Saturday, May 26, 2012

       In their article "Addiction," Robinson and Berridge (2003) explore the phenomenon of drug addiction from the perspective of seeking to answer the question of why it is that while many people experiment with drugs, only some become "addicts" (where "becoming an addict" is operationalized as developing a pattern of compulsive drug-seeking and self-administration which often comes at the expense of other activities). In particular, the seek to discover first, what it is about certain individuals which makes them particularly susceptible to the development of such habits, and second, what it is that makes it so difficult for these individuals to overcome their drug-taking habits once they are established.

       In attempting to answer these question, Robinson and Berridge (2003) begin by suggesting that the potent and addictive effects of drugs rely upon their ability to "hijack" the brain systems normally involved in the processing of learning about rewards and in enabling organisms to attribute motivational value to stimuli important to survival (Kelley and Berridge, 2002). They also argue that successive drug administrations can result in changes in these neural systems which can lead the drug-taking behavior becoming increasingly compulsory. Among the neural systems involved in these processes, they include those of the "... dopamine projections from the ventral tegmental area and the substantia nigra to the nucleus accumbens (NAcc) and striatum, as well as glutamate inputs from the prefrontal cortex, amygdala, and hippocampus and other key parts of the system to which [they] refer to as NAcc-related circuitry," (Robbinson and Berridge, 2003, p. 26).  According to Robinson and Berridge (2003), the connection between these systems and the process of addiction is rooted in first, the fact that drugs are able to engage these neural systems to a greater extent and more powerfully than can natural rewards, and second, the fact that over successive administrations, drugs can actually change the way in which these systems operate, in such a way as to make drug-taking behavior increasingly compulsory, (Robinson and Berridge, 1993, 2000).

Robinson and Berridge (2003) go on to present several possible accounts for what these drug-induced changes in psychological functioning might be, and of how they might come about as a result of drug-induced changes in brain circuitry.

         One of these involves the Opponent Processes Theory of Motivation (Solomon & Corbit 1973), in which a compensatory b-process (a process designed to return the system back to a state of homeostasis following a drug-induced disruption), which originally comes on only as a gradual decay in the intense reward state induced by drug self-administration, begins, over time, to come on sooner and be stronger when it does so. Over time, the b-process begins to come on earlier and to be stronger when it does so. This phenomenon of the b-process becoming stronger eventually allows it to compete successfully with the a-process (the set of physiological processes triggered by the ingestion of the drugs themselves- i.e., the rapid heart rate and feelings of euphoria which follow the ingestion of cocaine, for example). The result of this "competition" between the stimulus-bound, drug-induced a-process and the compensatory b-process is that the effects of the a-process come to be greatly attenuated (i.e., the addict obtains progressively less of the desired effects from each successive drug self-administration). Furthermore, the now-stronger b-process causes progressively more severe and debilitating withdrawal symptoms (the withdrawal symptoms come on as a result of the fact that, over time, the b-process becomes able to not only to counteract the effects of the a-process, but also to outlast its effects). Crucially, only the effects of the b-process change over time. The effects of the stimulus-dependent a-process neither increase not decrease over time; rather, they become increasinly attenuated solely as a result of the increasing ability of the b-process to counteract  them. The withdrawal symptoms tend to be particularly severe when the addict is exposed to the types of environments and other conditioned stimuli in the presence of which they would usually have taken the drugs, but is deprived of the opportunity to self-adminster the drugs (Siegel et al. 2000). At the same time, the increasing attenuation of the a-process results in the addict having to take ever-increasing amounts of the drug in order to obtain the same degree of desired effects as they had been able to before (the phenomenon of the buildup of "drug tolerance"). The overall result of these phenomena is the seemingly-paradoxical phenomenon of addicts continuously self-administering drugs, to the detriment of their health and personal well-being, not for the purpose of attaining any sort of pleasurable effects, but rather solely with the goal of avoiding the debilitating withdrawal symptoms which are certain to ensue should they cease to do so! In this way, as Robinson and Berridge argue, drug taking can become truly compulsory (Robinson and Berridge, 2003). Interestingly, according to Robinson and Berridge (2003), "Once the b-process is strengthened, even a small drug dose can instate it and thereby trigger withdrawal again. Conversely, prolonged absitnence from the drug would decay the b-process, and the ability to reactivate it would return back to normal. Once the b-process returns back to normal, the person would no longer be addicted," (Robinson and Berridge, 2003, p. 28). This presents a strong argument for treatment programs which emphasize total abstinence from alcohol. It also goes some distance in explaining the phenomenon of people who recently graduated from detoxification programs accidentally overdosing on their "one last time," intake of their drug of choice.

