Effects of Alcohol, Zolpidem, and Some Other Sedatives and Hypnotics on Human Performance and Memory

Mattila, Mikko; Vanakoski, Jyrki; Kalska, Hely; Seppαlä, Timo

doi:10.1016/s0091-3057(97)00506-6

Cited by 71 publications

(55 citation statements)

References 25 publications

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“…PAS LTP -induced LTP-like plasticity shares common mechanisms with motor skill learning (Elahi et al, 2013;Jung and Ziemann, 2009;Kang et al, 2011;Rosenkranz et al, 2007;Stefan et al, 2006;Ziemann et al, 2004) and acute EtOH ingestion has deleterious effects on memory formation and learning (Lister et al, 1991;Lowy, 1970;Mattila et al, 1998). Therefore, the present findings suggest a negative impact of EtOH on memory formation and learning at doses as low as reached by a single drink, but this will need to be tested in further experiments.…”

Section: Drug Effects On Pas Ltp -Induced Ltp-like Increase Of Mep Iomentioning

confidence: 67%

“…The cellular mechanisms of this detrimental low-dose EtOH effect cannot be disentangled at the systems level but likely relate to the potentiation of tonic inhibition mediated by extrasynaptic GABAARs and/or blockade of glutamatergic neurotransmission through NMDARs. Findings have potentially significant impact at the behavioral level, as acute EtOH ingestion impairs LTP-dependent processes such as learning and memory formation (Lister et al, 1991;Lowy, 1970;Mattila et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

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Deleterious Effects of a Low Amount of Ethanol on LTP-Like Plasticity in Human Cortex

Lücke

Heidegger

Röhner

et al. 2014

Neuropsychopharmacol

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Ingesting ethanol (EtOH) at low doses during social drinking is a common human behavior for its facilitating effects on social interactions. However, low-dose EtOH may have also detrimental effects that so far are underexplored. Here we sought to test the effects of lowdose EtOH on long-term potentiation (LTP)-like plasticity in human motor cortex. Previous cellular experiments showed that low-dose EtOH potentiates extrasynaptic GABAAR and reduces NMDAR-mediated currents, processes that would limit the expression of LTP. Paired associative transcranial magnetic stimulation (PAS LTP ) was employed in nine healthy subjects for induction of LTP-like plasticity, indexed by a long-term increase in motor-evoked potential input-output curves. Synaptic a1-GABAAR function was measured by saccadic peak velocity (SPV). Very low doses of EtOH (resulting in blood concentrations of o5 mM) suppressed LTP-like plasticity but did not affect SPV when compared with a placebo condition. In contrast, 1 mg of alprazolam, a classical benzodiazepine, or 10 mg of zolpidem, a non-benzodiazepine hypnotic, decreased SPV but did not significantly affect LTP-like plasticity when compared with placebo. This double dissociation of low-dose EtOH vs alprazolam/zolpidem effects is best explained by the putatively high affinity of EtOH but not alprazolam/zolpidem to extrasynaptic GABAARs and to NMDARs. Findings suggest that enhancement of extrasynaptic GABAARmediated tonic inhibition and/or reduction of NMDAR-mediated neurotransmission by EtOH blocks LTP-like plasticity in human cortex at very low doses that are easily reached during social drinking. Therefore, low-dose EtOH may jeopardize LTP-dependent processes, such as learning and memory formation.

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Section: Drug Effects On Pas Ltp -Induced Ltp-like Increase Of Mep Iomentioning

confidence: 67%

Section: Introductionmentioning

confidence: 99%

Deleterious Effects of a Low Amount of Ethanol on LTP-Like Plasticity in Human Cortex

Lücke

Heidegger

Röhner

et al. 2014

Neuropsychopharmacol

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“…For example, an acute dose of zopiclone can impair memory and psychomotor function (e.g. Mattila et al 1998). Although it is recommended that prescriptions for these drugs should be limited to 4 weeks, in practice this is not always the case and it is important that repeat prescribing is monitored.…”

Section: Methodological Considerationsmentioning

confidence: 99%

Older adults and withdrawal from benzodiazepine hypnotics in general practice: effects on cognitive function, sleep, mood and quality of life

Curran

Collins²,

Fletcher³

et al. 2003

Psychol. Med.

168

105

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“…With exponential increase in the number of motor vehicles on roads, it is inevitable that many of the patients taking these medications getting behind the wheel. Neurophysiological and neuropsychological experiments show that the CNS-depressant medications impair an array of cognitive functions underlying [44][45][46][47] driving and other everyday activities . The cognitive effects include impaired visual [47][48][49][50][51] attention and reaction time , attentional 5 2 5 3 switching , planning and working 54 memory .…”

Section: O G N I T I V E To X I C I T Y O F S E D a T I V E P S Y Cmentioning

confidence: 99%

Cognitive toxicity: from pesticides to pharmaceuticals

Dassanayake

2017

SL J. Med.

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Impairment of cognitive functions following neurotoxic exposure is collectively termed cognitive toxicity. This oration is based on a series of studies carried out over last 12 years on cognitive toxicity of two groups of substances, viz. organophosphate (OP) pesticides and sedative psychotropic drugs.OP pesticide poisoning is a major clinical and public health problem in South Asia. OPs act as cholinesterase inhibitors, and bring about acute neurological deficits following exposure. Using neurophysiological and neuropsychological techniques, we assess long-term neurocognitive deficits of OPs, a less known yet important adverse effect of OP exposure. The findings hitherto indicate both acute large-dose poisoning and subclinical occupational exposure are associated with long-term cognitive impairment.In the same way the pesticide use and misuse are common in agricultural communities, use and misuse of sedative psychotropic medications are common in urbanised societies. Sedative drugs, even in therapeutic doses impair driving and underlying cognitive functions, and increase the risk of traffic accidents. When taken in overdose, these drugs have cognitively impairing effects that last beyond clinical recovery from acute poisoning. These patients are more prone to traffic crashes at least up to 4 weeks following exposure, and the cognitive recovery over this period mirrors the crash risk at different post-overdose time points. The above findings raise a number of clinical and medico legal implications in post-discharge management of patients with sedative drug overdose.As the agricultural communities transform into urban industrialised societies in Sri Lanka, the pattern of poisoning changes from agrochemicals into pharmaceuticals, particularly psychotropic dugs. The two lines of research discussed above highlight how this changing social fabric poses new challenges for the neurophysiologists, neurologists and psychiatrists who study cognition and apply their findings in clinical settings. Our latest work in generating age-, sex-and education-adjusted norms for cognitive tests for Sri Lankans, would set the foundation in interpreting the cognitive test results of clinical populations.

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Effects of Alcohol, Zolpidem, and Some Other Sedatives and Hypnotics on Human Performance and Memory

Cited by 71 publications

References 25 publications

Deleterious Effects of a Low Amount of Ethanol on LTP-Like Plasticity in Human Cortex

Deleterious Effects of a Low Amount of Ethanol on LTP-Like Plasticity in Human Cortex

Older adults and withdrawal from benzodiazepine hypnotics in general practice: effects on cognitive function, sleep, mood and quality of life

Cognitive toxicity: from pesticides to pharmaceuticals

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