Effects of ethanol on eye movements in the monkey

Fuster, Joaquı́n M.; Willey, T. Joe; Riley, Darrell M.

doi:10.1016/0741-8329(85)90088-6

Cited by 11 publications

(4 citation statements)

References 11 publications

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“…This is consistent with a wealth of data in support of the notion that the different synaptic GABAAR subtypes mediate different functions: a1-GABAAR activation results in sedative and anticonvulsant effects, a2-GABAAR activation leads to anxiolytic and muscle relaxant effects, while the biological functions of the a3-GABAAR are as of yet unclear (Möhler, 2007;Möhler et al, 2002). EtOH at the low doses tested here had no effect on a1-GABAARmediated currents in acutely dissociated cells (Criswell et al, 2003) and did not affect SPV in monkeys (Fuster et al, 1985) while higher dosesX0.6% (E13.9 mM) resulted in SPV slowing (Fransson et al, 2010). Therefore, the lack of any SPV slowing in the EtOH o5mM (Figure 2c) condition provides further evidence that EtOH at very low doses has no significant action at the synaptic a1-GABAAR.…”

Section: Ethanol Suppresses Ltp-like Plasticity In Human M1supporting

confidence: 71%

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: Ethanol Suppresses Ltp-like Plasticity In Human M1supporting

confidence: 71%

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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“…However, an intoxicating amount of alcohol significantly reduces the amplitude of mono-and polysynaptic reflexes [4], and prolongs the latency and reduces the amplitude of long latency muscle responses [5]. Thus, alcohol leads to deleterious effects on both the sensory and motor systems [6] and is well known to result in impaired motor and balance control in experimental test setups [7].…”

Section: Introductionmentioning

confidence: 98%

Study I: Effects of 0.06% and 0.10% blood alcohol concentration on human postural control

Modig¹,

Patel²,

Magnusson³

et al. 2012

Gait & Posture

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“…Alcohol intoxication impairs vestibular senses (Kubo et al, 1990;Tianwu et al, 1995), reduces the amplitude of mono-and poly-synaptic reflexes (Ashby et al, 1977), and prolongs the latency and reduces the amplitude of long latency muscle responses (Woollacott, 1983). Therefore, alcohol intoxication leads to deleterious effects on both the sensory and motor systems (Fuster et al, 1985) and is likely to have profound effects on body movement control while standing.…”

Section: Introductionmentioning

confidence: 99%

Blood alcohol concentration at 0.06 and 0.10% causes a complex multifaceted deterioration of body movement control

Modig

Fransson

Magnusson

et al. 2012

Alcohol

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Link to publication Citation for published version (APA): Modig, F., Fransson, P-A., Magnusson, M., & Patel, M. (2012). Blood alcohol concentration at 0.06 and 0.10% causes a complex multifaceted deterioration of body movement control. Alcohol, 46, 75-88. DOI: 10.1016/j.alcohol.2011 General rights Copyright and moral rights for the publications made accessible in the public portal are retained by the authors and/or other copyright owners and it is a condition of accessing publications that users recognise and abide by the legal requirements associated with these rights.• Users may download and print one copy of any publication from the public portal for the purpose of private study or research.• You may not further distribute the material or use it for any profit-making activity or commercial gain • You may freely distribute the URL identifying the publication in the public portal AbstractAlcohol-related falls are recognized as a major contributor to the occurrence of traumatic brain injury. The control of upright standing balance is complex and comprises contributions from several partly independent mechanisms like appropriate information from multiple sensory systems and correct feedback and feedforward movement control. Analysis of multisegmented body movement offers a rarely used option for detecting the fine motor problems associated with alcohol intoxication.The study aims were: 1) to investigate whether alcohol intoxication at 0.06% and 0.10% blood alcohol concentration (BAC) affected linear body movement under unperturbed and perturbed standing; and 2) to investigate whether alcohol affected the ability for sensorimotor adaptation.Body movements were recorded in 25 participants (13 women and 12 men, mean age 25.1 years) at five locations (ankle, knee, hip, shoulder and head) during quiet standing and during balance perturbations from pseudorandom pulses of calf muscle vibration over 200s with eyes closed or open. Tests were performed at 0.00%, 0.06% and 0.10% BAC.The study revealed several significant findings: 1). An alcohol dose-specific effect; 2). A direction-specific stability decrease from alcohol intoxication; 3). A movement pattern change related to the level of alcohol intoxication during unperturbed standing and perturbed standing; 4). A sensorimotor adaptation deterioration with increased alcohol intoxication; and 5). That vision provided a weaker contribution to postural control during alcohol intoxication.Hence, alcohol intoxication at 0.06% and 0.10% BAC causes a complex multifaceted deterioration of human postural control.

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Effects of ethanol on eye movements in the monkey

Cited by 11 publications

References 11 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

Study I: Effects of 0.06% and 0.10% blood alcohol concentration on human postural control

Blood alcohol concentration at 0.06 and 0.10% causes a complex multifaceted deterioration of body movement control

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