Addiction to Altering States: Observable Tendencies Attributed to Learning and Neurology

Due et al. (2002) hypothesized that, although previous “addictive-cue” studies tended to focus on the limbic brain regions typically considered to be involved in reinforcement, two “distinctive neural circuits might be activated by smoking cues” (p. 954). The predicted circuits were a reward circuit and a visuospacial attention circuit. The reward circuit, which was previously identified in animal studies, consisted of the “mesocorticolimbic regions that include the ventral tegmental area, nucleus accumbens, amygdala, hippocampus, medial dorsal thalamus, ventral pallidum, and prefrontal cortex” (Due et al., p. 954). This circuit was already known to be activated by consumption of addictive substances, but the researchers predicted that it might be activated by predictors of the availability of the addictive substances (i.e. stimuli associated with the drug). The researchers’ prediction is a neurologically-founded support for the idea of conditioned homeostatic responses, in that the homeostatic responses could result from classically conditioned cues. So neural activity was predicted to occur in areas known to be highly associated with learning (via reinforcement) as a result of exposure to stimuli relating to smoking; if participants should show activation and report craving, it would support the idea of a homeostatic mechanism as the source of drug craving. The findings of the study support the ideas of salience, conditioned responding, and conditioned homeostatic responding.

Due et al. (2002) found that in the nicotine-deprived smokers, exposure to cigarette-related stimuli elicited greater neural activation in smokers than in non-smokers in mesocorticolimbic areas associated with reinforcement; also there was increased neural activity in areas involved in visuospatial attention. They report that their findings are consistent with the relatively new theories about the role of the “mesolimbic dopamine substrates in drug reinforcement” (Due et al., 2002, p. 959), which is part of the motivational control system (Due et al., 2002; Hyman et al., 2006; McKim, 2006). One of the key findings of this study was that activation occurred in the reward circuit, which traditionally has been thought to happen only in response to the use of drugs (not drug cues). The participants in the study received no drug, but the reward circuitry still showed activity.

The visuospatial activation seen in this study may be representative of the type of mechanism that allows the general search mode of appetitive behavior to succeed. After a stimulus is conditioned to signal the availability of a reinforcer, and has gained salience, it is believed to be integrated into the learning and memory system in the motivational control system of the brain (McKim, 2006).

From all that has here been presented, there are many questions and considerations that should be addressed in future research. A comprehensive model of addiction will be complex and will include recent neurological discoveries (e.g. neurotransmitters, specific pathways, cerebral blood flow, etc), traditional theories and proposed mechanisms, and the general neural systems, such as the motivation control system proposed by McKim (2006). There appeared to be a lack of studies on normal drinking and drug behavior.

To close this preliminary attempt it may be interesting to note that in the motivation control system, the cortex does not receive information from the reinforcement system, but does send information to it (McKim, 2006); this supposition lends itself to a possible explanation of the “irrational” behavior displayed by drug addicts who use in spite of negative consequences. Assuming the motivation system begins at the VTA (reinforcement system), after the nucleus accumbens removes inhibition of the basal ganglia and movement begins, the cortex is made aware of some sort of imbalance. The imbalance will only be corrected, however, when the VTA ceases eliciting a compensatory response. The cortex receives sensory information from the thalamus and communicates with the hippocampus and amygdala. It seems that the associations in the hippocampus and the amygdala would make the strongest contribution to the final response because they send memory and associative information (i.e. past response and following outcome) to the nucleus accumbens, which has ultimate control over the basal ganglia. If the taking of drugs is associated with alleviation of imbalance (withdrawal symptoms), then in a situation where there are several alternatives, the salience of drugs will make them the simplest, and most likely stimuli to engage. However, it seems that in the case of the addict, even if the cortex decides against taking drugs, perhaps because of a negative experience, the association of drugs and relief may be so strong that any inhibition on the part of the cortex will be insufficient to change the direction of the behavior as it is the nucleus accumbens, and not the cortex, that activate the general search movement. It follows from this type of system that an imbalance and strong salience might allow suppression of the cortex itself, leading to inability to “decide” to use a drug.

This discussion has touched on theories and behaviors (from neurological and observational studies) involving classical conditioning in general, sequential organization and directed behavior, set point or homeostatic theories and mechanisms, withdrawal as homeostatic (compensatory) response, the motivational control system and its subsystems, stimulus salience, stimulus generalization, schema theory, habituation and sensitization, and several other theories and research. Although this approach attempted to integrate some theories and more recent discoveries, addiction and drug use in general are still very complex. There is much more that needs to be addressed and follow-up research on this investigation will attend to applications of new research to specific learning theories in more depth with the aim of relating them to the mechanisms of addiction.

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