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The biochemical mechanisms in narcotic tolerance and dependence and recent developments of the drug therapy in narcotic detoxification are discussed in this review article. Several lines of evidence indicated that narcotic drugs may act at opiate receptors on noradrenergic nerve terminals in several brain areas to inhibit norepinephrine release. Chronic uses of opiate drugs and prolonged suppression at the noradrenergic system can cause post-synaptic receptor supersensitivity, which manifests tolerance, and overactivity of the system upon opiate withdrawal, which leads to withdrawal symptoms. For the treatment of narcotic addiction, several new drugs have been studied in the past ten years. LAAM (Levo-alpha-acetylmethadol) is the long acting derivative which, in the near future, may replace the presently widely used methadone. Long acting narcotic antagonist such as naltrexone may be beneficial in preventing readdiction. Clonidine, the α2-adrenergic agonist which acts presynaptically to inhibit norepinephrine release, has been successfully used in the treatment of withdrawal symptoms. The effectiveness of this drug supports the current hypothesis of noradrenergic overactivity in opiate withdrawal symptoms. One interesting proposal for the rapid opiate detoxification includes the use of naloxone to facilitate the detoxification, clonidine to suppress the withdrawal symptoms, and naltrexone to prevent reinitiation of narcotic usage. Since it is generally agreed that no single treatment approach is best for all patients, the concept of multi-modality treatment should be promoted so that patients can get the kind of help they need. Furthermore, the appropriate drug therapy may also improve efficiency of the rehabilitation and the overall treatment processes.
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