       In their explanation of how the Opponent Processes Theory of Motivation might work at the neural level,  Robinson and Berridge (2003) suggest that "... the positive a-process is caused by activation of mesolymbic dopamine projections to the nucleus accumbens and amygdala which in turn govern the reinforcing properties of drugs," (Robinson and Berridge, 2003, p.29) (Koob and Le Moal, 1997). Furthermore, they propose that the buildup of tolerance that comes as a result of repeated drug self-administrations comes as a consequence of a "... downregulation of in the mesolimbic dopamine system," (Robinson and Berridge, 2003, p. 29) which repeated drug self-administration causes. Furthermore, they note that sudden cessation of drug intake (i.e., as might come about when people quit "cold turkey"),  "... causes dopamine (and serotonin) levels to drop below normal levels... resulting in a dysphoric B-state of withdrawal," (Robinson and Berridge, 2003, p. 29). As if this were not enough, sudden cessation of drug self-administration apparently also causes the activation of "...additional compensatory b-processes via the hypothalamic-pituitary axis stress system, causing the release of corticotropin releasing factor (CRF) in the amygdala, as well as other stress responses," (Robinson and Berridge, 2003, p. 29) (Koob and Le Moal, 1997). As these researchers argue, such effects cause addicts to what has quickly become (as a result of these neurochemical changes) a negative emotional and motivational state. In order to escape the aversive nature of this state, addicts may attempt to "self-medicate" by resuming to take at least some amount of the drug to which they were previously addicted, rekindling their previous dependence upon it.

     Robinson and Berridge (2003) go on to offer several interesting criticisms of the Opponent Processes Theory of Motivation as applied toward explaining drug addiction. For one thing (they argue), withdrawal (induced by activation of the b-process, as noted above), may actually be a far less powerful motivator of drug-seeking behavior than either the pleasurable effects which come as a direct result of taking the drugs, or the effects of stress, (Stewart and Wise, 1992)  For example, Stewart and Wise (1992) performed a study involving rats and lever-pressing behavior as part of a study attempting to elucidate which factors might be responsible for stimulating relapse among rats which had previously been addicted to drugs (cocaine or heroin specifically) but who had since been deprived of the drugs for a sufficient amount of time to break their addiction. In that study, Stewart, Shaham, and other researchers measured the amount of lever-pressing which the rats were willing to perform under extinction conditions in order to obtain the reward of an injection of the drug to which they had previously been addicted (Stewart and Wise, 1992). In that study, the researchers performed the manipulation of activating either the "a process," or the "b process." "Activating the 'a' process was done by giving the rats a small injection of the drug to which they had previously been addicted (Stewart and Wise 1992).To activate the b-process, the researchers administered a drug called naltrexone to the rats (Stewart and Wise, 1992). Naltrexone is an opioid antagonist, which means that it blocks the brain's naturally-occurring opioid receptors, with the result that when it is administered to individuals who are dependent on the opioid drug heroin, these individuals begin experiencing withdrawal symtoms (Stewart and Wise, 1992). For a heroin addict, the state which they would be experiencing following an adminstration of naltrexone is similar to the type of drug-withdrawal state which they would be experiencing if they suddenly ceased self-administering heroin (Stewart and Wise, 1992). As Robinson and Berridge (2003) explain, in the context of the Opponent Processes Theory of Motivation as applied to drug addiction, the artificial "withdrawal" state which an administration of naltrexone induces among former drug addicts is likely to be the most powerful force for getting them to relapse and resume self-administering heroin (this is the case because, according to the Opponent Processes Theory of Motivation's explanation of drug addiction and relapse, the withdrawal symptoms which individuals experience following their ceasing to self-administer a drug are the most powerful force toward motivating them to relapse in their drug-taking habits. Interestingly, however, the results of the Stewart and Wise (2003) experiment would suggest that, actually, both the administration of a small amount of the drug of choice, or exposure to a stressor are actually much more powerful means by which to induce a relapse in drug-seeking behavior, than the naltroxene-induced experience of withdrawal symptoms! (Stewart and Wise 1992). In other words, activation of the A process (as operationalized by exposing the rats to a small amount of the drug to which they had previously been addicted), is actually much more powerful than activation of B-process withdrawal symptoms. This would imply that there must be another force at work, aside from the experience of the withdrawal symptoms alone, which would be motivating individuals to continue self-administering the drugs.

