Motivation and emotion/Textbook/Motivation/Motivational toxicity

Motivational Toxicity

This page is part of the Motivation and emotion textbook. See also: Guidelines.

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Overview

Cocaine is a highly addictive illicit substance

Pleasure is the subjective interpretation of the feelings of happiness and sense of satisfaction that is derived from an enjoyable event or stimulus (Adinoff, 2004). Pleasurable feelings are the brain’s way of rewarding particular behaviours and are experienced as the feeling of contentment after a good meal, the refreshing sensation of cold water easing a parched throat or the orgasmic rush of a sexual encounter (Foddy & Savulescu, 2007).

Pleasurable experiences are beneficial in a variety of ways. Pleasures often promote survival and reproductive behaviour, and some also reduce stress, stimulate personal growth and promote health and well-being (Esch & Stefano, 2004). But pleasure-seeking can get out of control. Addiction and motivational toxicity can be the negative outcomes of pleasure-seeking gone terribly wrong (Hyman, 2007).

What makes an addict capable of lying, stealing and cheating to get their hands on a drug? How can they take advantage of other people and cause such pain and destruction to their families? Why do they apologise and promise to stay sober only to quickly get drunk again? Are addicts morally weak individuals who choose their drug over everything else, or are they sufferers of a chronic disease that robs them of their self-control?

This chapter will explore the neurobiological structures and processes that underlie substance addictions and the associated drug-obsessed thoughts and compulsive, destructive behaviours. Addictions come in many forms and involve a variety of brain regions and neurotransmitters. Merely touching on research in all these areas would fill many books, therefore this chapter will focus mainly on drug and alcohol addiction and the role of the neurotransmitter dopamine in the brain’s reward system.

Motivation, addiction and motivational toxicity

Alcoholism is a family disease. It affects not only the drinker but those who care about him or her as well.

Motivation is a collection of fundamental brain processes that underlie the two basic behavioural drives – pleasure and pain. Appetitive motivation directs us to pursue particular pleasant rewards while aversive motivation steers us away from potentially negative or dangerous situations. Ultimately, motivation is what directs our attention and triggers the initiation, persistence and intensity of our daily behaviours, which create our experiences, that collectively become our lives (Esch & Stefano, 2004).

Drug addiction is a chronic disorder characterised by compulsive drug-seeking behaviours despite obvious negative health and social consequences and regardless of whether or not the drug provides pleasure (Niehaus, Cruz-Bermudez & Kauer, 2009). Withdrawal avoidance has long been considered the primary motive underlying drug addiction, suggesting that drug-seeking behaviours are a series of voluntary, planned actions that require flexible adaptability to changing conditions (Hyman, 2007). However, many experts now consider addiction to be a brain disease resulting from long-lasting neural changes and involving a complex interaction of biological and environmental factors (Volkow, Fowler & Want, 2003). Modern research identifies a reduced capacity for voluntary behavioural control due to the effects of long-term substance abuse on neural circuits (Bakalar, 2004).

Motivational toxicity refers to the powerful drug-obsessed drive that takes control of a drug addict’s thoughts and behaviours at the expense of all other things. The toxic motivation of chronic, long-term drug abuse steals behavioural control away from the brain’s natural reward system and commandeers the associated cognitions into the endless pursuit for drug use (Esch & Stefano, 2004). Motivational toxicity is the combination of the over-valuing of the abused drug, reduced sensitivity to natural rewards, impaired inhibitory control and disrupted cognitive functioning (Volkow et al., 2004).

The reward system and the pleasure pathways

In 1954, Olds and Milner famously enabled rats to electrically self-stimulate certain parts of their brains. Their research revealed particular areas in the brain that the rats persistently self-stimulated to the exclusion of all other behaviours. These areas are now known as the brain’s pleasure centres (Adinoff, 2004). Olds and Milner’s technique has been refined over the years and is now known as intracranial self stimulation. It has been widely used to identify the neurobiological reward pathways and structures (Schmitz, 2005).

"Oh man, this is my kind of reward!"

