Drugs and human memory: effects of low doses of nitrazepam and hyoscine on retention.

Jones, Dylan M.; Jones, Mark; Lewis, Malcolm J.; Spriggs, T. L. B.

doi:10.1111/j.1365-2125.1979.tb00989.x

Cited by 38 publications

(23 citation statements)

References 12 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, they found that intravenous diazepam (0.1 1 mg/kg) and scopolamine (5.7 pg/kg) had essentially similar effects. They also replicated the Jones et al (1979) finding that scopolamine affected both early and middle parts of a sequence, while diazepam caused most impairment in the middle part only (Jones et al, 1978). A second study at the MRC Clinical Research Centre failed to show any difference in the effect of diazepam and scopolamine on different types of distractors or cues on homophone and synonym word-list learning .…”

Section: The Nature Of the Amnesiasupporting

confidence: 51%

Benzodiazepines, amnesia and sedation: Theoretical and clinical issues and controversies

King

1992

Human Psychopharmacology

View full text Add to dashboard Cite

The amnestic effect of benzodiazepines, first described in 1965, and the subsequent attempts to identify the precise nature of this effect, are reviewed. The difficulty in deciding to what extent this effect is secondary to the sedative action of these drugs is shown by the lack of agreement between studies. Nevertheless, it is concluded that, given the right experimental design, all benzodiazepines can be shown to cause an anterograde amnesia which is probably primarily a result of reduced attention or rehearsal and secondary to sedation. Its onset, degree and duration are influenced by dose, rate of absorption, route of administration, potency and the receptor occupancy rate of the particular benzodiazepine involved, but plasma elimination t,,, appears to be relatively unimportant. The clinical relevance of this for the long-term use of hypnotics and anxiolytics is not clear. Tolerance appears to be greater than for the anxiolytic but less than the sedative or anticonvulsant effect of benzodiazepines. It seems that transient amnestic effects could occur in chronic users related to post-dose, peak benzodiazepine levels. The great variability in individual response means that transient amnesia is a potential adverse drug reaction in certain individuals taking benzodiazepines.KEY woms-Benzodiazepines, amnesia, sedation, tolerance, receptor occupancy. HISTORICAL BACKGROUNDThe amnestic effect of benzodiazepines appears first to have been noticed by Brandt and Oakes (1965), who found that half their patients given diazepam (20mg) orally as a premedication prior to general anaesthesia, compared to a quarter of those given pentobarbital (lOOmg), were unable to remember the events prior to induction on the day after their operation. This effect, which was regarded by anaesthetists as a desirable property, was extensively studied and reported in the anaesthetic literature in the 1970s. The psychological methodology was necessarily simple and rather crude, consisting of the recall of events or recognition of picture cards, sometimes tested before the administration of general anaesthesia but more often postoperatively. Nevertheless, several useful reproducible findings emerged.Anterograde amnesia was commonly found after intravenous (Brown and Dundee, 1968;Fox et al., 1968;Pandit et al., 1971;Dundee and George, 1976;George and Dundee, 1977) but not intramuscular (Pandit and Dundee, 1970) or oral (Harry and Richards, 1972;Wilson and Ellis, 1973) diazepam. Lorazepam became preferred for this effect since it occurred reliably after intravenous (Heisterkamp and Cohen, 1975;Conner et al., 1976;Dundee and George, 1976;Pandit et al., 1976), intramuscular (Cormack et al., 1976;Fragen and Caldwell, 1976;Dundee et al., 1977) and oral (Turner, 1973; Magbagbeola, 1974;Dundee et al., 1977;McKay and Dundee, 1980) administration. By showing a series of cards at frequent intervals during premedication George and Dundee (1 977) showed that intravenous diazepam (10, 20mg) and flunitrazepam (1, 2mg) had a peak amnestic effect at 2min and la...

show abstract

Section: The Nature Of the Amnesiasupporting

confidence: 51%

Benzodiazepines, amnesia and sedation: Theoretical and clinical issues and controversies

King

1992

Human Psychopharmacology

View full text Add to dashboard Cite

show abstract

“…While we know of no evidence relating drug effects to colour memory, we do accept that hyoscine does produce a fairly specific impairment in primary memory (e.g. Jones et al 1979;Preston et al 1988). It is not obvious what this might imply for colour memory, but to explain our data it would have to mean that impairment in colour memory increases the saturation of the remembered colour.…”