As Robinson and Berridge (2003) also note, another problem which the Opponent Processes Thoery of Motivation has difficulty explaining is that of the unfortunate case in which individuals who were previously addicted to drugs, but who have since been abstinent for a significant period of time suddenly begin self-administering drugs, seemingly of their own volition. This especially seems to be the case when one notes that, by this time, the b-process (which will have been causing negative withdrawal symptoms) should have decayed away a long time ago- and, thus, according to the Opponent Processes Theory of Motivation, these individuals should no longer be addicted to drugs!
A possible explanation for this, as Domjan notes, is that of the drug cues surrounding the  self-administration of a drug (i.e., being in a particular location, being surrounded by particular friends, etc.) becoming, over many consecutive drug self-administrations, conditioned to act as conditioned stimuli predicting the impending self-administration of drugs. This also allows them to stimulate the initiation of compensatory b-processes, allowing an individual's body to compensate ahead of time for the dose of the drug which the conditioned cues predict. In accordance with this, studies with both humans and animals have shown that indeed,  such conditioned cues can, indeed, elicit withdrawal symptoms- at least in theory (Robinson and Berridge, 2003). The problem, however, is that they often do not; in fact, as Robinson and Berridge (2003) report, many former addicts report that they fail to do so! The fact that conditioned cues related to the self-administration of drugs do not appear powerful enough, on their own, to explain why relapse occurs has led researchers to search for different explanations.

       One such alternative, which Robinson and Berridge (2003) also present, is the possibility is that addiction to drugs comes as the result of learning processes. According to Robinson and Berridge (2003),this view came about as a result of a series of findings illustrating the role of neural circuitry, particularly that associated with the nucleus accumbens, in learning about rewards. Most hypotheses attempting to explain drug addiction through the role of learning processes argue that what occurrs specifically is "... drugs produce abnormally strong or aberrant associations involved in reward learning, more powerful than natural reward associations," (Robinson and Berridge, 2003). According to Robinson and Berridge (2003), the specific type of learning occuring in these types of situations could be of pretty much any kind.