A delicious "natural" (non-drug) reward

The reward system is a complex structure of neuronal circuits in the central nervous system that are intricately connected with the limbic system and the frontal cortex to guide and govern behaviour (Esch & Stefano, 2004). Evolution has refined this system into complex biological mechanisms that promote goal-seeking by enabling us to create internal mental images of our desired rewards, assign them a value for comparison against other alternatives, learn automatic sequences of goal-attaining behaviours, suppress competing distractions and inhibit disruptive impulses (Hyman, 2007). These neural processes prioritise our needs and desires into a motivational hierarchy designed to promote survival, health and well-being (Esch & Stefano, 2004).

The basic premise of the reward system lies in the principles of operant conditioning. Rewards are the tools that control our motivation and guide our behaviour, when our actions are pleasantly rewarded they are more likely to be repeated (Schmitz, 2005). Getting the reward reinforces, strengthens and improves the efficiency of the behaviour (Hyman, 2007).

Pleasure and addiction may be two sides of a coin but they follow the same neural route - the pleasure pathways. As will be discussed below, these pathways are the mesolimbic dopamine tracts which are made up of the projected axons from dopamine neurons situated in the ventral tegmental area of the midbrain (Esch & Stefano, 2004).

Natural reinforcers

Natural rewards are the pleasant feelings of enjoyment and arousal that are experienced in relation to behaviours or stimuli that promote survival, health and well-being (Adinoff, 2004). These reinforcers are controlled by biological feedback mechanisms to help regulate the motivational hierarchy. For example, we eat when we are hungry and we stop eating when we feel full (Esch & Stefano, 2004). These reinforcers are prioritised by their fluctuating value and saliency in order to maintain an optimal level of homeostasis (Volkow, Fowlwer & Want, 2003). Rewards trigger the release of the neurotransmitter dopamine in the brain resulting in the feeling of pleasure and promoting learning and memory (Hyman, 2007).

Drug rewards

Natural and drug rewards act at the same brain sites and both trigger the release of dopamine. Chemical substances however, directly and strongly stimulate the CNS without any controlling mechanism to keep them in check (Bakalar, 2004). This direct and unregulated activation of the CNS earns the drug a fixed and super-potent reward value which contrasts with the fluctuating relative value of natural rewards (Esch & Stefano, 2004). Chronic drug use also results in phasic dopamine levels, a faster, more intense release followed by a rapid decrease, which strengthens the motivational properties of the drug well beyond that of natural rewards (Volkow & Li, 2004). Drug-induced dopamine bursts also enhance conditioned learning, supporting the growing connections between drug use and drug-predicting internal and environmental cues (Volkow, Fowler & Want, 2003).

Drug use vs. drug addiction

What are the differences between drug use and drug addiction? Researchers have compared laboratory rats with differential access to cocaine self-administration to explore this question. As expected, their findings indicate that addicted rats self-administer higher levels of cocaine than non-addicted rats. Additionally, when the cocaine is taken away, addicted rats are more motivated to get their dose, take increased risks in the process, persist longer with drug-seeking behaviours and have a higher prevalence of relapse (Ahmed & Koob, 2005).

Drug effects

Neurons are made up of a cell body, axons and dendrites. The synapse is a small junction where chemical messengers pass from the axon of a pre-synaptic neuron to receptors on a post-synaptic neuron.

Long-term use of alcohol, cannabis, opiates and psychostimulants have all been associated with neuronal injury, dysfunction and loss of brain volume (Yucel & Lubman, 2007). The maladaptive neuronal changes incurred by substances of abuse correlate with the dysfunctional behaviours of addiction (Niehaus, Cruz-Bermudez & Kauer, 2009). These substances disrupt brain function and cause physical changes that redirect the neural circuits involved in planning, decision making, inhibitory control and attention to compulsively respond to drug related stimuli, creating an incredibly strong motivational drive (motivational toxicity) to seek and use drugs even when they no longer provide pleasure (Adinoff, 2004).

Neural sensitisation

The drugs' ability to directly and intensely stimulate the CNS results in the assignment of a super-potent reward value that far outranks the value of natural reinforcers, reducing the ability of other stimuli to compete for the addicts attention (Bakalar, 2004). This is the concept of neural sensitisation which results in the excessive wanting of the drug, the motivation to get the drug as opposed to liking the effect it produces (Robinson & Berridge, 2003). It is important to note the difference between liking and wanting, as wanting can occur without liking. Liking refers to the pleasurable feelings experienced when a desired reward has been procured. Wanting refers to the motivational salience that makes the reward desirable, wanting transforms a reinforcer from a sensory representation into a desired reward capable of capturing attention and motivating behaviour (Zhang et al., 2009).

