Addictive Behaviours - Biological Explanations: Dopamine Flashcards
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What is a neurotransmitter and what does it do
- A chemical messenger
- it carries signals from one neurone to the next across the synapse
What is the neurotransmitter dopamine associated with
- often called the “feel good” neurotransmitter
- involved in reward, motivation, addiction and also schizophrenia
What key piece of research helped to establish the ‘reward centre’ of the brain
- Olds and Milner (1954)
- they conducted a study where they implanted electrodes in rats’ brains
- They found that rats enjoyed the stimulation from certain brain areas and repeatedly sought it out
- To explore this, they built a Skinner box, allowing the rats to self-administer the brain stimulation by pressing a lever
- rats would run across the electrified grid in order to press the lever, despite the shocks
- Shows the stimulation of this part of the brain must be rewarding and pleasurable
Which area of the brain is known as the ‘reward centre’ or ‘pleasure centre’
- the septal region (identified by Old and Milner’s research
- Its closely associated with the limbic system
- Found the rats would stimulate this region even at the expense of food and sex
- Later identified as the nucleus accumbens by Heath
How does the mesolimbic pathway work
- When exposed to a stimulus essential for survival (such as food and sex) the brain responds by increasing the release of the dopamine
- The dopamine pathway (called the meso-limbic pathway) starts in the Ventral tegmental area (VTA) —This is the principle dopamine producing area of the brain
- This is connected to the nucleus accumbens (which is associated with motivation and reward)
- Dopamine projects from the VTA to the NAc and the activation causes levels of dopamine there to rise —> results in a feeling of pleasure that’s rewarding —> encourages us to repeat the behaviour
How might the mesolimbic pathway lead to addiction
- This system evolved to reward behaviours that are good for us so we would repeat them
- however, in the case of addiction this reward system becomes maladaptive because it is rewarding actions that are harmful to us such as taking a drug or engaging in an addictive behaviour encouraging us to repeat
Which 2 research evidence shows that dopamine and the mesolimbic pathway is involved in addictive behaviours?
- Jousta et al (2012)
- Boileau et al (2003)
Describe what was done, what was found and what it suggests about the dopamine hypothesis in Jousta et al (2012)
- Took PET scans of 24 gamblers and non-gamblers whilst gambling on a slot machine when they win or lose to measure dopamine levels
- Found that dopamine was released during gambling (irrespective of winning or losing)
- This shows that the dopamine levels are raised during gambling, supporting the explanation that an increase in dopamine levels leads to addictive behaviour in behavioural addictions
Describe what was done, what was found and what it suggests about the dopamine hypothesis in Boileau et al (2003)
- Took PET scans of 6 people who either had alcohol in orange juice or just orange juice
- Found more dopamine released in the alcohol condition
- Shows that dopamine levels are raised when engaging in an addictive substance supporting the fact that it is this increase in dopamine that leads to the addictive behaviour in substance addictions.
How are addictive behaviour maintained
three ways
1. neuroadaption
2. Tolerance
3. Withdrawal
What is neuroadaption
- The brain adapts in response to experiences and strives to reach an equilibrium.
- when we take drugs or engage in an addictive behaviour the brain seeks to restore balance so adapts to the effect of the drug or behaviour.
Describe how tolerance occurs
- neuroadaption causes changes in the brain (specifically the dopamine reward pathway)
- Due to overstimulated by consistently high levels of dopamine = compensates to reduce this stimulation by anticipating this overstimulation and making corrections to ensure a normal balance.
- There are two ways it can do this:
1. decreasing production of dopamine
2. Reducing the number of receptors available for dopamine to dock with - The fewer receptors there are the less stimulation of the neuron occurs.
- This reduction in dopamine means that more and more of the drug/behaviour will be needed to achieve the same effect
Describe how withdrawal occurs
- due to the neuroadaption
- When a drug/behaviour is stopped, the brain becomes out of balance again and it takes a while for the brain to adapt.
- The very low levels of dopamine cause the symptoms of withdrawal which often causes people to start taking the drug again.
- The drug now is no longer being taken for its pleasurable effects, but rather to avoid the withdrawal symptoms.
Describe activity in the synapse: pre-drug use
- At a normal synapse the dopamine is released from the transmitting neuron and attaches to the receptors on the receiving neuron firing the receiving neuron at a normal rate
Describe activity in the synapse: during drug use
- When a drug is taken more dopamine is released (amphetamines) and/or less is retaken as the drug binds to the reuptake transporter (cocaine) leading to more dopamine in the synaptic cleft and more being received at the receptors causing more excitement.
- This increase in firing is what leads to the ‘high’
Describe activity in the synapse: after tolerance
- due to the overstimulation caused by the excess dopamine the brain seeks to readress the balance by reducing the number of D2 receptors
or the amount of dopamine produced to reduce the firing rate of the neuron. - Therefore to get the same feeling the person will need to take more more of the drug
Describe activity in the synapse: after tolerance with no drugs (withdrawal)
- the drug is stopped then due to the reduced number of receptors very little excitement occurs leading to withdraw symptoms.