The first possibility which Robinson and Berridge (2003) consider is that of drugs being involved in explicit learning, in which the association formed just happens to be abnormally strong. As Robinson and Berridge (2003) state, in such a case, individuals addicted to drugs will simply have formed an unusually strong action-outcome association between the action of self-administering drugs and the outcome of receiving them, as well as another, also unusually strong, association between perceiving certain environmental cues and the imepending delivery of drugs (Balleine and Dickinson, 1998).
       Evidence for the fact that humans establish Response-Outcome associations in this manner comes, for instance, from a study by Balleine and Dickinson (1998) establishing the existance of what they call a "contingency degradation effect"- the idea that reducing the contingency between an action and a desired outcome by adding extra instances of the delivery of the outcome (reinforcer) should (and does) reduce the number of instances of the action.
      Similarly, a study by Colwill and Resorla (1986) established the existance of what they called the "Reinforcer Devaluation Effect"- the idea of which is that, if a subject performs an action in order to get a desired effect, then reducing the desirability of the effect should lead to a decrease in the numnber of instances of the action preceding it (which is exactly what happens).
       The fact that Robinson and Berridge (2003) include animals, as well as people, in this category of individuals who can form such abnormally-strong associations
differentiates their work from, for example, that of Thorndike, who, as Domjan states, all throughout his studies involving animals learning to escape out of puzzle boxes and the like, remained convinced that the animals' escapes were merely the result of trial-and-error learning, rather than their becoming aware, in any kind of intelligent way, of their specific actions to escape the box and the ensueing positive outcome. Rather, he believed the animals initially made their escapes through trial-and-error, and then simply repeated the same type of escape over and over again.
        According to Robinson and Berridge (2003), "Abnormally strong explicit learning might distort declarative memories or expectations in two ways. (a) Conscious memories of the hedonic drug experience might be especially vivid and/or abnormally intrusive. (b) Drugs could exaggerate or distort declarative memories such that memory-based cognitive expectations about drugs become excessively optimistic," (Robinson and Berridge, 2003, p. 32). As Robinson and Berridge (2003) go on to explain, however, addicts' excessive drug-taking behaviors do not seem to be tied to distorted memories and excessively positive expectations about the consequences of doing so. Evidence for this comes through such sources as what the addicts themselves say about their lives and the amount of pleasure they expect from drug taking- which they themselves agree does not justify the excessive costs of  continuing to self-administer controlled substances (Robinson and Berridge, 2003).
These conclusions are also consistent with the results of the previously-mentioned study by Colwill & Rescorla (1986) establishing the existance of the reinforcer devaluation effect- the main conclusion of which was that devaluing the value of a desired reinforcer should lead a decrease in the occurences of actions being performed with the goal of obtaining that reinforcer. Since, as Robinson and Berridge (2003) claimed, most addicts do not have unrealistically positive expectations of regarding the types of outcomes which drug-seeking and drug-taking behaviors, it appears that the "outcome" in this situation (i.e., whatever sensations they obtain from taking the drugs that they do) has effectively been "devalued" for them. Given this, according to the results of the study by Colwell and Rescorla (1986), the drug-seeking behaviors should lessen or cease. Thus, it makes sense that Robinson and Berridge (2003) claim that drug addiction likely cannot be explained as being rooted in the formation of conscious, although overly-intense and overly-positive, response-outcome associations between the response of drug self-administrations and the outcome of drug-induced "highs."