Conditioned learning

Addicts also demonstrate an attentional bias towards drug-related stimuli. Drug-cues activate memories, sensations and emotions generating responses strong enough to induce cravings and relapse (Gardini, Caffarra & Venneri, 2009). Over-learning of drug-stimuli associations is due to the enhanced activation of the memory and learning circuits from drug-induced dopamine surges. This strengthened learning supports the development of behaviour sequences that are automatically elicited by drug-stimuli, further increasing the motivational salience of the drug, and links affective states to drug-use to form future drug effect expectations (Volkow, Fowler & Wang, 2003).

Conditioned learning is an important aspect of addiction, however problems arise with the ability to activate the neural motivational systems, as learning by itself does not generate compulsive behaviours. Robinson and Berridge (2003) suggest that the abnormalities of addiction do not lie in the conditioned learning itself, but in the response of the brain's motivational systems to the conditioned drug cues.

Test yourself

1 Motivational toxicity is the drive behind addiction behaviours.

	TRUE.
	FALSE.

2 Drug rewards have the same motivational salience as natural rewards.

	TRUE.
	FALSE.

Brain structures and functions

Modern fMRI research has revealed that drug use and associated cravings activate a complex pattern of interconnected brain areas that receive direct innervations from dopamine neurons. These areas include the ventral tegmental area of the midbrain, the nucleus accumbens, orbitofrontal cortex, anterior cingulate, prefrontal cortex, amygdala and hippocampus. These regions, and their involvement in rewards, motivation, memory, learning and cognitive control, mediate our everyday behavioural choices by formulating comparisons, expectations and associations (Volkow, Fowler & Want, 2003).

Modern researchers hypothesise that drugs of abuse may create an 'addiction signal' that begins in the ventral tegmental area and is passed along to the nucleus accumbens and other areas of the frontal cortex and limbic system by mechanisms similar to long term potentiation (LTP) or depression (LTD). We will explore LTP and LTD in the next section (Niehaus, Cruz-Bermudez & Kauer, 2009).

Neural structures of the reward system

Ventral tegmental area	The pleasure pathways start here in the midbrain. This is the home of dopamine neurons whose projected axons create the mesolimbic system that innervates and interconnects other regions. Natural and drug rewards stimulate the VTA to start the cycle of dopamine release. Reward-driven behaviours are processed to provide information for modifying future behaviours (Niehaus, Cruz-Bermudez & Kauer, 2009).
Frontal and prefrontal cortex	The large frontal lobes consist of many specialised sections with specific roles. Overall, the frontal cortex coordinates and processes the information that determines appropriate behaviour (Esch & Stefano, 2004). The prefrontal cortex houses our conscious goals, is involved in decision making, inhibitory control and reward values (Volkow, Fowler & Wang, 2003).
Nucleus accumbens	The primary region for the pleasurable experience of rewards, or the sensation of liking. Here, the motivational saliency (how important something is compared to other things) of an expected reward is calculated in relation to the current situation and previous experiences (Volkow, Fowler & Wang, 2003). This area plays a critical role in priming future drug use and is involved in the higher order sensory and motor processes that initiate goal-directed behaviours, regardless of the type of reinforcer (Adinoff, 2004).
Orbitofrontal cortex	A major component of the reward system, the OFC houses several functions that if disrupted produce addiction behaviours. Reward values are compared to alternative options, taking into consideration recent experiences and internal needs. Appropriate courses of action are determined for unpredictable situations or when there is limited information available. The OFC also assesses the relevance and value of behavioural options, the familiarity of situations and outcome expectancies and provides behavioural stop signals (Adinoff, 2004). A critical area for drive and motivation, conditioned responses, learning stimulus-reinforcement associations, inhibiting emotional responses, compulsive behaviours, perseveration and protecting reward-association behaviours from extinction (Volkow et al., 2004). Disrupting the OFC can lead to impulsivity, decision making and obsessive-compulsive disorders (Adinoff, 2004).
Anterior cingulate	Inhibitory control over behaviour, performance monitoring, consideration of available choices, error detection, prediction of potential conflicts between intended actions and their outcomes (Yucel & Lubman, 2007). Also responsible for emotional self-control, focused problem solving and the ability to adapt to changing conditions under the influence of current motivation and mood (Adinoff, 2004). Disrupting this region impairs ability to detect errors in behaviour reducing capacity to control actions in the face of negative outcomes (Yucel & Lubman, 2007). Also associated with emotion and attention disorders (Adinoff, 2004).
Amygdala	Consolidates memories of emotionally arousing events, assesses whether events are pleasant or unpleasant, and subsequently whether they should be repeated or avoided. Assigns reward values to stimuli and is involved in fear conditioning in new situations (Adinoff, 2004).
Hippocampus	Formation of new memories of personal experiences (episodic memory) and learning new factual information. Damage to the hippocampus can result in amnesia and is implicated in Alzheimer's disease (Adinoff, 2004).
Dorsolateral prefrontal cortex	Home of our working memory, conscious management of chunks of current information enables us to sequence events, and plan and select goals (Adinoff, 2004).

