Previous literature by Robinson and Berridge, (1993) posits that these neuroadaptation changes in the brain can help explain the transition from a more casual drug use to more of a wanting drug state. However, this fails to explain the reasoning behind why behavioural sensitization is also reported through persistent drug use. The basis of behavioural sensitization is dependent upon the changes within the nucleus accumbens produced by persistent drug intake and the sensitization of the neurotransmitter dopamine (Kalivas and Stewart, 1991). Evidence to support behavioural sensitization and relational changes in the brain was found by Ferrario et al., (2005). Rats that were given cocaine over a progressive period of weeks were tested for sensitization, those that had consecutive access to cocaine showed more robust psychomotor sensitization than those who were received less access (Ferrario, et al., 2005). In contrast, Ben-Shahar, Ahmed, Koob, Ettenberg, (2004) found that extended access to cocaine results in a loss of sensitization. There is a clear discrepancy in findings between the two studies and therefore subsequent methodological issues can be determined. Ferrario et al., (2005) concluded that previous literature on behavioural sensitization failed to distinguish and measure the more complex qualitative changes. By failing to acknowledge the more complex qualitative changes including the context of drug inhibition renders the latter research careless in the overall conclusion and the critique thus can be nulled.
Evidence for the increased behavioural sensitization effects in humans was concluded by Strakowski et al., (1996). Through repeated amphetamine usage, they found that activity/energy and eye blink rate also increased, furthermore, findings were consistent with the hypothesis that ratings of drug liking did not increase through repeated drug use, therefore, again finding flaws in the hedonic reinforcement model (Strakowski et al., 1996). Whilst this does provide evidence for significant behavioural sensitization in humans who take drugs, the evidence has yet to be completely grounded with precise consistencies. Research by Rothman et al., (1994) failed to find evidence for increased psychomotor activities in humans. However, these findings were dismissed by the researcher in a later review as it was found that the studies participants had prior extensive cocaine exposure which would seem to suggest that the low dosage study would have no effect, therefore the research fails to be credited (Gorelick and Rothman, 1997). The difference in results could be further explained by the role of individual differences, as the results concluded different levels of susceptibility. From the literature, it is evident that individual differences play a key role in the susceptibility and thus sensitization to drug addiction. Robinson, (1998) suggested that genetic variation accountability may explain individual differences, as it has been reported that rats with a marked strain difference in genes reported being more susceptible to sensitization. Much of the research into psychomotor sensitization and self- administration has looked into the wrong behaviours, whereby researchers have mostly generalised behavioural sensitization into just locomotor activity. Not only does this generalise the behaviour but subsequently fails to measure the more intense psychomotor sensitization (Robinson and Berridge, 2008). As a result, the finding are impossible to interpret as they fail to relate to the correct behavioural measure and so the findings are unrelated to the incentive sensitization theory. In addition to this, Volkow, Fowler and Wang, (2004) further critiqued sensitization in humans as cocaine addicts have been shown to have a reduced count of dopamine D2 receptors, which may suggest that the state is more of a hyperdopaminergic state rather than a fully sensitized one.
It is now clear that to understand incentive sensitization, one must understand the role of incentive motivation and the reason people seek and intake drugs. The role of the mesocorticolimbic dopamine system is primarily focussed on the reinforcement properties of certain stimulant drugs such as cocaine and amphetamines (Taylor and Robbins, 1984). These drugs increase dopamine within the mesolimbic dopamine system, through reinforcing a sense of euphoria. The increased motivation behind drug addiction and the role of dopamine has been found in numerous studies whereby after administration of the drug, there has been an increase in dopamine in the nucleus accumbens (Mocsary and Bradberry, 1996). Lingford-Hughes, (2005) alternatively concluded that dopamine is only released when related to a drug-related cue and not due to the reward process. Additionally, more recent research by Witteman, et al., (2015) further evidenced that drug addiction becomes a pathological incentive when the mesolimbic system becomes sensitized and hyper-reactive to the incentive salience of cues. Through up to date research, the findings have found a cause and effect relationship between the role of cues and sensitization (Witteman et al., 2015). Despite this strong relationship, Lingford- Hughes, (2005) raised the issue of interpreting such studies that look into dopamine and the role of the nucleus accumbens, as the studies have only looked into the role of food and so fail to be extrapolated to drug-behaviours.
