Drugs of abuse
Drugs of abuse are perceived to stimulate significant surges of dopamine in nucleus accumbens, which is an extracellular limbic region. Human imaging studies have demonstrated correlations in indicators of reward such as euphoria and the “high” with drug-induced nucleus accumbens (NAc) dopamine escalations. Additionally, there is also a concern of reward saliency that is typically facilitated by the activity’s unexpectedness or novelty. Research harnessing imaging techniques has uncovered most of the convoluted nature of dopamine as presented in the process of addiction, for instance, dopamine alterations with drugs of abuse, metabolic and neurochemical processes measurements, and plastic changes with brain dopamine and their impact on addiction patients.
Positron emission tomography (PET) analysis has demonstrated that intravenous stimulant administration results in rapid dopamine changes. However, oral dosing results in slower surges of dopamine. A correlation of the speed of entry of substance into the brain and the degree of reinforcement is noteworthy. For instance, rapid brain dopamine changes are stimulated following an event of substance abuse such as tobacco smoking. Such findings have led to the decryption that substances of abuse are able to mimic, however, significantly exceed the typical psychologic phasic of dopamine firing. Often, the primary dopamine trafficking pathway becomes compromised. Moreover, Volkov et al. (2017) assert that on the verge of intoxication, there is an increment in synaptic dopamine in participants (both with and without an addiction). Nevertheless, a small percentage of the participants suffers addiction and, in turn, engages in compulsive abuse of drug or substance. This study further proposes that vulnerable individuals experience surges in neuroadaptations of systems of dopamine, such as motivation, memory, conditioning circuitry, saliency, and reward (Volkov et al., 2017). Volkov et al. (2011) further confirm the evidence demonstrating the effects of nicotine, opiates, or stimulants exposure producing consistent adaptive transitions of the dendritic trees where there is the location of reward circuitry in the brain.
Other studies reveal that patients with multiple substances or drug addictions such as alcohol, methamphetamine, cocaine, and heroin demonstrate reduced dopamine 2 receptor density in the striatum. For instance, the nucleus accumbens that persist even after significant detoxification. Such findings provide a clinical glimpse of vulnerability and relapse issues even after the suspension of substances from the patients. Other scholars posit that there are metabolic and functional implications of prolonged dopamine imbalances triggered by abuse of the substance. For example, Ersche et al. (2006) revealed using PET that abusers of cocaine, marijuana, and alcohol have a reduced dorsolateral prefrontal cortex, orbitofrontal cortex, and cingulate gyrus activity. Indeed, there is an existing correlation between such events and reductions in dopamine and receptor density striatum. Moreover, in alcohol abusers, it has been linked with craving severity and significant inductions of cue-activators of medial prefrontal cortex and anterior cingulate gyrus.
Additionally, dopamine is crucial for memory, conditioning, and habit formation within the regions of the brain (hippocampus, amygdala, and dorsal striatum). Deciphering the vulnerability of particular patients compared to other patients to becoming addicted poses a significant clinical relevance. Accordingly, patients exhibiting substances as pleasurable have deescalated their dopamine receptor levels compared to those loathing the substances (Volkov et al., 2011). Assertions are that high receptor density and dopamine may guard against addiction. This assumption follows a theory that supposes higher dopamine metabolism in patients within the orbitofrontal cortex and cingulate gyrus results in the dampening of the frontal circuits involved in limbic area silencing or inhibition.
Furthermore, Volkov et al. (2011) opine that dopamine is involved in motivation, such as persistence, the pursuit of reinforcing stimuli, and vigor through its regulation on various targeted regions of the brain such as ventral pallidum, amygdala, and dorsal striatum. The hallmark of addiction is demonstrated through the enhanced motivation to procure the substance. Individuals with a substance addiction will often defy the odds to obtain the drug or substance no matter the repercussions. Therefore, substance taking and seeking become their motivational drive and displace other vital activities. However, the addict is motivated and aroused while procuring the substance and tends to be apathetic and withdrawn while exposed to non-substance-related activities. Volkov et al. (2011) identify this shift and compare brain activation patterns stimulated with exposure to conditioned cues with non-conditioned cues.
Conversely to the de-escalation of prefrontal activity demonstrated in detoxified abusers of cocaine lacking drug stimulation, these prefrontal regions are activated when these abusers have an exposure to craving induced stimuli that is either cues or drugs. In like manner, cocaine abusers investigated after a cocaine binging episode demonstrated increments in metabolic activities of the dorsal striatum, ACC, and OFC, which were linked with craving (Volkov et a., 2011). Nevertheless, comparisons of the responses to intravenous intake between addicts of cocaine and non-addicts, it was evident that only the addicts exhibited escalations in medial OFC and ventral ACC metabolism. On the other hand, non-addicts of cocaine demonstrated a decreased metabolism in the regions, as mentioned above of the brain. As a result, stimulation of these prefrontal regions, owing to drug exposure, accounts only for addiction. Also, associations with an enhanced desire for drug accounts for the activation. Additionally, other studies dealing with cocaine-addicted participants demonstrated that subjects who managed to inhibit their craving had a reduction in medial OFC (processes of motivation) and NAc (predict rewards) metabolism.