Dopamine and the pleasure pathways

Neurotransmitters are chemical messengers released from one neuron, across the synapse (the tiny gap between cells) to be taken up by receptors on other neurons (Volkow et al., 2004). The activation of the mesolimbic pathways releases dopamine into the synapses, producing feelings of pleasure and enabling the determination and recording of motivational saliency (reward value) for the particular reinforcer (Adinoff, 2004).

Dopamine is naturally released at a slow, steady rate to consistently regulate mood and drive motivation (Esch & Stefano, 2004). Unexpected, new or better than anticipated experiences trigger the release of dopamine to enhance motivation encoding, new learning, information processing, reward prediction and reinforcement. Addictive drugs trigger a flood of dopamine release that creates the euphoric sensation of a drug high and strongly facilitates drug learning (Volkow et al., 2004).

Drug-induced higher levels of stimulation are adapted to by the resetting of reward values that further enhance the value of the drug and decrease sensitivity to natural reinforcers. Simultaneously the over-activated motivational and memory circuits start to take over from the frontal cortex, reducing inhibition functions and creating a positive feedback loop that results in compulsive drug-taking (Volkow, Fowler & Wang, 2003). The phasic dopamine levels induced by drugs eventually result in chronically reduced levels of dopamine and dopamine receptors in the mesolimbic system and reward circuitry, this renders the addict hyper-sensitive to the substance and strengthens the motivation to get and use the drug (Bakalar, 2004).

The dopamine pathways originate in the midbrain and spread out to innervate the striatum, hippocampus, amygdala (not shown), nucleus accumbens and frontal cortex

Dopamine receptors and reward deficiency syndrome

There are two main families and five sub-types of dopaminergic receptors. D2 dopamine receptors are the ones most commonly associated with addiction (Adinoff, 2004).

The amount of dopamine receptors that an individual has is influenced by both genetic and environmental factors. A person who has more receptors is likely to be less affected by drugs of abuse as there will be less dopamine free-floating at the synapse, this may offer a higher level of protection against addiction. Conversely, a person with less receptors may be predisposed to use drugs as a means of compensating for decreased reward circuit stimulation (Volkow et al, 2004).

Reward deficiency syndrome (RDS) refers to chronically low levels of dopamine and dopamine D2 receptors, a common factor in a variety of addictive behaviours including drugs, obesity, compulsive gambling and sex addiction. RDS reduces the level of pleasure experienced from normal rewarding stimuli, such as a good book or friendly social interaction. Binging on addictive substances increases dopamine release and may be a form of self-medication to compensate for an under-active reward system. Unfortunately binges are quickly followed by the down-regulation of dopamine D2 receptors returning levels to their chronically low state and creating a vicious cycle of craving and compulsion (Fortuna & Smelson, 2008).

Synaptic plasticity and long term potentiation

Various drugs exert different effects, but all of them alter the strength of the synapses stimulating VTA dopamine neurons, suggesting that all addictive substances may alter brain reward circuitry through the same mechanisms early in addiction (Niehaus, Cruz-Bermudez & Kauer, 2009).

Synaptic plasticity refers to the ability to alter the synaptic connections between neurons by a mechanism known as long term potentiation or depression (LTP or LTD), a long-lasting increase or decrease in synaptic transmission hypothesised to underlie information storage in the brain (Kauer & Malenka, 2007).

