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Next - Psychology & Neuroscience of Addiction [Private] > Biological basis of addiction > Flashcards

Biological basis of addiction Flashcards

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1
Q

What are the three components of the addiction cycle?

A
  1. Binge intoxication
  2. Negative withdrawal effect
  3. Preoccupation anticipation
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2
Q

What does the binge intoxication in the addiction cycle lead to?

A
  • Tolerance
  • Withdrawal
  • Compromised social, occupational or recreational activities
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3
Q

What are the negative withdrawal effects?

A
  • Persistent physical problems
  • Persistent psychological problems
  • Preoccupation with obtaining drugs
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4
Q

How is the preoccupation and anticipation in the addiction cycle characterised?

A

Persistent desire to take more drugs to relieve the withdrawal

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5
Q

What is the direct reward pathway?

A

Ventral tegmental area (VTA) releases dopamine directly into nucleus accumbens

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6
Q

What is the indirect reward pathway?

A

GABA inhibits the VTA from firing dopamine in nucleus accumbens

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7
Q

What is the action of nicotine (or MDMA) on the reward pathway?

A

Nicotine or MDMA increase firing of dopamine neurone (from VTA)
-> increased amount of dopamine in the Nucleus accumbens

= Pleasure

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8
Q

What is the action of cannabis on the reward pathway?

A

Cannabis prevents inhibitory GABA transmission to VTA
-> Increased amount of dopamine transmitted to the Nucleus accumbens

= Pleasure

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9
Q

What are the roles of the shell and the core of the Nucleus accumbens?

A

NAc -> PFC

  • Core: cognitive effects of motor function (plan and get)
  • Shell: wanting and reward
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10
Q

What did Olds and Milner (1954) show using intracranial self-stimulation in rodents?

A

When stimulants location was put in NAc and VTA
-> rats would press the stimulation lever almost to the exclusion of everything else (food, water)

“potency of the stimulation will not fade, and rodents will narrow their behavioural repertoire and ignore other priorities”
= behaviour of human addict

-> we can surgically cut the VTA-NAc reward pathway; or administer dopamine antagonists

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11
Q

Which type of scans are used to explore the reward pathway?

A
  • PET

- SPECT: Single Photon Emission Computed Tomography

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12
Q

What is observed with scans when we show addicts conditional stimuli (e.g. drug paraphernalia, such as needles)?

A

Significant increases in glucose and metabolism in the VTA and Frontal Cortex

-> increased activity even though no drug is actually given to participants

<=> reward pathway activated independent of the drug

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13
Q

What are the neurotransmitters involved in reward?

A

> Dopamine

> Cannabinoids

> Serotonin

> Opioid Peptides

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14
Q

Which function do dopamine neurotransmitters address?

A

Pleasure, euphoria, mood, motor function

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15
Q

Which function do cannabinoids (neurotransmitters) address?

A

Pain, appetite, memory

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16
Q

Which function do serotonin (5-HT) neurotransmitters address?

A

Mood, impulsion, anxiety, sleep, cognition

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17
Q

Which function do opioid peptides (neurotransmitters) address?

A

Pain

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18
Q

What are the dopamine receptors?

A

G protein-coupled receptors (GPCRs)

  • D1-like: D1 and D5
  • D2-like: D2, D3, D4
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19
Q

What characterises D1-like dopamine receptors?

A

D1 and D5

  • generally post-synaptic
  • generally produce excitation through activation of Gs
  • increases cyclic adenosine monophosphate (cAMP) levels
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20
Q

What characterises D2-like dopamine receptors?

A

D2, D3, D4

  • generally pre and post-synaptic
  • generally produce inhibition through activation of Gi
  • decreases cyclic adenosine monophosphate (cAMP) levels
  • may also open potassium (K+) channels leading to hyperpolarisation
21
Q

What is the effect of drugs of abuse (e.g. amphetamine, cocaine, nicotine, ethanol) compared to natural rewards (e.g. food, sex)?

A

These drugs act like natural rewards in the NAc and Caudate, but with a significantly higher magnitude

22
Q

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

A

The number of available receptors

23
Q

What is the effect of cocain in the synapse?

A

Cocaine blocks the DA reuptake
- it binds to the dopamine transporter (DAT) and inhibits it -> slowing transport

  • > increased synaptic concentration of DA
  • > continual binding to DA postsynaptic receptors
24
Q

How does alcohol (ethanol) modulate the effects of dopamine?

