The differential effects of flumazenil on the psychomotor and amnesic actions of midazolam

Birch, Brian; Curran, H. Valerie

doi:10.1177/026988119000400105

Cited by 26 publications

(8 citation statements)

References 15 publications

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“…β-CCt failed to block the amnesic actions of chlordiazepoxide in the passive avoidance test and the radial arm maze in mice (Belzung et al 2000). Similarly, several human studies found that flumazenil blocked the sedative and psychomotor effects of benzodiazepines, but not their amnesic effects (Birch and Curran 1990;Curran and Birch 1991;Hommer et al 1993;Birch and Miller 1995), while in others (Dorow et al, 1987;Ghoneim et al 1989;Preston et al 1989;McKay et al 1990), the effective reversal of amnesic effects of benzodiazepines was obtained. Hence, Curran (1991) concluded that, in humans, the sedative effects of benzodiazepines are much more easily reversed than their amnesic effects.…”

Section: Discussionmentioning

confidence: 95%

Bidirectional effects of benzodiazepine binding site ligands on active avoidance acquisition and retention: differential antagonism by flumazenil and β-CCt

et al. 2005

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Section: Discussionmentioning

confidence: 95%

Bidirectional effects of benzodiazepine binding site ligands on active avoidance acquisition and retention: differential antagonism by flumazenil and β-CCt

et al. 2005

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“…Such a result would provide evidence that implicit and explicit memory are mediated by different memorial factors. 1 Studies using the benzodiazepine antagonist flumazenil have shown evidence inconsistent with the hypothesis that midazolam amnesia is due to a state-dependent memory effect in free recall (Birch & Curran, 1990;File, Goodall, Mabbutt, Harris, & Skelly, 1993). Specifically, such studies show that although flumazenil reverses midazolam's major sedative effects (e.g., psychomotor performance returns to normal levels), midazolam's amnesic effects remain, and are as strong as in a condition where participants are administered an injection of saline prior to free recall.…”

Section: Characteristics Of Midazolam Amnesiamentioning

confidence: 99%

The effect of midazolam on implicit and explicit memory in category exemplar production and category cued recall

Arndt

Passannante

Hirshman

2004

Memory

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Transfer-appropriate processing theory (Roediger, Weldon, & Challis, 1989) proposes that dissociations between performance on explicit and implicit memory tests arise because these tests often rely on different types of information processing (e.g., perceptual processing vs conceptual processing). This perspective predicts that implicit and explicit memory tasks that rely primarily on conceptual processing should show comparable results, not dissociations. Numerous studies have demonstrated such similarities. It is, however, possible that these results arise from explicit memory contamination of performance on implicit memory tasks. To address this issue, an experiment was conducted in which participants were administered the sedative midazolam prior to study. Midazolam is known to create a temporary, but dense, period of anterograde amnesia. The effects of blocking stimulus materials by semantic category at study and generation at study were investigated on category exemplar production and category-cued recall. The results of this study demonstrated a dissociation of the effects of midazolam on category exemplar production and category-cued recall. Specifically, midazolam reduced the effect of blocking stimulus materials in category-cued recall, but not in category exemplar production. The differential effect of midazolam on explicit and implicit memory is at odds with transfer-appropriate processing theory and suggests that theories of memory must distinguish the roles of different types of conceptual processing on implicit and explicit memory tests.

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“…This selective pattern of cognitive dysfunction may serve as a model for clinical cognitive syndromes. [ 112,216,217] A variation of the hypoxia model is that of hyperventilation-induced cognitive dysfunction. This model has previously been shown to be more valid for the simulation of ischaemic events in the brain than the hypoxia model and also that it is a sensitive model to test the neuroprotective effects of nootropic drugs such as aniracetam.l 60 ] Recently, hyperventilation-induced cognitive dysfunction was demonstrated employing a variety of cognitive tests.…”

Section: Future Possibilitiesmentioning

confidence: 99%

Cognition Enhancers in Age-Related Cognitive Decline

Riedel

Jolles

1996

Drugs & Aging

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A review of recently published studies on the effect of cognition enhancers in non-demented human study participants is presented. The heterogeneity of the therapeutic target, age-associated cognitive decline, can be improved by separately treating groups in whom age-extrinsic factors may underlie cognitive pathology. Standardisation of cognitive assessments is necessary, since many different tests are applied to answer the same question. Modelling cognitive dysfunction, either by pharmacological or nonpharmacological means, in humans is highly recommended since it allows hypotheses to be tested in a clearly operationalised way. Predictive validity of the currently applied models for the clinical situation remains a problem, however. The scopolamine (hyoscine) model has, to a reasonable extent, predictive validity for the cholinergic agents. The results of 67 single-dose studies and 30 multiple-dose studies are summarised. All single-dose studies and 14 multiple-dose studies were carried out in young or elderly human volunteers. In 45 of 81 volunteer studies, models of cognitive dysfunction were employed. The scopolamine model was the most used (n = 21); the other studies induced cognitive dysfunction by means of benzodiazepines (8), hypoxia (7), alcohol (5) and sleep-deprivation (4). The remaining 16 multiple-dose studies were clinical trials of a duration varying between 2 weeks and 1 year (average duration was 14 weeks). In these trials, the effects of cognition enhancers were assessed in elderly people in whom impairment of memory, psychomotor performance or cognitive function was determined. These included age-associated memory impairment (AAMI) and age-associated cognitive decline (AACD). There were many studies in which the cognition enhancing properties of substances in humans were reliably demonstrated. The cognition enhancing properties of substances that are widely used, such as caffeine, nicotine and vitamins, may already be active against AACD. New developments such as serotonin (5-hydroxytryptamine3; 5-HT3) antagonists and N-methyl-D-aspartate (NMDA) antagonists have provided marginal and disappointing results in AAMI. There is no cognition enhancer that has reliably and repeatedly been demonstrated to be efficacious for the treatment of AACD. However, this situation may change as the selectivity, specificity and adverse effect profiles of substances that are being developed for the treatment of AD may be expected to be improved in the future.

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The differential effects of flumazenil on the psychomotor and amnesic actions of midazolam

Cited by 26 publications

References 15 publications

Bidirectional effects of benzodiazepine binding site ligands on active avoidance acquisition and retention: differential antagonism by flumazenil and β-CCt

Bidirectional effects of benzodiazepine binding site ligands on active avoidance acquisition and retention: differential antagonism by flumazenil and β-CCt

The effect of midazolam on implicit and explicit memory in category exemplar production and category cued recall

Cognition Enhancers in Age-Related Cognitive Decline

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