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How the brain adapts Flashcards

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1
Q

What is a receptor?

A
  • Protein
  • Located in cell surface membrane
  • Characteristic 3D structure
  • target of specific drug/ligand
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2
Q

What is the effect of an agonist binding to a receptor?

A

Activation, producing biochemical/cellular effects

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3
Q

Which receptors are glutamate ionotropic receptors?

A
  • AMPA
  • NMDA
  • Kainate (several types)
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4
Q

Which receptor is a glutamate metabotropic receptor?

A

mGluR1-8

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5
Q

Which receptor is a GABA ionotropic receptor?

A

GABA(A) receptor

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6
Q

Which receptor is a GABA metabotropic receptor?

A

GABA(B) receptor

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7
Q

Which receptors are acetylcholine ionotropic receptors?

A

nACh (several types)

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8
Q

Which receptors are acetylcholine metabotropic receptors?

A

M1-5

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9
Q

Which receptor is a serotonin ionotropic receptor?

A

5-HT_3

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10
Q

Which receptors are serotonin metabotropic receptors?

A

13 different types

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11
Q

Which receptors are dopamine ionotropic receptors?

A

None

- dopamine has no ionotropic receptors

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12
Q

Which receptors are dopamine metabotropic receptors?

A

D1-5

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13
Q

What are ionotropic receptors?

A
  • Ligand-gated ion channels,
  • comprised of several subunits,
  • that mediate/modulate fast synaptic potentials
  • immediate changes in milliseconds
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14
Q

What are metabotropic receptors?

A
  • G-protein-coupled receptors,
  • that mediate/modulate slow synaptic transmission
  • long-term changes in seconds, activating biochemical pathways
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15
Q

What is the action time scale of kinase-linked receptors?

A

Hours

- e.g. cytokine receptors

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16
Q

What is the action time scale of nuclear receptors?

A

Hours

- e.g. oestrogen receptors

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17
Q

What are the key steps in synaptic transmission?

A

Pre-synaptic:

  1. Action potential arrives
  2. Depolarisation
  3. Opens voltage-gated Ca2+ channels
  4. Ca2+ flood in -> change in vesicular proteins (surrounding stored NTs)
  5. Diffusion in synaptic cleft

Post-synaptic:

  1. Activation of NT receptors
  2. Removal of NT
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18
Q

How do drugs interfere at all stages of the synaptic transmission?

A

> Pre-synaptic:
- drugs interfere with synthesis, storage and release of NTs

> Post-synaptic:
- drugs interfere with receptors and removal mechanisms

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19
Q

How do drugs interfere with the synthesis of neurotransmitters?

A
  • Removal or enhanced synthesis of NTs

- Slow onset of action: need to remove NTs that have been synthesised and stored

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20
Q

How does L-dopa interfere with the synthesis of neurotransmitters?

A

Enhances dopamine synthesis in Parkinson’s Disease

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21
Q

How do drugs interfere with the storage of neurotransmitters?

A
  • “Leakage” of NTs into nerve terminals
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22
Q

How does amphetamine interfere with the storage of neurotransmitters?

A

Causes release of dopamine and noradrenaline

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23
Q

What does the neurotransmitter release depend on?

A

Voltage and calcium:

  • NT release requires depolarisation to activate voltage-gated calcium channels (VOCCs)
  • > VOCCs play pivotal role in synaptic transmission
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24
Q

Which drug blocks voltage-gated calcium channels?

A

Conotoxin

- toxins produced by marine snails

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25
Q

What is the effect of conotoxin on the synapse?

A
  • Blocks voltage-gated calcium channels
  • > preventing NT release

-> Paralyses synapses

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26
Q

What are the two types of post-synaptic receptors?

A

Ionotropic and metabotropic receptors

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27
Q

What is a homomer receptor?

A

Ionotropic receptor composed of similar subunits

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28
Q

What is a post-synaptic heteromer receptor?

A

Ionotropic receptor composed of different subunits

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29
Q

What are the two types of pre-synaptic receptors?

A
  • Autoreceptors

- Heteroreceptors

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30
Q

What are autoreceptors?

A
  • Presynaptic receptors,
  • that mediate the transmission of neurotransmission back to itself
  • α_2-adrenoceptors
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31
Q

What are heteroreceptors?

A
  • Presynaptic receptors,
  • that mediate the inhibitory effects of one neurotransmitter on the release process of another
  • opioid receptors (kappa, mu, delta)
32
Q

What is the action of antagonists at pre-synaptic inhibitory receptors?

