They salience. This can provide evidence as to

They also suggested that dopamine usually functions to attribute incentive salience to stimuli associated with rewards such as food and sex, and triggers reward desire/wanting. Drugs overtake this “wanting” response and the these ‘neuroadaptations’ make these brain circuits hypersensitive (‘sensitized’). They suggest this results in pathological levels of incentive salience (‘wanting) being attributed to drugs and drug-associated triggers following frequent drug exposure. The dopamine system becomes hyper-responsive and drug cues become hyper-salient(FIND EVIDENCE). Meaning that drug cues/triggers are virtually impossible for addicts to overlook, and when encountered they can lead to intense drug cravings. This sensitized cue-triggered pathological incentive motivation could last for years after the addict recovers from the chemical addiction, and long after drug withdrawal has ceased. Sensitized incentive salience could be shown in behaviour via either implicit (unconscious wanting) or explicit (conscious cravings) processes, this can be manifested in deifferent ways according to individual cases. This finding may shine light on why some former addicts have the tendency to relapse to drug use after recovery, sometimes even after many years of abstinence. This doesn’t necessarily mean that the addicts like the drugs but rather they have a pathological ‘wanting’ for drugs, this was highlighted when Berridge & Robinsons (1998) found that dopamine is a distinct component of incentive salience (desire and wanting) but it is not necessary for liking what is wanted, and for acquisitions of new ‘likes’ and ‘dislikes’. This poses a interesting view on addiction suggesting that addicts may not necessarily like the drugs but rather have a sensitized ‘wanting’ of said drugs, which can be perceived as a need. However the role of learning is quite an important one, as the learning of the triggers/ cues, we can argue, is what leads to the relapse and it specifies the target of desire. Associative learning processes can control the way in which neural sensitization is demonstrated in behaviour in particular circumstances, as it directs the attribution of incentive salience. This can provide evidence as to why behavioural sensitisation usually occurs in contexts which have been previously associated with drug taking experiences (Anagnostaras & Robinsons 1996, Robinsons et al. 1998). However learning alone cannot be made responsible for the one’s pathological motivation for drugs. Dalley and Everitt (2009) conducted a review of existing literarure on dopamine receptors and their involvement in memory, learning and drug reward system, suggesting an interesting complementary argument to berridge and robinson’s original theory. They argued that addiction develops due to a series of learning transitions, from goal-oriented or reward seeking behaviour eventually leading to a pathological stimulus-response habbits it can then be supposed that by its own nature, the S-R habbits then confer compulsivity to drug-seeking behaviour (Tiffany 1990; Berke & Hyman 2000; Everitt et al. 2001; Hyman et al. 2006). This means that drug-seeking behaviour are automatically produced and sustained by the reward associated with the cues. This view compliments the original theory as it supports its view of addiction stemming from a pathological wanting of drugs, however poses an interesting perspective on the role of dopamine suggesting that it aids not just incentive salience but also the learning transitions that lead one’s motivation of drug-seeking behaviour. This also suggests that the drug intakes inhibit inputs from the pre frontal cortex, responsible for between many things, decision making, as well as inputs from the orbitofrontal cortex and anterior cingulate cortex. This suggest that drug-seeking behaviour may takes not account of consequences, which explains why addicts continue to seek drugs despite adverse consequences it may cause to their lives.

However, it is commonly doubted that addictive behaviour can be cause just by learning itself. We perform tasks every day that are very well learned such as brushing teeth, tying shoe laces or driving but we’re not necessarily addicted to those behaviours, even after carrying these out thousands of times. Therefore, it can be assumed that for a behaviour to be become compulsive a motivational component must exist to explain why addicts sometimes can adapt new behavioural patterns (act out of character) in order to obtain the drug. Such fixated and adaptable behaviour must derive from a pathological motivation (incentive salience). The idea of automatic S-R behaviour would suggest that when the drug is not available, addicts would still carry out the same behavioural patterns, as it suggested to be an involuntary response. In reality, we see that addicts have different methods of acquiring the desired drug, even going to extreme measure such as scamming and stealing. However these S-R habit can be more prominent once addicts have access to the drug and subsequently automatized behaviour of drug consumption (tiffany, 1990). It has been found in animal studies that treatment with drugs can facilitate the development of S-R habits (miles et al 2003, nelson and killcross, 2006). Animal studies have provided some insight on how drugs encourage the learning od S-R habits and drug consumption behaviour in addicts.

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One of the main aspects of this theory is that sensitisation is caused by repeated drug use, which changes neural pathways in the VTA-nucleus accumbens pathways. This creates a strong and even pathological incentive salience of drug associated cues, leading to a pathological ‘wanting’ that drives drug seeking behaviour. It is also thought to cause sensitization of locomotor activity, however locomotor is an example of many different psychomotor effects of drug use that undergo sensitization, and most of these are dissociable (Robinson & Becker 19986). The increasing response to drug effects can be expressed in different ways i.e. behavioural (increased eye blink responses in amphetamine users, Strakowski, Saz, Setters & Keck, 1996); Neurological ( L-DOPA induced spiked levels of dopamine in the ventrial striatum of Parkinson’s patients who compulsively take medication, Evans et al., 2006);  subjective to individuals ( changing vocabulary of drug craving throughout the course of abuse, Everitt & Robbins, 2005).

