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2nd Year: Drugs and the Mind > Transmitter systems > Flashcards

Transmitter systems Flashcards

1
Q

What does an agonist do?

A

Stimulates a receptor by mimicking an NT, thus increasing the effects of that NT.

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2
Q

What does an antagonist do?

A

Blocks a receptor, thus preventing an NT binding and diminishing its effects.

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3
Q

“The CNS is inherently changeable and non-static.” True or false?

A

True.

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4
Q

What do the dendrites do?

A

Receive inputs from other neurons.

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5
Q

What does the axon do?

A

Propagate the AP.

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6
Q

Which part of the neuron generates the AP?

A

The soma.

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7
Q

Why is it difficult to localise drug effects to the CNS?

A

Because the same receptors are found throughout the body in the PNS.

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8
Q

What is meant by a ‘disorder of the CNS’?

A

Disorders that arise from abnormal neuronal function in the brain and spinal cord. Often this is closely linked to mental function.

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9
Q

Why is it difficult to measure drugs for CNS disorders?

A

Results are subjective, e.g. pain is not the same for everyone.

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10
Q

NTs only have effects in the brain. True of false?

A

False: they are also found throughout the body.

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11
Q

Define an NT.

A

A chemical that allows signal transduction between neurons, thus conveying information.

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12
Q

NTs are always agonists. True or false?

A

True.

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13
Q

Why does changing NT activity to treat disease have adverse effects?

A

Because the same NTs have multiple functions and numerous receptors throughout the body.

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14
Q

NT action can be a) fast and b) slow. Which kinds of receptors are involved in each case?

A

a) Ligand-gated ion channels

b) Modulated receptors (GPCRs)

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15
Q

Where are NTs synthesised?

A

In nerve terminals.

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16
Q

What does a transporter do?

A

Removes excess NT from the synapse. This terminates its effects and recycles it (NTs are re-uptaken into the neuron).

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17
Q

List 3 methods for increasing the effects of an NT.

A
  1. Add precursor molecules to increase synthesis
  2. Block re-uptake by transporters
  3. Excite receptors
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18
Q

Give examples of drugs that block re-uptake by transporters.

A

Cocaine, MDMA, depression treatments like SSRIs

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19
Q

Give examples of 4 drugs that excite receptors in place of endogenous NTs. State the receptors they excite.

A
  1. Heroin, opioid receptors
  2. Nicotine, nicotinic cholinergic receptors
  3. LSD, 5HT2A
  4. Cannabis, cannabinoid receptors
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20
Q

What is epigenetic regulation?

A

Changes to gene expression. There are NO physical changes to DNA sequences.

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21
Q

Give an example of how gene expression can be regulated.

A

By histone winding or methylation. Increased histone winding or methylation means transcription factors cannot access the genes, thus transcription is down-regulated and less protein is produced.

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22
Q

NTs can affect gene transcription. True or false?

A

True.

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23
Q

Why do drugs affect everyone differently? Refer to genes.

A

Genes are the basis of individual differences. Drugs mimic NTs and can thus regulate gene transcription.

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24
Q

What causes the release of NTs?

A

Ca2+

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25
Q

Describe how NTs are released.

A

An AP causes voltage-gated ion channels to open.
Ca2+ floods into the cell.
This causes mobilisation of vesicles to undergo membrane fusion.

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26
Q

There are 4 types of Ca2+ channel. What are they?

A

N, P, R and T

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27
Q

Receptors can be a) intrinsic or b) extrinsic. What do these terms mean?

A

a) Strings of amino acids that link in and out of the membrane.
b) Sit on the membrane, are not embedded in it

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28
Q

If a drug targets a pre-synaptic receptor, what does it affect?

A

NT release.

29
Q

If a drug targets a post-synaptic receptor, what does it affect?

A

Activity of the post-synaptic neuron.

30
Q

When dosing a drug, threshold value must be overcome. True or false?

A

True.

31
Q

Does a higher dose of a drug increase its effects?

A

Yes.

32
Q

In terms of maximal response, what do a) full agonists, b) agonists and c) partial agonists achieve?

A

a) Always reaches maximal response
b) Reaches maximal response but a higher dose is required than with a full agonist
c) Never reaches maximal response REGARDLESS OF DOSE

33
Q

What are the monoamine neurotransmitters?

A

Dopamine, noradrenaline and 5HT.

34
Q

What is dopamine involved in? List 4 things.

A
  1. Reward, stimulates the nucleus accumbens in the VTA
  2. Motor function
  3. Psychosis
  4. Nausea and vomiting
35
Q

What is dopamine made from?

A

Tyrosine (an amino acid)

36
Q

Give the synthesis pathway for dopamine.