A

They will increase the release of NTs

33
Q

What are pre-synaptic nicotinic acetylcholine receptors?

A

Excitatory pre-synaptic receptors

34
Q

What is the action of co-agonists?

A
  • They cannot activate a receptor alone
  • Act at separate sites on receptor protein
  • e.g. Activation of NMDA receptors requires binding of both glutamate and glycine
35
Q

What is the action of competitive antagonists?

A

They compete for the same site on receptor protein

36
Q

What is the action of non-competitive antagonists

A

They act by another mechanisms

  • e.g. PCP “angel dust” blocks the channel of NMDA receptor
37
Q

What is the composition of GABA A receptors?

A
  • Have an allosteric modulatory site = benzodiazepine (BDZ) site
  • Multiple subunits: GABA, BDZ, ethanol, neurosteriods, barbiturates
  • > heteromer ionotropic opening chloride ion channel
  • hyperpolarisation of neuron
38
Q

What is the action of benzodiazepine agonists?

A

Potentiate GABA
- through GABA A receptor BDZ site

  • e.g. Diazepame (Valium)
39
Q

What is the action of benzodiazepine inverse agonists?

A

Inhibit GABA
- through GABA A receptor BDZ site

  • e.g. experimentally used only
40
Q

What is the action of benzodiazepine antagonists?

A
  • Block effects of BDZ agonists or inverse agonists
  • no effects on GABA
  • e.g. Flumazenil used for BDZ overdose
41
Q

What are the two removal mechanisms of neurotransmitters?

A
  1. Enzymatic destruction
    - ACh is broken down by Acetylcholinesterase
    - Monoamine oxidase (MOA) breaks down dopamine (DA), serotonine (5-HT), norepinephrine (NE)
  2. Active reuptake
    - e.g. DA uptake via dopamine transporter (DAT)
42
Q

What is the effect of blocking the removal mechanisms of neurotransmitters?

A

It will potentiate the life of the neurotransmitter in the synapse
-> increase of synaptic concentration of NTs

  • e.g. cocaine, Prozac (fluoxetine), Rivastigmine work by blocking removal mechanism
43
Q

How does Rivastigmine work?

A

Prevents breakdown of ACh
- via inhibition of Acetylcholinesterase

-> enhances ACh synaptic concentration

44
Q

How does Prozac (fluoxetine) work?

A

Serotonin reuptake inhibitor

-> increased 5-HT synaptic concentration

45
Q

How does cocaine work?

A

Binds to dopamine transporter (DAT)
- blocking DA reuptake

-> increased DA synaptic concentration

46
Q

What do the effects of neurotransmitters on the central nervous system depend on?

A

On the role played by the target neuron

  • e.g. inhibition of inhibitory nerve in a circuit
  • > disinhibition and overall increase in excitability
47
Q

What determines whether a neurotransmitter is excitatory or inhibitory?

A

Determined by the receptor it acts on at target cell

48
Q

What is the action of dopamine D1-like receptors?

A

D1 and D5 receptors activate adenylyl cyclase (which synthesizes cAMP)

49
Q

What is the action of dopamine D2-like receptors?

A

D2, D3 and D4 receptors inhibit adenylyl cyclase (synthesizer of cAMP)

50
Q

What is the effect of an increase in adenylyl cyclase activity?

A

Can lead to changes in protein transcription
- i.e. synthesis of receptors or ion channels expressed by particular nerve cell

  • slow changes (hours to days)
51
Q

Why do changes in protein transcription in a cell are slow (i.e. hours to days)?

A

Cell has to synthesise these new proteins and then insert them correctly into cell surface membrane

52
Q

What are the four characteristic behaviours on the spectrum of psychoactive substance use?

A

> Beneficial use
- positive health, spiritual or social impacts

> Casual non-problematic use
- negligible health or social effects

> Problematic use
- negative consequences for individual, others, society

> Chronic dependance
- habitual and compulsive

53
Q

What are the common pharmacological processes of drugs of abuse?

A

> Rapid and effective delivery to the brain
- more likely to be dependent

> Release of DA in reward pathway

> Potential development of neuroadaptation or tolerance
-> withdrawal symptoms

54
Q

What is the typical psychoactivity associated with drugs of abuse?

A

Release of dopamine in the reward pathway

55
Q

Are all drugs of abuse associated with withdrawal symptoms?

A

No

- e.g. LSD, cannabis

56
Q

What are the two types of drug dependence?

A
  1. Psychological
    - long lasting compulsion driven by rewarding effects of the drug
  2. Physical
    - physical withdrawal symptoms
57
Q

What are the two pillars of psychological drug dependence?

