[Functional involvement of cerebral diazepam binding inhibitor (DBI) in the establishment of drug dependence].
Mechanisms for formation of drug dependence and emergence of withdrawal syndrome are not yet fully understood despite of a huge accumulation of experimental and clinical data. Several clinical features of withdrawal syndrome are considered to be common (i.e., anxiety) among patients with drug dependence induced by different drugs of abuse. In this review, we have discussed the possibility of the functional involvement of diazepam binding inhibitor (DBI), an endogenous neuropeptide for benzodiazepine receptors with endogenously anxiogenic potential, in the development of drug dependence and emergence of its withdrawal symptom. The levels of DBI protein and its mRNA significantly increased in the brain derived from mice dependent on alcohol (ethanol), nicotine and morphine, and abrupt cessation of these drugs facilitated further increase in DBI expression. In the cases of nicotine- and morphine-dependent mice, concomitant administration of antagonists for nicotinic acetylcholine and opioid receptors, respectively, abolished the increase in DBI expression. Therefore, these alterations in DBI expression have a close relationship with formation of drug dependence and/or emergence of withdrawal syndrome and are considered to be a common biochemical process in drug dependence induced by different drugs of abuse.
Katsura
M
M
Department of Pharmacology, Kawasaki Medical School, Kurashiki 701-0192, Japan. mkatsura@med.kawasaki-m.ac.jp
D000818:Animals; D001921:Brain / Q000378:metabolism*; D002352:Carrier Proteins / Q000378:metabolism / Q000502:physiology; D026261:Diazepam Binding Inhibitor; D000431:Ethanol; D006801:Humans; D009020:Morphine; D009538:Nicotine; D013375:Substance Withdrawal Syndrome / Q000209:etiology; D019966:Substance-Related Disorders / Q000209:etiology
D002352:Carrier Proteins; D026261:Diazepam Binding Inhibitor; D000431:Ethanol; D009538:Nicotine; D009020:Morphine