Chronic Pain and Addiction (Advances in Psychosomatic

Sufferers with power ache understandably search reduction from their misery and soreness, yet many medicines that alleviate discomfort are in all likelihood addictive, and such a lot continual ache stipulations merely have a brief reaction to opiate analgesic medications. This quantity experiences the basic issues that underlie the complicated relationships of this debatable domain.

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Additional resources for Chronic Pain and Addiction (Advances in Psychosomatic Medicine, Vol. 30)

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Lewis rats are naturally highly addictive-drug-preferring and drug-seeking. Fischer 344 rats are naturally highly addictive-drug-avoidant. e. by exposing animals to repeated administration of addictive drugs. Nestler and Kosten and colleagues [86, 87] studied the dopaminergic brain reward circuits of laboratory rats made vulnerable (or resistant) to addictive drugs by both genetic and experiential means. They found that in animals displaying the behavioral phenotype of high addictive drug acceptance and high addictive drug seeking – whether this behavioral phenotype was imparted genetically or experientially – there exists a pathological atrophy of the neurofilamentous transport system for the dopamine-synthesizing enzyme tyrosine hydroxylase in the dopamine axons of the second-stage medial forebrain bundle neurons of the brain’s reward circuitry.

Time-line graph of reinstatement (relapse) to addictive drug-seeking behavior. Means ± SEM. 001. To model relapse in this model, the animal is allowed to acquire a conditioned place preference to an addictive drug. Then the animal is repeatedly exposed to the conditioned place preference test chamber (with open access to all compartments), day after day, until the drug-induced place preference is fully extinguished. Then, on the test day, the animal is exposed to relapse triggers, and the amount of drug-seeking behavior is measured as the amount of time spent in the previously drug-paired compartment.

Thus, the reward deficiency hypothesis seeks to explain drug addiction as a type of self-medication, ultimately damaging and self-destructive though it may be. The brain substrate of this reward deficiency syndrome may be mechanistically referable to more than a single deficiency in the functioning of the brain’s dopaminergic reward circuitry. Comings and Blum [70] and Blum et al. [72] have hypothesized that it is referable to a deficiency of dopaminergic D2 receptors in the brain’s reward circuitry, a view congruent with reports – including neuroimaging of the brain – by Volkow et al.

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