After drug use, changes in synaptic plasticity are equivalent to changes in behaviours. More importantly, sometimes when the synaptic changes are reversed, some of the behavioural effects are reversed along with them. It is theorised that addictive drugs use LTP or LTD to alter dopamine synapses in the reward circuits. This either promotes or blocks plasticity of learning and memory circuits, hence influencing the over-learning and long-term storage of the reward-related memories involved in addiction (Niehaus, Cruz-Bermudez & Kauer, 2009).

Non-chemical addictions

Gambling is an impulse-control disorder that can become an addiction

Both substance-related and impulse-control disorders can be considered addictions. Although there are notable differences between the various disorders many appear to share common pathways. Pathological gamblers in search of a particular state of arousal stimulate the same dopaminergic reward and pleasure pathways as drug addictions, and demonstrate similar forms of tolerance and dependence. Like chemical addictions, pathological gamblers demonstrate increased rates of comorbid mood disorders, attention deficit/hyperactivity disorder, substance-related disorders, and personality disorders (Schmitz, 2005).

Binge-eating disorder, also known as food addiction, is defined by a lack of control over eating larger than normal amounts of food. Research has suggested similar decreases in dopamine D2 receptors may lead food addicts to seek out tasty rewards. Also in line with drug addictions, research recently identified the nucleus accumbens as the main site for the sweet tooth, sparking suggestions that food binges are a form of addictive behaviour that increase levels of dopamine (Fortuna & Smelson, 2008).

Test yourself

1 Phasic dopamine eventually results in chronically decreased levels of dopamine.

	TRUE.
	FALSE.

2 Reversing changes to synaptic plasticity also reverses addiction.

	TRUE.
	FALSE.

Vulnerability to addiction

A woman addicted to morphine. Painting by Santiago Rusiño, last decade of the 19th century.

Even with an extremely addictive drug like cocaine, only about 15% of users will become addicted. So what makes those people vulnerable to addiction? Although genetics are estimated to account for 40 to 60% of addiction vulnerability, other well known influential factors include stress, mental illness, social status and environmental factors (Volkow & Li, 2004). Increased risk of substance abuse and addiction may also be related to a decreased sensitivity to natural rewards, genetic or stress related deficiencies in D2 dopamine receptors, reduced activity of dopamine circuits or increased sensitivity to drug-stimuli by learning or motivation circuits (Volkow, Fowler & Wang, 2003). Adolescents have a particularly high susceptibility to addiction as their developing brains will not reach full maturity until into their 30’s. Research consistently shows higher levels of disruption and increased addiction due to the vulnerability of teenage brains to the neurotoxic effects of drugs (Yucel & Lubman, 2007).

Opponent-process theories of drug addiction

Drug-induced over-activation of the reward system eventually results in chronically decreased responsivity. According to opponent-process theories, this occurs due to an anti-reward system that counter-balances the natural reward system to maintain a narrow range for reward thresholds and an optimal level of homeostasis (Ahmed & Koob, 2005). The concept of opponent-processes is a common feature in biological systems but has not been as extensively researched in relation to addiction. Researchers suggest that the anti-reward process may manifest as withdrawal symptoms and involve stress hormones such as corticotrophin releasing factor (CRF), norepinephrine and dynorphin (Koob & Le Moal, 2005).

The general concept of opponent-process theories is that an a-process moves a biological system out of its normal range, closely followed by a slower b-process designed to gradually reinstate stability. In relation to drug use, initial drug consumption may boost the reward system responsivity well outside of normal range, the closely following opposing b-process works to stabilise the reward threshold resulting in the symptoms of withdrawal. During drug-binge use, the anti-reward b-process may not have sufficient time to successfully return the system to normal before the next drug hit delivers another surge. By this unbalanced process the drug may eventually reset the reward threshold, producing tolerance and gradually increasing the required dosage strength (Ahmed & Koob, 2005).

Robinson and Berridge (2003) identify limitations of the opponent-process theories. They note that often the symptoms of withdrawal are simply not potent enough to motivate drug-seeking behaviours. Additionally, withdrawal symptoms generally peak within a few days and then taper off, hence the short-term nature of withdrawal is an insufficient explanation for the long term potential to relapse.