- Engaging in the behaviour then becomes about avoiding withdrawal symptoms rather than experiencing pleasure.
What is the research evidence that neuroadaptation to dopamine is involved in addictive behaviours
- Volkow et al (1997)
- carrred out PET scans of cocaine addicts and non addict controls after giving them a drug similar to cocaine.
- they found the cocaine addicts showed a reduced release of dopamine in response to the drug compared to controls
- The brain of the addict had adapted so it doesnt release as much dopamine in order to reduce the overall dopamine levels causing tolerance
- Also did PET scans for a variety of different drug addictions (cocaine, meth, alcohol and heroin) + control and found decreased D2 receptors in addicts —> further supports neuroadaption
Explain how the maintenance and relapse of addictive behaviours work
- high levels of dopamine caused by addiction alter the functioning of parts of the frontal cortex, which persist even when the drug is no longer being taken or the behaviour no longer engaged in.
- It explains why addicts feel compelled to engage in their addiction, even though they no longer gain any pleasure from it.
- Research evidence suggests changes like reduced blood flow to the prefrontal cortex, reduced activity and reduced volume and that it is these changes, which affect decision making, attention and memory that really turn engaging in a behaviour into an addiction.
- Volkow argues that these changes alter our attention —> pay more attention to stimuli related to the addiction
- Robinson and Berridge (2013) suggests it cause the addict to want to engage, rather than just like it
What is the research evidence of the altering functioning of the prefrontal cortex due to dopamine is involved in addictive behaviours (substance example)
- Volkow et al (1992)
- PET scans of 21 cocaine users 1-6 weeks after their last cocaine use and also after 3 months. Compared with controls for glucose metabolism (shows brain activity)
- Found cocaine users had significantly less glucose metabolism (therefore brain activity) in the frontal cortex persisting up to 4 months of abstinence
- Suggesting that cocaine use and the associated high levels of dopamine has changed brain activity in the frontal cortex long term and it’s still apparent after the drug use has stopped, offering support for dopamine being the explanation for the maintenance of drug addiction long term
What is the research evidence of the altering functioning of the prefrontal cortex due to dopamine is involved in addictive behaviours (behavioural example)
- Bolla et al (2003)
- Looked at blood flow in the frontal cortex via PET whilst carrying out a decision making task (the IOWA gambling task) versus a non decision making task in cocain users who were 25 days abstinent
- During the decision making task, cocaine users showed greater activation in the areas of the frontal cortex that are related to anticipation and reward and less activity in the part of the frontal cortex related to planning and memory
- The increased dopanine level caused by cocaine addiction causes functional abnormalities in decision making. They pay more attention to the short term reward and less to the long term consequences and so are more likely to continue their addictive behav.ours. This offers support for the dopanine explanaton as the increased level of dopamine has made changes the frontal Cortex that encourage the addictive behaurour.
What is the research evidence of the altering functioning of the prefrontal cortex due to dopamine is involved in addictive behaviours (paying attention to stimuli to do with addiction)
- Want et al (1999)
- Carried out PET scans on 13 cocaine abusers, once during an interview about cocaine related themes (designed to elicit cravings) and once during an interview about neutral themes
- Found during the cocaine themed interviews the cocaine abusers had higher metabolic activity in the frontal cortex, suggesting that being exposed to ‘cues’ associated with cocaine and expectancy which explains why addicts are likely fo relapse.
- This is evidence do support the dopamine explanation that high levels of dopamine in addiction lead to changes in the frontal cortex which encourage continuation of addictive behaviours. In this case because more attention is paid to the cues associated with the addiction.
Based on this explanation, the method of modifying should work by…
- reducing dopamine levels in the synapse and therefore reducing stimulation and pleasure and reward.
A method of modifying addictive behaviours could be using….
- agonist or antagonist drugs.
- Agonist drugs mimic the action in the brain of the additive drug (e.g. heroin) being taken, by binding to and activating the same receptors causing the release of dopamine.
- This dopamine release causes the same pleasurable effect as the addictive drug (without creating the same intensity high) and therefore reduces withdrawal symptoms and cravings.
- Antagonist drugs block the effect of the addictive drug by binding to the same receptors but not activating them, so when the drug is taken no dopamine is released so no pleasure is felt removing the reinforcing effect
Give an example of an antagonist drug + how it works
- Naltrexone is an opioid antagonist.
- It binds to and blocks the opioid receptors but doesn’t activate them so when an addict takes an opioid such as heroin there are no receptors for the heroin to bind to so no dopamine is released and no high is felt, breaking the reinforcing effect of taking heroin.
Give an example of a drug that is both an agonist and an antagonist
- Varenicline
- it works as an agonist and antagonist drug and is used to treat nicotine addiction.
- It works by binding to the nicotine receptors and activating them to a small extent releasing a small amount of dopanine to allieviate windawal symptoms and crawings for nicotine.