 In the context of addiction, sensitization refers to an increase the effect of the drug caused by repeated exposure to said drug (Robinson & Berridge, 2008). Psychomotor activation can reflect the involvement of the brain incentive systems, which includes the mesotelencephalic dopamine systems (Wise & Bozarth 1987). This can be used as indirect evidence of hypersensitivity in relevant motivation circuitry which contributes most to addictive wanting of drugs (Robinson & Berridge 2008). It is quite interesting to note that drug abuse sensitizes only motivational neural processes, but not systems that generate subjectively enjoyable effects of the drugs, this can result in a dissociation of these processes over time (Robinson & Berridge, 1993). This means that repeated drug use doesn’t change how much pleasure one derives from the experience. The neural systems that mediate craving do however appear to be affected by this repeated administration, as the incentive value of these drugs become sensitized over continued dosings as the drug   attributes the associated stimuli with salience. Stimuli acquire this salience by being associated with reward and conditioned-stimuli that have been imbedded with incentive salience and have three fundamental features (Berridge 2001; Cardinal et al. 2002): (i) they can elicit approach towards them acting as ‘motivational magnets'( measure by Pavlovian conditioned approach behaviour); (ii) they can encourage on going actions by provoking cue-triggered wanting for the associated reward ( measure by Pavlovian instrumental transfer) and (iii) they can act as reinforces on its own, reinforcing the acquiring of new responses ( measurable by conditioned reinforcement). We can say that the most direct evident for incentive sensitization comes from studies showing past drug treatment that produces psychomotor sensitisation, facilitates all features of incentive stimuli: Pavlovian conditioned approach behaviour (Harmer & Phillips 1998); Pavlovian instrumental transfer (Wyvel & Berridge 2001); and conditioned reinforcement (taylor & Horger 1999; Di Ciano 2007). However it is important to acknowledge that in most studies, natural rewards such as food or water, and not drugs were used to pair conditioned stimuli with incentive motivational properties. Although the same neuroanatomical system are being used, these studies will not show how these may be affected by the neural changes cause by drugs use. Nevertheless Di Ciano(2007) found that cocaine sensitisation facilitated the conditioned reinforcement effects of a cocaine-associated stimulus, concordant with incentive sensitisation.

However it is important to question how incentive salience happens and if it happens to everyone in the same manner. Robbinson & Berridge (2003) suggest that there is a big  individual variation in susceptibility  to sensitisation,  where some individual show rapid sensitisation to even one dose of the drug and other that show high tolerance sensitizing very little, if at to the drug. They suggest this could be due to a number of factors such as genes, hormones levels and experiential factors but also that it is largely unknown how these individual differences occur.

There has however, been some insight on how incentive sensitisation occurs in the brain. Studies have shown that sensitisation increases neural activations in the brain’s systems that are responsible for incentive value given to a reward stimulus (Tindel et al. 2005; Boileau et al. 2006; Evans et a; 2006). Amphetamine sensitisation in rats increases specific firing patterns of neurons in the mesolimbic structures that code the incentive salience of a reward conditioned stimuli (Tindel et al. 2005). It has also been shown that in humans, repeated amphetamine treatment sensitises amphetamine-stimulated dopamine release in the ventral striatum even some time after the last drug treatment (Boileua et al. 2005). Sensitisation of dopamine release has also been found in patients with dopamine dysregulation syndrome (Evans et al. 2006).

Drug use and abuse is responsible for many changes in the brain (its structures and chemistry), even though there isn’t much evidence that indicates which of these changes exactly is responsible for the psychological change of incentive sensitisation, evidence has indeed suggested that repeated drug use modifies relevant behaviours, psychological processes and brain structures in a way that supports the thesis of the original theory.

As mentioned earlier, drug effects can be expressed in different way, and evidence of some ways in which humans showed incentive sensitisation that could not be explained by other theories of drug addiction. However, there are many studies which shows conflicting evidence towards the idea of dopamine changes in the brain of addicts. Even though some finding need to be carefully interpreted as variable interact in complex ways when determining whether sensitisation is expressed in a particular circumstance. It has been reported that recovered cocaine addicts in reality show a decrease in produced dopamine release rather than a sensitised increase as suggested above (Volkow et al. 1997; Martinez et al 2007).

Animal studies have shown that expression of sensitisation is significantly moderated by the context in which drugs exposure occurs (Robinson et al. 1998), humans are possibly even more sensitive to psychological contexts (Leyton 2007). This was evidenced when studies found that sensitisation and increased dopamine release usually are not expressed if animals are tested in a context which is not directly associated with drugs (Fontana et al 1993; Duvauchelle et al 2000). From these studies one could argue that drug addicts should not experience or display behavioural sensitisation or sensitised dopamine release if the environment in which they’re given the drug is dramatically different form the ones previously experienced by the addict. This shows that in order for studies to have relevant ecological validity, experimental contexts should be taken into high importance for the results to be considered to reflects the experience of addicts in reality.

In conclusion, Addiction is very complex disorder which has been vastly studied but it is still not completely understood, or at least not all its components are. Addiction involves drug induced changes in behaviour and neuroanatomical function. Robinson & Berridge (2003) suggested that ‘loss of inhibitory control over behaviour and poor judgement, combined with sensitisation of addicts’ motivational impulses to obtain and take drugs, makes for a potentially disastrous combination. Even though vastly studied, and a significant amount of evidence shown in support of the theory’s idea that addiction is a disorder of aberrant incentive motivation due to drug-induced sensitization of neural systems that attribute salience to a particular stimuli, they still don’t answer perhaps the most important question in addiction, which is why even though one third of adults (16-59) have tried a potentially addictive drug in their lifetime, on a relatively small percentage of those become addicted. However their theory proposes a well evidenced explanation of processes that may lead to addictive behavioural patterns, highlighting that incentive salience is distinct from pleasure or liking processes and sensitisation given a pathological drug wanting that can endure a lifetime (Robinson & Berridge 2003), this has potentially changed some perspectives that addiction is a condition of the weak willed but rather a disease of the brain.  


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