplies us with the brakes

203
Q

Why do we need GABA?

A

GABA provides the necessary inhibitory effect that we need in order to block out excessive brain activity that in depression may lead to excessive negative thinking

204
Q

What are tranquilizers?

A

Drugs that affect GABA receptors

205
Q

What is a well known category of anxiolytic drugs?

A

Benzodiazepine

206
Q

Benzodiazepine is a(n)… for the GABA receptor

a. Indirect antagonist
b. Direct antagonist
c. Indirect agonist
d. Direct agonist

A

c. Indirect agonist

207
Q

What are the 2 drugs used for tranquilizing effects?

A

1) Valium (diazepam)
2) Xanax (Alprazolam)

208
Q

Describe acetylcholine. List 3 points (i.e. where is it found, what paralyses/blocks the transmission, what receptors it uses)

A

1) Acetylcholine is the transmitter at the neuromuscular junction connecting motor nerves to muscles

2) The paralytic arrow-poison curare acts by blocking transmission at these synapses

3) Acetylcholine also operates in many regions of the brain, but using different types of receptors (nicotinic and muscarinic)

209
Q

Describe GABA. List 3 things (i.e. is it inhibitory or excitatory, tranquilizers, etc)

A

1) GABA is used at the great majority of fast inhibitory synapses in virtually every part of the brain

2) Many tranquilizing drugs act by enhancing the effects of GABA.

3) Correspondingly glycine is the inhibitory transmitter in the spinal cord.

210
Q

Describe dopamine. List 2 things

A

1) Dopamine plays a critical role in the reward system

2) Dysfunction of the dopamine system is also implicated in Parkinson’s disease and schizophrenia.

211
Q

Describe Serotonin. List 2 things (i.e. what does it do, how does it relate to depression)

A

1) Serotonin regulates appetite, sleep, memory and learning, temperature, mood, muscle contraction, and function of the cardiovascular system and endocrine system

2) It plays a role in depression (lower concentrations of serotonin in their CSF and brain tissue).

212
Q

Describe glutamate. List 3 things (i.e. is it inhibitory or excitatory, where is it used, etc)

A

1) Glutamate is used at the great majority of fast excitatory synapses in the brain and spinal cord

2) It is also used at most synapses that are “modifiable”, i.e. capable of increasing or decreasing in strength

3) Modifiable synapses are thought to be the main memory-storage elements in the brain.

SEM 2 Brain & Behaviour (10 decks)

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