Sensitization is not something that happens through repeated exposure; instead it has been found that the cues in which the individual inhibits the drug play a crucial role in the overall modulation of sensitization (Robinson, Browman, Crombag and Badiani, 1998). Anagnostaras and Robinson, (1996) investigated the phenomenon known as context-specific sensitization which suggests that animals that receive drug injections in a unique test environment compared to those in a different environment usually express sensitization. Context-specific sensitization has been directly evidenced by research that has focussed on prior exposure to addictive drugs and the link to a later acquisition. Deroche, Le Moal and Piazza, (1999) reported that those that have previously self- administered cocaine encourages the motivation to seek cocaine in a runway apparatus. This study provides strong evidence to support the relationship between the drug-seeking behaviour and drug sensitization, as it demonstrates that upon recollection of previous drug-seeking behaviour it elicits an accompanied locomotor response. On the contrary, if this was the case for all drug addicts then it can be assumed that neural sensitization would be peaked when drugs have been taken before. Although an association was suggested by Deroche et al., (1999), there is evidence that neural sensitization can occur even if they do not express behavioural sensitization. Henry and White, (1991), concluded that neural sensitization was apparent even in tissues of anaesthetised animals, not only does this prove the existing studies to be incorrect also infers that neural sensitization can happen well before the contextual stimuli are present.
To understand the concept of drug-seeking behaviour and drug sensitization, it is crucial to understand the way researchers interpret “wanting vs liking”. The phrase “wanting vs liking” has been widely researched, with findings concluding to different biological substrates. Koob and LeMoal, (1997) found the hedonic agent of drugs was not primarily linked to an increase but in fact, drug-addicts take more drugs to restore the dopamine to a normal level through “hedonic homeostasis”. However, in a separate account by the same researchers they found contrasting evidence as dopamine was found to be linked to the reinforcing agent of drug addiction, as well as being linked to an increase in the drugs positive effects (Koob and LeMoal, 1997). Inconsistencies are clearly apparent in terms of studies that look into “wanting vs liking”, nevertheless the overarching argument shares a similar viewpoint whereby the hedonic state is involved in drug-seeking and drug- taking behaviours. This viewpoint clearly differs from the incentive sensitization theory as it states that the positive effects of drug addiction are associated with “liking” which from previous research is understood to not be a component of the drug reward process. From the evidence, there is a separate component of the drug reward system as noted by the “wanting” aspect, which is named the incentive salience.
The impulsive behaviour that underlines the pathological sense of wanting drugs can also be extrapolated to similar impulsivities in those that have been diagnosed with Attention Deficit/Hyperactivity Disorder (ADHD). Through studying a reward processing task, those with ADHD have been found to have a positive relationship between impulsivity- related measures and brain activity within the ventral striatum (Kirsch et al., 2003). The direct connection between ADHD and substance use disorders has been reported by Biederman, Newcorn and Sprich, (1991) however, the connection is one that should be interpreted with caution as only 30% have the diagnosis of ADHD through to adulthood therefore the results are difficult to generalise. Whilst previous research was crucial in advancing research into the connection between ADHD and substance abuse disorders, more recently it was reported that this prior research often identified ADHD as “hyperactive” (Biederman et al., 1991). Therefore, the established link that was made was not sound which makes it difficult to compare to more recent findings in relation to ADHD and subsequently fails to be valid in the comparison to drug addiction and incentive sensitization theory (Disney, Elkins, McGue and Lacono, 1999).
To some extent, the overarching conclusion is that according to the incentive sensitization theory addictive drugs are involved in the psychological process of incentive salience attribution (“wanting”). From the given evidence, the development of addiction is characterised by the detachment between the wanting value of drugs and the subjective pleasurable effects. To a state that is shown by cravings which is not associated with the liking quality which was previously thought, although the validity of these studies can be questioned. Furthermore, findings have concluded that environmental stimuli may play an important role into inducing cravings, through having a heightened incentive salience towards the stimuli as found by Deroche et al., (1999). Due to the neurochemical complexities of substance abuse on humans, these studies highlight the need for additional research into the neuropharmacology of the incentive process. Further research should address chronic drug alterations in humans and the subsequent relevance to wanting and craving. Whilst there has been partial evidence of the motivational process, often the studies are cluttered with inconsistencies.