In response to this, Robinson and Berridge (2003) came up with an alternative explanation for drug addiction- that of it being the result of the establishment of deeply-ingrained and implicit (rather than declarative) S-R (stimulus-response) or S-S (stimulus-stimulus) habit associations within an addict's mind. As Robinson and Berridge (2003) note, the most promising of these possibilities is that of addicts' drug habits progressing from what are initially readily-verbalized, declarative-memory associations between the action of taking a drug (a response) and the outcome of a "high,"which, based on previous congitive expectations has been labeled a "desirable outcome," to to more automatic, stimulus-response guided behavior. As habits, the latter associations occur without the involvement of conscious memory processes. Essentially, such hypotheses suggest, that, as was suggested in my Fundamentals of Learning class lecture, over-learned action patterns often become automatic habits. What Robinson and Berridge (2003) add to this is the idea that, over time, such habits can actually become compulsive.
This idea also makes sense in light of a study conducted by Adams (1982), which sought to investigate the question of why behavior is mediated by goal-directed, stimulus-response associations at some times, and by habitual, stimulus-response assocations at other times. In that study, rats were initially trained to press a lever (make a response) in order to obtain the reward of one sucrose pellet (an outcome/reinforcer) (Adams 1982). Initially, the schedule of reinforcement in this study was one of "continuous reinforcement," or a "fixed response or Fr1 schedule"- that is, the rats were rewarded with a sucrose pellet for every lever press they made (Adams 1982). The rats were then divided into two groups: one group received 100 trials of training, while another group received 500 trials of training (Adams 1982). Then, the rats in each of these two groups were further divided up into two groups (i.e., the rats in the "500 trial group" were divided into two groups, as were the rats in the "100 trial group")(Adams 1982). For one of the two groups of rats in each of the trail conditions (i.e., the 500-trial group, and the 100-trial group, respectively), the sucrose-pellet outcome was then devalued though pairing the administration of the sucrose-pellet outcome with the administration of an aversive lithium chloride stimulus (Adams 1982). For the other half of the rats in each number-of-tirials condition, the stimulus was not devalued (i.e., the sucrose pellets were still delivered normally(Adams 1982).Then, both groups of rats were tested under extinction conditions in order to see how many lever pressess they would make (Adams 1982). Fascinatingly, for the rats in the 100-trial group, the lever-pressing behavior remained goal-directed; that is, the rats would only press the lever if doing so allowed them to attain a desired outcome (that of being rewarded with regular sucrose pellets, which they saw as desirable, and not lithium-chloride sucrose pellets, which they saw as undesirable)(Adams 1982). Among the rats in the "500 trail group," however, all rats continued to press the lever, whether or not the sucrose-pellet outcome for doing so had been devalued! (Adams 1982). The results of this experiment by Adams (1982) lend further support to the idea that overtraining a behavior can cause it to transition from being a goal-directed behavior to becoming one that is habitual and mindlessly insensitive to the outcome it might result in.

However, in response to this, Robinson and Berridge (2003) offer the interesting criticism that while an overtrained behavior is indeed likely to become habitual, in their words, "... habits are not necessarily likely to become compulsive in any motivational sense, no matter how automatic they are,"(Robinson and Berridge, 2003, p. 33). To this ends, Robinson and Berridge (2003) present the examples of habits such as brushing one's teeth and the like and argue that, while these are habits and thus require minimal cognitive attention, they are not motivationally compulsive; people, with very few exceptions,  feel absolutely compelled to do them, even in the face of great sacrifice. Indeed, Robinson and Berridge (2003) argue that the sheer flexibility and the great range of behaviors in which addicts are willing to engage in order to obtain the drugs they crave, as well as the severely agitated and distressed manner in which many addicts react when they are suddenly deprived of a routine dose of the drugs to which they have become accustomed mandates a search for further explanations of drug addiction, beyond simply the formation of strong habits.

Similarly, while Robinson and Berridge (2003) briefly consider the possibility that perhaps drug addiction is mediated by a distorted form of learning in which an addict might form an unreasonably strong association between, for instance, a particular location and the environmental stimuli present there, and the administration of a drug, they ultimately dismiss the possibility that such actions might be able to elicit compulsive drug taking. Rather, they suggest that "... most S-S associations may actually remian normal in addicts. What is aberrant in aberrant in addiction is the response of brain motivational systems to Pavlovian-conditioned drug cues," (Robinson and Berridge, 2003, p. 35).

Thus, in sum, Robinson and Berridge (2003) argue that ".. learning and incentive motivational processes are joined in the transition to addiction," (Robinson and Berridge, 2003, p. 36). Their view that learning and motivational processes are joined in the development of addictions is evident in their own theory of drug addiction, which they refer to as that of "incentive sensitization," (Robinson and Berridge, 2003, p.36).

