Diazepam-induced impairment in the acquisition of verbal material
Date
1988
Authors
Rich, Jill Bee
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Abstract
Research has indicated that the tranquilizer diazepam produces a transitory amnesia by selectively impairing the acquisition phase of new learning while the retrieval of previously-learned information remains intact. This study was conducted to determine the underlying component deficit in memory processing that ultimately leads to impaired acquisition of newly-presented material. Word lists, composed of 16 common nouns each, were presented on a computer at a rate of 2 or 8 seconds per word to 48 healthy subjects during both a training and an experimental session in which either diazepam or placebo was administered in a double blind manner. As predicted, diazepam subjects were impaired relative to placebo subjects on their immediate free recall of the word lists at both presentation rates. Further, the drug group demonstrated improved recall when presentation time was increased, consistent with the impaired acquisition hypothesis. This deficit was attributed in part to a reduction in short-term memory (STM) capacity, as measured by the number of different words rehearsed aloud between successive word presentations. However, two other measures involving an analysis of the recency portion of the serial position curve, which purportedly reflects recall from STM, yielded equal performance for the two groups. Drug subjects were also consistently impaired on a measure of vigilance that was administered throughout the session during each of the 3-minute intervals separating the lists. Thus, lowered attention and arousal could not be ruled out as confounds of the memory deficit, contrary to the prediction that memory and vigilance measures would manifest different patterns of impairment. Other analyses indicated that, although the drug subjects appeared similar to alcoholic Korsakoff amnesics in many respects, they did not exhibit an excessive build-up of proactive inhibition as Korsakoff patients do. Instead, their similarity to patients and experimental animals with hippocampal damage supported the view that suppression of hippocampal areas, which contain a high density of benzodiazepine receptors, by high-affinity diazepam binding may be the physiological mechanism by which diazepam impairs memory.