A
  1. Compulsion
    - long lasting
  2. Withdrawal
    - emotional
    - important to prevent relapse
58
Q

What is psychological drug dependence driven by?

A
  • Effects in limbic system (reward pathway)

- Cognitive and behavioural reinforcement
sense of relief after taking drug

59
Q

What is the positive reinforcement in psychological drug dependence?

A

Pleasure from compound (drug), through the reward pathway

60
Q

What is the negative reinforcement in psychological drug dependence?

A

Relief from withdrawal symptoms

61
Q

What are the two types of drug tolerance?

A
  1. Acute
    - short lasting
  2. Chronic
    - following prolonged exposure
    - pharmacodynamic (cellular) tolerance
    - pharmacokinetic (metabolic) tolerance

-> tolerance once developed, may not last indefinitely

62
Q

What is cross-tolerance?

A

Tolerance developed between members of the same class of drug

63
Q

When does acute tolerance occur?

A

When a drug acts at a receptor which becomes desensitised by the first dose
- e.g. alcohol

64
Q

What is the ‘Mellanby effect’?

A

George Mellanby, study in early 1900s:

- effects of alcohol are more pronounced when blood alcohol level (BAL) is rising

65
Q

What is pharmacokinetic tolerance?

A

Chronic tolerance due to an increase in the metabolism of the drug

  • e.g. drugs causing induction of CYP450
  • e.g. amphetamine
66
Q

How do drugs causing an induction of the CYP450 enzymes generate a pharmacokinetic tolerance?

A

More CYP450 = more drug molecules being broken down = drug around for less time

-> diminished response per dose of the drug

67
Q

How can amphetamine generate a pharmacokinetic tolerance?

A

Tolerance = increased urine pH

-> increases excretion of amphetamines

68
Q

What is the process of G-protein-coupled receptor desensitisation?

A
  1. Binding of drug to GPCR produces beta-gamma subunit, which dissociates together with alpha subunit
  2. Phosphorilation of GPCR by enzymes:
    - G-protein-coupled kinases (GRKs) which bind to GPCR
  3. Dynamin binds to phosphorylated GPCR
    - > causes internalisation of the receptor in clathrin-coated tips
    - once phosphorylated GPCR is internalised, it’s de-phosphorylated

Either:
4. GPCR is put into recycling vesicle and re-inserted back into cell surface membrane
or
5. GPCR is sent to lysosome for degradation

69
Q

What does the internalisation of a G-protein-coupled receptor via binding of dynamin consist of?

A

Removing GPCR away from cell surface membrane and internalising it

70
Q

What are lysosomes?

A

Subcellular organelles

  • surrounded by a semipermeable membrane,
  • contains numerous hydrolytic enzymes,
  • involved in digestion, defense, and reproduction
71
Q

How does cross-tolerance develop in individuals?

A

Individuals who are already tolerant to one drug can develop tolerance to other drug from the same class

e. g. Heroin -> cross-tolerance to opioid painkillers
e. g. Alcohol -> cross-tolerance to benzodiazepines

72
Q

What is the lifespan of physical drug dependence?

A

Relatively short

- approx. 2 weeks

73
Q

How is the duration of the physical drug dependence related to the half-life of the drug?

A

Longer half-life of drug = longer syndrome duration

74
Q

How is the magnitude of the physical drug dependence related to the half-life of the drug?

A

Negative correlation:

shorter half-life = more intense syndrome

75
Q

How can the syndrome of physical drug dependence be reversed?

A

By administration of an agonist

76
Q

What is the cycle of physical drug dependence?

A

> Chronic drug administration
- adaptions occur at various levels (genetic, cellular)

  • > Drug use stops
  • adaptations persist and act unopposed -> withdrawal
  • > Withdrawal syndrome
  • depends on drug characteristics
  • generally short term
  • can be medicated
  • > Negative reinforcement
  • can be uncomfortable and can motivate avoidance of withdrawal symptoms by continued drug use

-> Chronic drug administration

77
Q

What are the six factors that need to be taken into account to understand the effects of drugs on the central nervous system?

A
  1. Pharmacodynamics
    - affinity for and intrinsic activity at site of action
  2. Pharmacokinetics
    - drug concentration - metabolism
  3. Biology of the patient (genetics, age, disease)
  4. Neuroadaptive processes to primary interaction of drug and target
  5. Blood-brain barrier
  6. Drug’s site of action in the brain

Next - Psychology & Neuroscience of Addiction [Private] (14 decks)

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