Addiction as a form of pleasure-seeking

Some researchers disagree with the chronic-disease model of addiction. Foddy and Savulescu (2007) suggest that addiction is neither a brain disease nor a moral condition but an unusually strong, socially unacceptable pleasure-seeking preference that has been labelled a disease in order to allow the medical treatment of behaviours that challenge social norms. Foddy and Savulescu compare drug addiction to the the nineteenth century disorder of drapetomania, which caused slaves to run away from their masters, and people to mountain climb, suggesting that research is devoted to drug addiction over mountain climbing due to the sociopolitical context of the twenty-first century. Opiate-addicted returning Vietnam soldiers are offered as evidence that many addicts simply stop using or mature out of their addiction. Hence, in the view of Foddy and Savulescu, addiction is nothing more than a strong drive to experience pleasure.

Reversing motivational toxicity

Despite the increased value of drugs, the stronger and well-learned drug cues and the damaged neural control mechanisms, addictions can be overcome. Recovery requires a drug-free environment, strong support system, and the understanding that multiple relapses are likely and should be accepted as a temporary setback rather than a personal failure (Hyman, 2007). Effective treatments need to adopt multi-modal methods combining pharmacological, cognitive and behavioural therapies targeted at decreasing drug reward values, increasing natural reward values, weakening learned drug responses, extinguishing drug-cue associations and differential reinforcement of other behaviours (Volkow, Fowler & Wang, 2003).

There are two main pharmacological interventions used when treating addictions. The first type of medications interfere with the reinforcing effects of the drug by triggering aversive responses or interfering with their binding, the drug-induced dopamine increase, the postsynaptic response, or the drug's ability to reach the brain. The second type compensate for the long-term adaptations of addiction by decreasing the drugs motivational value, enhancing the motivational saliency of natural rewards, or interfering with conditioned responses, stress and withdrawal symptoms (Volkow & Li, 2004).

Meditation promotes mindfulness - remaining in the present moment, watching your thoughts without reaction or judgement.

Alternative and adjunctive treatments may help reduce symptoms and support pharmacological and behavioural therapies. Sensory stimulation, for instance music, may influence the limbic and reward pathways involved in feelings of pleasure and happiness, thus helping to reduce anxiety, depression and stress (Esch & Stefano, 2004). Auricular acupuncture stimulates branches of the cranial nerves that affect the limbic system, resulting in the production of the calming neurotransmitter serotonin. Research demonstrates this may help improve sleep, confidence, concentration, energy and physical and psychological well being, and reduce anxiety, cravings and stress (Handley, 2009). The Buddhist mindfulness practice of Vipassana meditation teaches objective, self-observation without reaction. Research by the University of Washington found Vipassana mediation to be a low-cost adjunctive treatment that helps to reduce substance use and associated psychiatric symptoms, and increase optimism and substance-use related locus of control (Monti, 2007).

Designing effective preventative methods requires early onset drug use research, increasing adolescent education and early identification of comorbid conditions and characteristic behavioural problems such as impulsivity and emotional dysregulation (Yucel & Lubman, 2007).

Questions to make you think

1. Can you define motivational toxicity?
2. What is the difference between appetitive and aversive motivation?
3. Do you consider addiction a disease? Why or why not?
4. Can you describe the reward system?
5. How is liking different to wanting?
6. What processes does dopamine facilitate?
7. Can you define synaptic plasticity and long term potentiation?
8. What methods would you use to treat an addiction?

