No abstract

Two experiments were designed to test whether the memory impairment induced by benzodiazepines (BZDs) is due to impaired memory for temporal context. In both experiments, subjects were administered either diazepam (15 mg oral) or placebo, and a standard BZD impairment on prose recall as well as a decreased subjective arousal was found. Key tasks to explore temporal context memory were an A-B A-C proactive interference paradigm and a list discrimination task. Initial learning of both groups on these tasks was broadly matched. In experiment 1, diazepam did not increase susceptibility to proactive interference using semantically related words. However, in experiment 2, using unrelated word pairs, diazepam markedly increased the number of prior list intrusions. Furthermore, after diazepam intake, subjects were clearly impaired in learning unrelated word pairs. Subjects after diazepam intake were not impaired in the list discrimination task. We conclude that (1) diazepam impairs the forming of new associations, whether this is the formation of links between two or more targets or between targets and context, (2) a temporal context encoding deficit cannot account for a broader diazepam-induced memory impairment.

Benzodiazepines are known to induce amnesic effects. To specify these effects more precisely, 40

Benzodiazepines (BZDs) give rise to memory impairments. It has been questioned whether or not these impairments are related to the drug's sedative, alertness-reducing effects. Therefore, in this study, alertness was reduced in healthy subjects both pharmacologically (15 mg diazepam) and non-pharmacologically (24-h sleep deprivation, SD) in order to assess whether these manipulations both gave rise to memory impairments. Twelve subjects were tested using a repeated measures cross-over design. Drug administration was placebo-controlled and double-blind. A subjective alertness reduction was established after diazepam intake and even more after SD. Additionally, performance-disruptive effects were found on psychomotor tasks after both SD and liazepam intake. However, only diazepam, and not SD, impaired delayed recall of a word list and recall of paired associates. Thus a reduction in alertness, i.e. sedation, cannot fully account for BZD-induced memory impairments.

It was tested whether a depletion in resources can account for the benzodiazepine-induced memory impairment. In two experiments, it was examined whether dividing attention had a disproportionately detrimental effect on learning semantically related and unrelated word pairs after diazepam intake. Word pairs had to be learned in both a single task condition and while performing a visual discrimination task concurrently (dual task condition). Moreover, the complexity of the visual discrimination task was manipulated systematically. Diazepam (15 mg, orally) or placebo was administered in a double-blind, between-subjects design. Subjects after diazepam intake were clearly impaired in learning unrelated word pairs, but not in learning related word pairs. Dividing attention in the dual task condition was associated with a reduction in learning unrelated word pairs, but this was not disproportionately reduced after diazepam intake. Moreover, the magnitude of resource depletion did not correlate with the severity of the diazepam-induced memory impairment. In general, the pattern of results does not support the hypothesis that a depletion of resources can explain the benzodiazepine-induced memory impairment.