Addiction- brain chem explanation for nicotine addiction Flashcards

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1
Q

What are the two parts of the neurochemistry explanation

A

Smoking initiation- genes and dopamine function

Smoking maintenance- increased dopamine activity

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2
Q

What gene is involved with smoking addiction

A

A1DRD2 candidate gene

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3
Q

What does the A1DRD2 candidate gene cause/do

A

Seems to code for defective and insufficient dopamine receptors in the brain’s reward circuitry, which means they can not produce pleasure naturally

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4
Q

Is nicotine a stimulant or depressant

A

Stimulant

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5
Q

What does a stimulant drug do

A

It increases the production and activity of dopamine in the brain.

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6
Q

Why do stimulants lead to repetitive behaviour

A

Because we find the dopamine release rewarding

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7
Q

What does nicotine stimulate

A

Specific acetylcholine (nicotinic acetylcholine receptors - NAcR) receptors

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8
Q

What does the stimulation of NAcRs cause

A

Increased alertness, memory function and learning

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9
Q

What is the ventral tegmental area

A

A critical area in the brain’s reward circuitry which is highly populated with NAcR.

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9
Q

What does the stimulation of NAcRs do to dopamine

A

Causes a rise in dopamine activity in the ventral tegmental area (VTA):

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10
Q

What gives nicotine a rewarding sensation

A

A rise of DA in the VTA

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11
Q

What causes VTA activity

A

Nicotine

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12
Q

Where is VTA activity (causes by nicotine) projected onto

A

The nucleus accumbens

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13
Q

What is the nucleus accumbens

A

A producer of DA

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14
Q

Where is the nucleus accumbens located

A

Deep in the mesolimbic pathway

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15
Q

What is the primary reward centre in the brain

A

The nucleus accumbens

16
Q

What does increased activity in the nucleus accumbens lead to

A

DA rise

17
Q

What happens when smokers encounter a DA rise

A

Causes them to evaluate ‘smoking’ as very pleasurable, compelling further use.

18
Q

What does nicotine also stimulate besides DA

A

Endorphins

19
Q

What do endorphins do to GABA

A

Reduce its activity

20
Q

What does a decrease in GABA correlate with

A

A rise is DA

21
Q

What does more and more DA do to smokers

A

Forces them to engage with further use

22
Q

Who proposed the nicotine regulation model

A

Shachter

23
Q

With long term use, what does the NRM suggest

A

That the smokers ‘reward system’ becomes temporarily less active/sensitive (downregulation)

24
Q

What causes anxiety, sadness and lethargy in down regulation

A

Specific acetylcholine receptors become unavailable and inactive.

25
Q

How to smokers avoid the negative side effects

A

Smoke more to maintain a certain level of nicotine in their bodies

26
Q

What is smoking more to avoid unpleasant side effects and example of

A

Negative reinforcement

26
Q

Where does down regulation occur

A

Mesolimbic pathway

26
Q

With the down regulation in the mesolimbic pathway what is needed for the same initial ‘kick’

A

An increased amount of nicotine

27
Q

Why do LT smokers need more nicotine for the same initial ‘kick’

A

Receptors have been ground down

28
Q

What happens to the nicotinic receptors when an individual is smoking

A

They are desensitised
Cravings and withdrawal symptoms are held off

29
Q

What happens when smokers go without nicotine for a long period of time

A

Nicotine disappears from the body.
This allows more nicotine receptors to become functional again (upregulation).

30
Q

What is up regulation

A

Allowing more nicotine receptors to become functional again (upregulation).

31
Q

Evaluation, evidence
Paterson et al

A

P- Paterson et al. (2002) found support for the role of nicotine and dopamine through research with epilepsy drug (Gamma-vinyl GABA).

E-This drug reduces the surge of dopamine in the nucleus accumbens that occurs after nicotine. This effectively reduces the addictive properties of nicotine, without major side effects.

L- This suggests that nicotine is does activate DA and stopping this can help with cessation

32
Q

Evaluation, practical applications

A

P- The bio chem explanation as led to some useful practical applications

E-Delivering therapeutic doses of nicotine (without the undesirable parts of tobacco) in the early stages of stopping smoking.

E- This release of nicotine is absorbed much more slowly and steadily than in tobacco.

L- This implies the brain chem account of smoking addiction has the potential to help the 19% of smokers in the UK to ditch the habit.

33
Q

Evaluation, beta bias

A

P- However the explanation seems to suffer a beta bias

E-Nerin and Jane (2007) argue the onset of smoking addiction is significantly different between the sexes - i.e., women typically start smoking much later than men.

E- The biological reasoning for this is ignored.

L- This could imply the explanation suffers from an implicit gender bias

34
Q

Evaluation, neglects role of nurture

A

P-Neglects to consider the role of nurture.

E- Perhaps the rewarding qualities of nicotine are also gained through the environment - for example the peer acceptance and approval that have been shown to be positively reinforcing.

E- Research has shown that nicotine activates dopamine - but studies have also shown peer approval activates dopamine as well.

L- This could imply that the explanation could be more comprehensive if it takes into account nurturing influences of nicotine addiction

35
Q

Evaluation, scientific

A

P- Explanation can be praised for being scientific

E-The dopamine account uses both empirical and falsifiable methods to help identify the biochemical action of nicotine.

E- For instance, dopamine and NAcR can be objectively measured through cerebrospinal fluid (CSF), sophisticated PET scans as well as carefully examining urine for waste products.

L- This implies that the DA account for nicotine addiction is more trustworthy and reliable.