Addiction - biological explanation of addiction Flashcards
What is the main function of Acetylcholine (Ach) in the brain?
Ach helps the transmission of other neurotransmitters across the synapse, which increases Dopamine levels in the brain. Dopamine is involved in the brain’s reward pathway, particularly in the Nucleus Accumbens.
How does nicotine affect Dopamine levels in the brain?
Nicotine increases Dopamine levels in the ventral tegmental area by mimicking Ach’s effects. This interaction makes nicotine act like a rewarding substance, contributing to its addictive nature. Dopamine travels through the mesolimbic pathway to the nucleus accumbens, simultaneously dopamine travels through the mesocortical pathway to the frontal cortex. This causes mild euphoria and a reduction in anxiety.
How does nicotine affect the Nicotinic receptors after use?
Unlike Ach, nicotine temporarily shuts down the Nicotinic receptors after use. This downregulation or desensitization results in lower-than-average Dopamine levels, leading to a feeling of low pleasure, which makes individuals crave another cigarette.
Outline what happens in the brain after ingesting nicotine.
the nicotine binds to the Ach receptors (nAchR’s), which causes dopamine release throughout the brain. The nAchR’s then shut down causing downregulation (no longer sensitive to any other neurochemical). Once the nicotine is metabolised, the nAchR’s go through upregulation and are sensitive to neurotransmitters again.
What is the nicotine regulation model?
The nicotine regulation model explains how nicotine addiction is maintained. It suggests that the cycle of nicotine intake, followed by withdrawal, leads to increased sensitivity of Nicotinic receptors, causing a desire to replenish nicotine levels, thereby reinforcing the addiction.
What is the role of Glutamate in neuron activity?
Glutamate speeds up the activity of neurons, helping to increase dopamine release, which contributes to the pleasurable effects of nicotine.
What is the role of GABA in neuron activity?
GABA slows down neuron activity, helping to reduce the release of dopamine and counteracting the stimulating effects of other neurotransmitters like Glutamate.
How does nicotine affect Glutamate and GABA?
Nicotine increases Glutamate’s activity, which speeds up dopamine release, and prevents GABA from slowing down dopamine release. This combination leads to longer-lasting pleasurable effects from nicotine.
What is the role of Monoamine Oxidase (MAO) in the brain?
Monoamine Oxidase (MAO) is an enzyme responsible for breaking down dopamine after it has been released, helping to regulate dopamine levels in the brain.
How does nicotine affect Monoamine Oxidase (MAO)?
Nicotine contains an unknown substance that blocks the action of MAO, leading to increased dopamine levels and the amplification of nicotine’s rewarding properties.
What is the result of nicotine’s effects on dopamine, GABA, and MAO?
Nicotine leads to increased dopamine levels by enhancing Glutamate, inhibiting GABA, and blocking MAO. This results in amplified rewarding effects of nicotine, reinforcing the smoking habit.
What happens to nicotine-dependent neurons over time?
Repeated nicotine intake changes the sensitivity of dopamine-enhancing neurons, leading to tolerance, dependence, and eventually addiction.
Why is the first cigarette of the day often described as the most enjoyable by smokers?
The first cigarette after a period of abstinence (e.g., overnight) is often the most enjoyable because the smoker has gone through withdrawal and the nicotine provides a quick dopamine ‘rush’, temporarily relieving withdrawal symptoms.
What is downregulation of nicotinic receptors (nAChRs)?
Downregulation refers to the temporary shutdown of nicotinic receptors after nicotine use, leading to desensitisation and a reduction in receptor activity, which makes the brain less responsive to nicotine over time.
How does upregulation of nicotinic receptors (nAChRs) contribute to withdrawal?
Upregulation of nicotinic receptors occurs when nicotine is absent, making the receptors more sensitive and increasing the smoker’s desire for nicotine. This contributes to withdrawal symptoms when the person tries to stop smoking.
How does the repeated activation of nicotinic ACh receptors change brain neurochemistry?
Repeated activation of nicotinic ACh receptors by nicotine creates permanent changes in brain neurochemistry, reinforcing the addictive cycle and making it more difficult to quit smoking over time.
What research support is there for the neurochemical explanation of nicotine addiction?
A strength of the neurochemical explanation is that it has research support from the treatment of patients with Parkinson’s disease (PD). Fagerstrom et al (1994) found that nicotine gum and patches significantly improved symptoms of PD, likely by increasing dopamine levels. This suggests that nicotine does have an impact on dopamine.
What is a limitation of the neurochemical explanation of nicotine addiction? (Issues and debates)
A limitation is that the neurochemical explanation is reductionist, simplifying addiction to just the activity of neurotransmitters and ignoring other factors, such as social influences or learning processes like operant conditioning or social learning theory.
What practical applications does the biological explanation of nicotine addiction have?
The development of nicotine replacement therapies (NRT) like patches and inhalers. By mimicking the effects of nicotine, stimulating dopamine release and reducing withdrawal symptoms, which makes it easier for individuals to quit smoking and avoid relapse. Nicotine addiction is also strongly associated with conditions like schizophrenia, depression, and alcoholism, and NRT can help reduce smoking in individuals suffering from these disorders, providing additional benefits beyond just treating addiction.
What does Cosgrove et al. (2014) suggest about gender differences in nicotine addiction?
Cosgrove et al. (2014) found that women experience a stronger dopamine response in the dorsal putamen while smoking, while men show a stronger response in the ventral striatum, suggesting that men smoke for the nicotine effect itself, while women may smoke more to manage stress or improve mood. This is not included in the biological explanation, suggesting it doesn’t take all factors into account, and therefore has a beta bias.
What is a limitation of the research by Cosgrove et al. (2014)?
A limitation is that the study had a small sample size (16 smokers), and further research with a larger sample is needed to increase confidence in the conclusion. There may also be an issue of beta bias, as current explanations might overlook gender differences in nicotine addiction.