A
  • Binds to GABAa receptors

- > Increased dopaminergic activity in the VTA via inhibition of GABAergic interneurons

25
Q

How does cannabis modulate the effects of dopamine?

A

Binds to cannabinoid receptors (GPCRs)

26
Q

How does nicotine modulate the effects of dopamine?

A

Binds to nicotinic acetylcholine receptors

-> increased dopaminergic activity in the VTA

27
Q

How do opiates modulate the effects of dopamine?

A

Bind to opioid receptors (GPCRs)

-> reduced overall neurotransmission at the synapse
decrease cAMP and open potassium K+ channels

28
Q

What are the types of opioid receptors and their function?

A

All GPCRs (coupled via Gi/o)

  • Mu (µ): analgesia (beneficial), euphoria, respiratory depression (hypoventilation) and dependence
  • Delta (ẟ): contribute to analgesia
  • Kappa (k): mixed actions at spinal cord
29
Q

What is the action of opioid receptors at the synaptic level?

A
  • Reduce neurotransmission

- Can lead to inhibition of inhibitory synapses -> excitation

30
Q

What is the action of heroin on the reward pathway?

A

Binds to opioid receptors that inhibit GABAergic neurons that project to dopaminergic neurons in the VTA

31
Q

What are the two current drugs used as pharmacotherapies for addiction?

A
  • Varenicline

- Naltrexone

32
Q

What is the action of the pharmacotherapeutic drug Varenicline for addiction?

A

Blocks actions of acetylcholine

-> smoking cessation

33
Q

What is the action of the pharmacotherapeutic drug Naltrexone for addiction?

A

Blocks opioid receptors

34
Q

What are the synaptic changes associated with addiction?

A
  • Sensitisation/Desensitisation (brain trying to restore normal functionning - homeostasis)
  • Changes in size of neurons
  • Increased glutamate neurotransmission
  • Increased tyrosine hydroxilase (TH) (dopamine synthesis)
  • Alterations in synaptic proteins
  • Changes in transcription factors
  • Decreases brain D2 receptor expression
35
Q

How does addiction affects behaviour?

A

Reward pathway projects to areas of the brain that control movement
- reward pathway + motor pathway

-> Reward seeking pathway (i.e. getting more drugs)

36
Q

How does withdrawal happen?

A

Abrupt stop to drug taking

after addiction making synaptic changes

37
Q

What are the neurobiological symptoms in a withdrawal syndrome?

A

> Disturbance of autonomic nervous system

> Activation of thalamus

> Release of corticotrophin releasing factor (CRF)

> Activation of locus ceruleus (LC)

38
Q

What are trophic factors?

A

Proteins that can promote cell growth and viability

39
Q

What is observed in dopamine and serotonin levels addicted animals (i.e. who have been exposed to drugs)?

A

Reduced levels of DA and 5-HT in addicted animals

- v.s. animals who have not been exposed

40
Q

Which neurotransmitters have reduced levels in withdrawal and what are the consequences?

A
  • Dopamine -> dysphoria
  • Serotonin -> dysphoria
  • Opioid peptides -> increased pain
  • GABA -> anxiety, panic attacks
  • Neuropeptides (NPY) -> anti-stress
  • Dynorphin -> dysphoria
41
Q

Which neurotransmitters have increased levels in withdrawal and what are the consequences?

A
  • Corticotrophin releasing factors (CRF) -> stress
  • Norepinephrine -> stress
  • Glutamate -> hyper-excitability
42
Q

Why does the number of receptors increase in addiction?

A

To counteract with the continuous presence of the drugs

43
Q

Why does the amount of neurotransmitters decrease in addiction?

A

They are depleted, or because of feedback inhibition

44
Q

What are the structural changes on the brain associated with long term drug abuse?

A

Decreases metabolism in the Orbito Frontal Cortex

- involved in decision making and planning

45
Q

What are the functional changes on the brain associated with long term drug abuse?

A
  • Decreases CREB transcription factor in the NAc
  • Decreases in dopamine D2 receptor binding
  • > reduced availability of dopamine transporters (DAT)
46
Q

What is the role of the CREB transcription factor?

A

Activates transcription of target genes
- in response to a diverse array of stimuli, including peptide hormones, growth factors, and neuronal activity, that activate a variety of protein kinases

47
Q

What is the cognitive dependence of dopamine transporters (DAT) related to?

A

Verbal memory

48
Q

What is the association between dopamine transporter (DAT) availability and cognitive ability?

A

Positive correlation between DAT availability and recall

  • More DAT available = increased cognitive ability
  • Less DAT available = reduced cognitive ability

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

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