Summary

Motivational toxicity is the potent maladaptive drive that directs an addict to acquire and use their drug (Esch & Stefano, 2004). Compulsive addiction behaviours are the direct result of neural damage that is caused by substances of abuse (Adinoff, 2004). Addictive drugs directly and intensely stimulate the brain reward system and dopaminergic pathways causing physical damage and disruption to learning, memory, motivation, reward and cognitive control circuits (Bakalar, 2004). The reward system is a collection of neural structures originating in the midbrain and incorporating the frontal lobes and limbic system,. The system is innervated and interconnected by the mesolimbic dopamine pathway (Volkow, Fowler & Wang, 2003). Stimulating the dopaminergic neurons triggers dopamine release which produces feelings of pleasure, codes motivational saliency and enhances learning (Volkow & Li, 2004). Continuous drug stimulation of the pleasure pathways incurs phasic bursts of dopamine that lead to neuronal damage and eventually result in chronically reduced levels of dopamine and dopaminergic receptors (Fortuna & Smelson, 2008). Neural sensitisation, synaptic plasticity and long-term potentiation are suggested mechanisms for drug-induced neural disruption (Kauer & Malenka, 2007). Addiction theories have moved away from being predominantly withdrawal-avoidance based towards chronic disease and opponent-process models. Opponent-process theories suggest an anti-reward system attempts to counter-balance the drug effect and restabilise homeostasis after drug use (Ahmed & Koob, 2005). Not all researchers agree. Foddy and Savulescu (2007) claim that addiction is merely extreme pleasure-seeking using socially unacceptable behaviours. Common neural pathways, structures and processes have been identified in substance abuse disorders and impulse control disorders indicating shared foundations (Schmitz, 2005). However, not all people that experiment with illicit drugs will become addicted. Vulnerability is influenced by genetics, age, stress, mental health, social status and environmental factors (Volkow & Li, 2004). Addiction and motivational toxicity can be overcome with time, support, understanding and multi-modal treatment strategies (Hyman, 2007). Combining pharmacological, behavioural, cognitive and adjunctive therapies enhances recovery by targeting multiple levels of neural dysfunction, cognitive control and mental and physical health and well-being (Handley, 2009). Like other chronic conditions, drug addiction has known risk factors, a typical course and outcome, equivalent relapse and recovery rates, physiological underpinnings and a genetic influence. Treating drug addiction as a disease reduces the associated stigma, shame and moral devaluation, and offers families and individuals hope and understanding for recovery (Volkow & Li, 2004).

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Glossary

Addiction - Chronic brain disease characterised by compulsive behaviour and poor inhibition.

• Amygdala - Fear conditioning area of the limbic system.
• Anterior cingulate - Performance monitoring and behaviour control.
• Appetitive motivation - Drive that directs us towards pleasurable events.
• Aversive motivation - Drive that steers us away from aversive events.
• Drapetomania - Nineteenth century mental disorder that caused slaves to flee captivity, now considered a pseudoscience.
• Dopamine - Neurotransmitter critical to mood, reward, motivation and learning
• Dopaminergic receptor - Five subtypes of D1 and D2 receptors take up dopamine at the synapse.
• Dorsolateral prefrontal cortex - Working memory.
• Frontal lobe - Executive functions.
• Hippocampus - Memory, implicated in Alzheimers disease.
• Homeostasis - The optimal, stable, internal condition.
• Liking - Pleasurable feeling in response to attaining a desired reward.
• Long term potentiation - A long lasting increase in synaptic transmission.
• Motivational toxicity - Strong, maladaptive drive to procure drugs in addiction.
• Nucleus accumbens - Pleasure centre and motivational saliency.
• Opponent processes - Concept of paired processes in biological systems, b-process counter-balances a-process to maintain homeostasis.
• Orbitofrontal cortex - Compares alternatives to determine behaviour.
• Pleasure pathways - Tracts of dopamine axons that innervate reward system structures.
• Prefrontal cortex - Conscious goals and decision making.
• Reward deficiency syndrome - Reduced amount of dopamine and D2 dopamine receptors in the reward circuits.
• Reward system - motivational brain system that guides behaviours.
• Saliency - Stands out in comparison to alternatives, grabs our attention.
• Synapse - Tiny junction where messages pass between neurons.
• Synaptic plasticity - Ability of a synapse to change in strength.
• Ventral tegmental area - Start of the pleasure pathways, processes reward-driven behaviours.
• Wanting - Motivational drive to procur a desired reward.

See also

• Addiction (Textbook chapter)
• Gambling (Textbook chapter)

References

Adinoff, B. (2004). Neurobiologic processes in drug reward and addiction. Harvard Review of Psychiatry, 12, 305-317. doi:10.1080/10673220490910844

Ahmed, S. H., & Koob, G. F. (2005). Transition to drug addiction: A negative reinforcement model based on allostatic decrease in reward function. Psychopharmacology, 180, 473-490. doi:10.1007/s00213-005-2180-z

Bakalar, J. B. (2004). The addicted brain. Harvard Mental Health Letter, 21, 1-4. Retrieved from http://web.ebscohost.com.ezproxy1.canberra.edu.au

Esch, T., & Stefano, G. G. (2004). The neurobiology of pleasure, reward processes, addiction and their health implications. Neuroendocrinology Letters, 25, 235-251.