A

Tyrosine, L-DOPA, dopamine, DOPAC and HVA

37
Q

What are DOPAC and HVA?

A

Inactive metabolites

38
Q

How many types of dopamine receptor are there?

A

5.

39
Q

What pathway is noradrenaline involved in?

A

The sympathetic adrenomedullary system (the fight or flight response).
Noradrenaline is involved in arousal and fear.

40
Q

When the body reacts to a stressor, noradrenaline is released. List 4 physiological effects of noradrenaline release.

A
  1. Increased heart rate
  2. Increased blood pressure
  3. Increased blood flow to muscles
  4. Increased mobilisation of glucose stores
41
Q

What happens if a person has too little noradrenaline?

A

They suffer from motor retardation (lethargy) and are sleepy.

42
Q

What happens if someone has too much noradrenaline?

A

They are nervous, have racing thoughts and high blood pressure etc.

43
Q

If injected peripherally, noradrenaline cannot enter the CNS. Why?

A

It cannot cross the blood-brain barrier.

44
Q

What kind of receptor does 5HT act on?

A

Always modulated receptors, these are slow acting

45
Q

There are only a small number of small 5HT circuits, thus 5HT has a small effect in the brain/body. True or false?

A

False: it is true that there are only a small number of small circuits, but serotonin controls numerous functions so its effects are always profound.

46
Q

List 9 things that 5HT is involved in.

A
  1. Pain, e.g. migraine
  2. Mood
  3. Attention
  4. Sleep
  5. Depression
  6. Hallucination
  7. Fear
  8. Anorexia
  9. Anxiety
47
Q

What is glutamate?

A

The main excitatory NT in the brain, is always depolarising (generates APs).

48
Q

Glutamate pathways are always short. True or false?

A

False: they are v. long

49
Q

Glutamate is involved in LTP or ‘long term potentiation’, meaning it creates a lasting response. True or false?

A

True.

50
Q

List 5 things glutamate is involved in.

A
  1. Pain
  2. Memory
  3. Attention
  4. Cognition
  5. Epilepsy
51
Q

Glutamate is the only NT that causes excitotoxicity. What happens in excitotoxicity?

A

Glutamate receptors are inappropriately activated, e.g. prolonged synaptic levels cause continued stimulation of the post-synaptic neuron.
This results in the death of the post-synaptic neuron.
This leads to pain, memory loss or even death.

52
Q

When can excitotoxicity occur? Give an example.

A

After ischemia (restriction of blood flow to tissues).

53
Q

Glutamate has 4 major receptors. What are they and what are they involved in?

A
  1. AMPA = Na+ transport
  2. Kainate = Na+ transport
  3. NMDA = Na+ and Ca2+ transport
  4. Metabotropic (these are GPCRs)
54
Q

What is the role of ACh?

A

Main motor NT.

55
Q

There are 2 types of ACh receptor. What are they?

A
  1. Nicotinic

2. Muscarinic

56
Q

Nicotinic cholinergic receptors are ligand-gated ion channels with fast responses. True or false?

A

True.

57
Q

Muscarinic cholinergic receptors are ligand-gated ion channels with fast responses. True or false?

A

False: they are GPCRs and have slow responses as they involve second messengers.

58
Q

What is GABA?

A

The main inhibitory NT, is always hyperpolarising to prevent the generation of NTs

59
Q

What chemical is GABA made of?

A

Gamma-aminobutyric acid.

60
Q

GABA is synthesised from glutamate. True or false?

A

True.

61
Q

GABA only has localised effects. True or false?

A

True.

62
Q

There are 2 main receptors for GABA. What are they?

A
  1. GABA-A: ligand-gated ion channel, causes a Cl- influx

2. GABA-B: GPCR modulated receptor

63
Q

Describe how alcohol affects GABA transmission in a) low and b) high doses.

A

a) Alcohol causes GABA disinhibition, i.e. it prevents GABA from acting so the subject is energetic and chatty.
b) Alcohol stimulates GABA, so the subject becomes lethargic and sleepy.

64
Q

Give examples of peptide NTs.

A

Substance P and opioids.

65
Q

Opioids have 4 main receptors. What are they?

A

Mu, delta, kappa and ORL-1.

66
Q

What do endogenous opioids do?

A

Modulate the pain response.

67
Q

What can a) low and b) high doses of opioids produce?

A

a) Depression, Parkinson’s and Alzheimer’s

b) Pain, epilepsy and positive schizophrenia

68
Q

Why is it that some people do not gain pain relief from opiate drugs like codeine?

A

They do not have sufficient enzyme to metabolise codeine into morphine.

2nd Year: Drugs and the Mind (12 decks)

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