 According to the "incentive sensitization," (Robinson and Berridge, 2003, p. 36) view of addiction pioneered by Robinson and Berridge (2003), drug addiction involves "drug-cues triggering excessive incentive motivation for drugs, leading to compulsive drug seeking, drug taking, and relapse," (Robinson and Berridge, 2003, p. 35), (Robinson and Berridge, 1993, 2000).The main idea behind this theory is that the self-administration of drugs creates lasting changes in the brain's nucleus accumbens-related structures. The structures which drugs tend to modify are those which attribute salience (or lack thereof) to various environmental stimuli. As a consequence of these drug-induced modifications, areas in the nucleus accumbens become lastingly hypersenstive [or as Robinson and Berridge call it, "sensitized," (Robinson and Berridge, 2003, p. 36) to the effects of particular drugs and to the stimuli predicting their administration. These changes lead areas in the3 nucleus accumbens area of the brain to attribute excessively-high ratings of stimulus salience to drugs and cues related to their self-adminstration- a process which, on a psychological level, leads to extreme and abnormal desire to take drugs. As Robinson and Berridge (2003) go on to explain, such abnormal "wanting" "...can sometimes become manifest implicitly in drug-seeking behavior," (Robinson and Berridge, 2003, p. 36). The fact that this often happens at an implicit level means that individuals often remain unaware, on a conscious level, of the processes taking place [although Robinson and Berridge (2003) go on to explain that sometimes other cognitive processes can sometimes cause these representations which these processes involve to become consciously manifest, resulting in the affected individuals developing a very consciously-noticable desire to take drugs.
       Significantly, Robinson and Berridge (2003) draw a distinction between "the sensitized neural systems responsible for incentive salience," (Robinson and Berridge, 2003, p. 36)- in other words, those responsible for how much a particular drug might be "wanted"- and "the neural systems that mediate the hedonic effects of drugs, how much they are 'liked,'" (Robinson and Berridge, 2003, p. 36). They further suggest that these two processes are governed by different areas of the brain, and thus largely operate independently of each other.
       In defining "sensitization," Robinson and Berridge (2003), speak of it being largely the opposite of tolerance; that is, in sensitization, with each subsequent self-administration of a drug actually increases its effects. According to Robinson and Berridge (2003), there are two major classes of sensitization: psychomotor sensitization, and motivational sensitization. Both, however,are sensitive to changes in the neural structure of the nucleus accumbens- a process which they argue takes place when individuals repeatedly self-administer drugs. Interestingly, psychomotor sensitization, at least, is context-specific; for instance, rats which had been exposed to stimulants which resulted in their exhibiting symptoms of psychomotor sensitization only showed these symptoms when they were subsequently tested in an environment that contained many of the same cues as had been present when the drugs were orginally being administered to them (Robinson and Berridge, 2003).
       Interestingly, as Robinson and Berridge (2003) note, individuals can differ in their degree of susceptibility to sensitization- something which they argue can be helpful in unraveling the puzzle of why some individuals, but not others, become drug addicts. Furthermore, they note that "... once sensitized, most individuals show cross-sensitization, which means that sensitization to one drug can cause sensitized effects for other drugs as well," (Robinson and Berridge, 2003, p. 38).  Finally, Robinson and Berridge (2003) note that cross-sensitization can even occur between drugs and nondrug stress! Taken together, these factors begin to suggest how such factors as gateway drugs and exposure to stress may come into play in addiction.

In terms of the specific changes in the brain involved in sensitization, Robinson and Berridge (2003) argue that "sensitization-related changes have been described in many neurotransmitter systems that are integral to the function of NA-cc related circuits including serotonin, norepinephrine, acetylcholine, opioid and GABA systems," (Robbinson and Berridge, 2003, p. 38). Thus, the changes in the nucleus accumbens by sensitization appear to be quite widespread. Furthermore, drug-induced changes in the nucleus accumbens occasionally occur even at the length of neurons, with neurons in the nucleus accumbens and in the prefrontal cortex often showing "...changes in the lengths of dendrites and the extent to which dendrites are branched," (Robbinson and berridge, 2003, p. 38). Furthermore, "...changes can also occur in the density and types of dendritic spines, which are primary site of excitatory gluatamate synapses," (Robinson and Berridge, 2003, p. 39). As Robinson and Berridge (2003) argue, such changes may significantly alter the way information about rewards is processed in this area of the brain.

Overall, these effects can  go some distance in explaining not only why it is that some people become addicted to drugs, but also why many of these individuals continue self-administering them, even in the face of deriving little pleasure and, often, much suffering as a result of continuing to do so.


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