Addiction- brain chem explanation for nicotine addiction Flashcards

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

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

23
Q

With long term use, what does the NRM suggest

A

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

24
What causes anxiety, sadness and lethargy in down regulation
Specific acetylcholine receptors become unavailable and inactive.
25
How to smokers avoid the negative side effects
Smoke more to maintain a certain level of nicotine in their bodies
26
What is smoking more to avoid unpleasant side effects and example of
Negative reinforcement
26
Where does down regulation occur
Mesolimbic pathway
26
With the down regulation in the mesolimbic pathway what is needed for the same initial 'kick'
An increased amount of nicotine
27
Why do LT smokers need more nicotine for the same initial 'kick'
Receptors have been ground down
28
What happens to the nicotinic receptors when an individual is smoking
They are desensitised Cravings and withdrawal symptoms are held off
29
What happens when smokers go without nicotine for a long period of time
Nicotine disappears from the body. This allows more nicotine receptors to become functional again (upregulation).
30
What is up regulation
Allowing more nicotine receptors to become functional again (upregulation).
31
Evaluation, evidence Paterson et al
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
Evaluation, practical applications
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
Evaluation, beta bias
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
Evaluation, neglects role of nurture
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
Evaluation, scientific
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.