- It also blocks the nicotine recaptor so when cigarettes are smoked nicotine can’t bind to the receptors which helps reduce the rewarding effect of smoking as the addict gets less pleasure from it.
What is the research evidence that shows Varenicline as being effective
- Taylor et al (2016) followed 220,136 smokers.
- Half were prescribed Varenicline and half Nicotine Replacement therapy.
- They found that after 2 years those prescribed Varenicline were more likely to have successfully quitted smoking then those prescribed NRT.
When evaluating this explanation, what are the different points you can make
- contradictory evidence — Stokes et al (2009) + stokes et al (2012)
- Reductionism — weakness
- Methodological issues with supporting research — David Nutt et al (2015)
- Use of non-human animal studies — low generalisability + counter of strengths
- Determinism - strength of how it changes stigma of addiction + counter of feeling powerless
Evaluate the explanation using contradictory evidence
P: A lot of evidence assumes all drugs would have a similar effect on dopamine, more recent research shows this isn’t the case, particularly when comparing the effects with cannabis addictions
E: Stokes et al (2009) 13 volunteers with previous cannabis experience underwent 2 PET scans to measure dopamine levels following either 10 mg of THC (the main active ingredient of cannabis) or a placebo. Finding that even though the THC caused psychosis like symptoms there was no significant effect on dopamine levels.
T: Therefore this shows that significant amounts of dopamine are not released when using cannabis suggesting dopamine isn’t a cause of addiction to cannabis.
C: furthermore this is supported by his later research, Stokes at al (2012) when he compared PET scans of 10 volunteers who had a lifetime use of cannabis (with an average of 2032 sessions of cannabis use in their lifetime) with 10 controls who had never used cannabis. They found that a history of use of cannabis was not associated with alterations in dopamine receptor availability. This means that dopanine explanation of addiction cannot be used to explain all addictive behaviours at any stage ef addiction initration, maintence, tolerance a mindrawal).
Evaluate the explanation for it being reductionist
P: could be considered reductionist as it offers an oversimple explanation, (altered levels of dopamine), for a complex behaviour that may be effected by a person’s social situation and circumstances, such as acceptability or availability.
E: Studies also suggested that dopanine levels increase in response to aversive stimuli as well as pleasurable ones suggesting the mesolimbic system encourages us to avoid unpleasant stimuli as well as encouraging us to seek out pleasurable ones.
E: research by Liberzon showed increased activation in the nuceus accumbens in war veterans suffering from PTSD when reminded of baltle via combat sounds.
T: This does not match the idea of this area simply being about pleasure, suggesting that the explanation is therefore oversimplified and incomplete
Evaluate the explanation having methodological issues with its supporting research
P: Other psychologists, such as David Nutt, criticise suppporting research of the dopamine explanation due to issues with the sample used
E: David Nutt et al (2015) critiques samples being too small and therefore not very generalisable. He also brings attention to the difficulty of souring participants that are generalisable to other addicts due to the fact that they are sourced from treatment centres, where they all share similar characteristics and attitudes that make their drug experiences different to others.
T: both these factors of the sample’s size and its characteristics contribute to most supporting research having a low population validity and therefore generalisability of the research itself.
C: furthermore Nutt also notes that the drugs are administered in different forms than everyday situations (e.g. THC in oral form rather than cannabis joints smoked.). Paired up with the highly sterile lab conditions and machinery that don’t reflect a more natural setting, it lowers the ecological validity of this research as well as the overall validity of the explanation itself
Evaluate the explanation using non-human animal research to support it
P: a number of research into the role of dopamine and the frontal cortex involve use of non-human animal research
E: This works well because it allows us to manipulate drug use so that we can observe their brains before and after drug use, seeing the effects of tolerance and withdrawal. Animals are also very similar to humans in terms of biology and brain structure/function especially in terms of the reward pathway . Rats for example have a very similar pathway as well as the same neurotransmitters and system for the release of neurotransmitters.
T: Therefore, it allows us to carry out research on the cause and effect relationships on some of the factors that the explanation is based on (tolerance and withdrawal)
Evaluate the explanation for being deterministic
P: it’s a deterministic explanation of addictive behaviours because it suggests it’s caused by altered levels of dopamnine, a biological process beyond our control. In addition if domaine is causing changes to the frontal cortex influencing decision making then the addicts are no longer in control of their own behaviour.
E: Heather, N., & Robertson, I. (1981) found individuals with alcohol addiction are more likely to seek help when their behavior is framed as being influenced by external factors (such as biological predispositions). Proposing the idea that when addiction is seen as “out of control” or beyond personal responsibility, individuals are less likely to feel shame and are more open to seeking treatment.
T: If viewed as beyond the addicts control = help decrease the stigma assocated with addiction + if we can encourage individuals with addiction to seek help —> proves useful for helping promote treatment
C: alternatively, it may mean the addict feels that their addictve behaviours are beyond their control so they feel powerless to change —> so they don’t bother trying to
