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Drug Reinforcement:

Drug abuse and addiction is a detrimental public health concern for in endangers both users and nonusers by spreading communicable diseases and inciting violent and other criminal behaviors. A new wave of studies have revealed a more comprehensive and multifaceted profile of addiction, involving environmental and neurobiological events that foster drug reinforcement. Most scientists agree that addiction -- the obligation to fulfill drug dependence -- occurs by reinforcement and reward pathways. Imaging studies depict the reinforcing effects of drugs in humans dependent on surges of dopamine initially exceeding rises from natural reinforcers (i.e. food). The scientific concord often remains intact when illustrating the reinforcement mechanisms at work implicating altered dopamine neurotransmission and higher-level processes. There are two such viewpoints that essentially build on each other.

Carlson (2004) essentially describes drug addiction as interplay with physiological and psychological dependencies. Addictive drugs generate positive reinforcement by conditioned responses that eventually solidify to dependence. He depicts a process that very much involves a basic neurochemistry underpinning mainly in the mesolimibic region for reinforcement that is significantly correlated with the drug effect timing. Whereas Carlson casually explicates reinforcers as largely biochemical disturbance that mediates conditioned reinforcing responses for drug abuse, Goldstein and Volkow (2002) propose a high-order progression of salience/reward modulation. Using neuroimaging techniques, they further establish the theory by implicating frontal neuroanatomy and thus behavioral and cognitive attributes to reinforcement. Addictive drugs hyper-activate certain neurophysiology, namely altered dopaminergeric systems as well as changes in neural architecture and brain structures, which may reset the thresholds of environmental events. Decreased sensitivity to nondrug-related stimuli, frontal inhibition, and increased attribution to the drug contribute to compulsive drug intake. In summary, a series of nurophysiological events, comprising both limbic and frontal structures, and altered cognitive modulation of reinforcers, increases motivation drive for the drug and thereby reinforces drug addiction.

Further biomedical, psychological, and sociological research is necessary to illustrate a comprehensive viewpoint for addiction. Understanding the basic mechanisms of drug abuse and addiction may improve treatment strategies. Moreover, neurofunctional imaging reveals similarities between drug addiction and obesity (Wang, 2004) which expands the practical benefits of such research. Perhaps the future will hold interventions that alter reward values for drugs and nondrugs and the discovery of pharmaceuticals that target dopamine and other implicated neurotransmission systems.

References

Carlson, N. R. (2004). Chapter 18: Drug Abuse. In Physiology of Behavior (pp. 572-600). Boston: Allyn & Bacon.

Goldstein, R. Z., & Volkow, N. D. (2002, October). Drug Addiction and Its Underlying Neurobiological Basis: Neuroimaging Evidence for the Involvement of the Frontal Cortex. American Journal of Psychiatry, 159, 1642 1652. Retrieved from ProQuest database.

Wang, G. J., Volkow, N. D., Thanos, P. K., & Fowler, J. S. (2004). Similarity between obesity and drug addiction as assessed by neurofunctional imaging: a concept review. Journal of Addictive Diseases, 23(3), 39 53. Retrieved from PubMed database (15256343).

 

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