Foddy, B., & Savulescu, J. (2007). Addiction is not an affliction: addictive desires are merely pleasure-oriented desires. The American Journal of Bioethics, 7, 29-32. Retrieved from http://web.ebscohost.com.ezproxy1.canberra.edu.au

Fortuna, J. L., & Smelson, D. A. (2008). The phenomenon of drug craving. Journal of Psychoactive Drugs, 40, 255-261. Retrieved from http://web.ebscohost.com.ezproxy1.canberra.edu.au

Gardini, S., Caffarra, P., & Venneri, A. (2009). Decreased drug-cue-induced attentional bias in individuals with treated and untreated drug dependence. Acta Neuropsychiatrica, 21, 179-185. doi:10.1111/j.1601-5215.2009.00389.x

Handley, A. (2009). Straight to the point. Nursing Standard, 23, 23-24. Retrieved from http://web.ebscohost.com.ezproxy1.canberra.edu.au

Hyman, S. E. (2007). The neurobiology of addiction: Implications for voluntary control of behaviour. The American Journal of Bioethics, 7, 8-11. doi:10.1080/15265160601063969

Kauer, J. A., & Malenka, R. C. (2007) Synaptic plasticity and addiction. Nature Reviews Neuroscience, 8, 844-858. doi:10.1038/nrn2234

Koob, G. F., & Le Moal, M. (2005). Plasticity of reward neurocircuitry and the dark side of drug addiction. Nature Neuroscience, 8, 1442-1444. Retrieved from http://web.ebscohost.com.ezproxy1.canberra.edu.au

Monti, P. M. (2007). Mindfulness meditation promising as SUD treatment. The Brown University Digest of Addiction Theory and Application, 2-3. Retrieved from http://web.ebscohost.com.ezproxy1.canberra.edu.au

Niehaus, J. L., Cruz-Bermudez, N. D., & Kauer, J. A. (2009). Plasticity of addiction: A mesolimbic dopamine short-circuit? The American Journal on Addictions, 18, 259-271. doi:10.1080/10550490902925946

Robinson, T. E., & Berridge, K. C. (2003). Addiction. Annual Review of Psychology, 54, 25-53. doi:10.1146/annurev.psych.54.101601.145237

Schmitz, J. M. (2005). The interface between impulse-control disorders and addictions: Are pleasure pathway responses shared neurobiological substrates. Sexual Addiction & Compulsivity, 12, 149-168. doi:10.1080/10720160500203641

Volkow, N. D., Fowler, J. S., Wang, G. J., & Swanson, J. M. (2004). Dopamine in drug abuse and addiction: results from imaging studies and treatment implications. Molecular Psychiatry, 9, 557-569. doi:10.1038/sj.mp.4001507

Volkow, N. D., Fowler, J. S., & Wang, G. (2003). The addicted human brain: insights from imaging studies. The Journal of Clinical Investigation, 111, 1444-1452. doi:10.1172/JCI200318533

Volkow, N. D., & Li, T. (2004). Drug addiction: the neurobiology of behaviour gone awry. Nature Reviews, 5, 963-971. Retrieved from http://web.ebscohost.com.ezproxy1.canberra.edu.au

Yucel, M., & Lubman, D. I. (2007). Neurocognitive and neuroimaging evidence of behavioural dysregulation in human drug addiction: implications for diagnosis, treatment and prevention. Drug and Alcohol Review, 26, 33-39. doi:10.1080/09595230601036978

Zhang, J., Berridge, K. C., Tindell, A. J., Smith, K. S., & Aldridge, J. W. (2009). A neural computational model of incentive salience. Computational Biology, 5, 1-13. doi:10.1371/journal.pcbi.1000437

External links

• Alcoholics Anonymous Australia - http://www.aa.org.au/
• Alcohol and Drug Foundation ACT - http://www.adfact.org/index.htm
• Centre for Addiction and Mental Health (CAMH) - http://www.camh.net/
• Directions ACT - http://www.directionsact.com/
• Narconon Australia - http://www.getoffdrugs.com.au/Addiction2.htm
• National Institute on Alcohol Abuse and Alcoholism (NIAAA) - http://www.niaaa.nih.gov/
• Salvation Army - http://www.salvos.org.au/need-help/drugs-and-alcohol/
• The Sober Recovery Community - http://www.soberrecovery.com/forums/
• Wildmind Buddhist Meditation - http://www.wildmind.org/