The biological basis of benzodiazepine dependence

Authors:
  • MLMalcolm Lader
    Malcolm Lader
  • SFSandra File
    Sandra File
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Abstract
The biological basis of benzodiazepine dependence 1 Benzodiazepines are the most widely prescribed psychotropic drugs and while the specific neural pathways mediating their several therapeutic effects remain largely unknown, at least their initial site of action has been identified. For the last decade we have known that the central nervous system contains high affinity, stereospecific binding-sites for the benzodiazepines. These sites are found on a supramolecular complex with y-aminobutyric acid (GABA) receptors and with a chloride ionophore (channel across the cell membrane), which also has binding-sites for drugs such as the barbiturates (Olsen, 1982). Recently there has been a growing appreciation that benzodiazepines induce dependence and that tolerance can occur to their behavioural effects. Although initially these phenomena were linked with long-term use, more recent evidence suggests that similar changes can be observed after short-term or even a single administration. This review covers both the clinical evidence and relevant experimental studies and attempts to explore the possible underlying mechanism(s). Although the precise mechanism is still unknown, we conclude that both rebound and withdrawal symptoms are reflections of a common dependence mechanism and also that tolerance is simply another manifestation of this same mechanism. We further conclude that the same underlying mechanism mediates the rebound phenomena and tolerance seen after short-term or acute benzodiazepine administration.

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