Section: Discussionmentioning

confidence: 93%

The McCollough effect as a measure of central cholinergic activity in man

Byth

Logue

Bell³

et al. 1992

Psychopharmacology

View full text Add to dashboard Cite

The McCollough Effect (ME) is an orientation contingent colour after-effect which has been proposed as an indicator of central neurotransmitter activity. Shute (1979) suggested that the ME could reflect a hippocampal "forgetting" mechanism which should be inhibited by GABAergic neurones and stimulated by cholinergic neurones. The purpose of the present study was to demonstrate that the ME is in fact sensitive to cholinergic and anticholinergic drugs and to compare its sensitivity to more conventional tests of psychomotor and cognitive function. Ten healthy subjects received single doses of physostigmine (0.75 mg SC), hyoscine (1.2 mg), temazepam (20 mg), flecainide (200 mg) or placebo in a double-blind double-dummy presentation. Subjects were tested on a battery of psychomotor and cognitive function tests at baseline and 1 h, and adapted to the ME at 1.5 h. Visual analogue rating scales and conventional tests of psychomotor function and saccadic eye movements indicated that both subjective and objective measures of arousal were impaired by temazepam. The subjective, but not the objective, measures of arousal were also impaired by both hyoscine and physostigmine, but not by flecainide. Initial strength and duration of the ME were decreased by physostigmine and increased by hyoscine and temazepam, relative to placebo (P less than 0.01). Thus, the ME is capable of detecting cholinergic, anticholinergic and GABA mimetic drug effects in man, in therapeutic doses.

show abstract

“…In normal human volunteers, it is well established that scopolamine, a muscarinic receptor antagonist, impairs the acquisition of new information and disrupts the process of memory consolidation (Drachman and Leavitt 1974;Petersen 1977;Jones et al 1979;Broks et al 1988) as well as impairing continuous performance in a task that challenges sustained attentional mechanisms (Colquhoun 1962;Wesnes andWarburton 1983, 1984;Broks et al 1988). These findings clearly implicate the cholinergic system in both attentional and memory processes, but the precise relationship between these two functions is far from resolved.…”

mentioning

confidence: 99%

Cholinergic Modulation of Visual Attention and Working Memory: Dissociable Effects of Basal Forebrain 192-IgG-saporin Lesions and Intraprefrontal Infusions of Scopolamine

Chudasama¹,

Dalley²,

Nathwani³

et al. 2004

Learn. Mem.

132

View full text Add to dashboard Cite

Two experiments examined the effects of reductions in cortical cholinergic function on performance of a novel task that allowed for the simultaneous assessment of attention to a visual stimulus and memory for that stimulus over a variable delay within the same test session. In the first experiment, infusions of the muscarinic receptor antagonist scopolamine into the medial prefrontal cortex (mPFC) produced many omissions but did not impair rats' ability to correctly detect a brief visual stimulus. However, these animals were highly impaired in remembering the location of that stimulus following a delay period, although in a delay-independent manner. In the second experiment, another group of animals with selective 192 IgG-saporin lesions of the nucleus basalis magnocellularis (nBM) were not impaired under conditions of low-attentional demand. However, when the stimulus duration was reduced, a significant memory impairment was observed, but similar to the results of the first experiment, the nBM-lesioned animals were not impaired in attentional accuracy, although aspects of attention were compromised (e.g., omissions). These findings demonstrate that (1) cortical cholinergic depletion produces dissociable deficits in attention and memory, depending on the task demands, (2) delay-independent mnemonic deficits produced by scopolamine are probably due to impairments other than simple inattention, and (3) working memory deficits are not simply dependent on attentional difficulties per se. Together, these findings implicate the nBM cortical cholinergic system in both attentional and mnemonic processing.

show abstract

Drugs and human memory: effects of low doses of nitrazepam and hyoscine on retention.

Cited by 38 publications

References 12 publications

Benzodiazepines, amnesia and sedation: Theoretical and clinical issues and controversies

Benzodiazepines, amnesia and sedation: Theoretical and clinical issues and controversies

The McCollough effect as a measure of central cholinergic activity in man

Cholinergic Modulation of Visual Attention and Working Memory: Dissociable Effects of Basal Forebrain 192-IgG-saporin Lesions and Intraprefrontal Infusions of Scopolamine

Contact Info

Product

Resources

About