Acute and chronic effects of ethanol on learning-related synaptic plasticity

Zorumski, Charles F.; Mennerick, Steven; Izumi, Yukitoshi

doi:10.1016/j.alcohol.2013.09.045

Cited by 142 publications

(131 citation statements)

References 259 publications

(350 reference statements)

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“…Surprisingly, alcohol can both enhance and impair memory, depending on when it is administered. Alcohol impairs learning when it is present during encoding (Zorumski et al, 2014), whereas it enhances learning and memory for salient environmental stimuli when it is present during consolidation. Parker et al (1980Parker et al ( , 1981 first demonstrated this in humans, showing that alcohol improved memory when it was administered immediately following stimulus presentation (i.e., during memory consolidation).…”

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confidence: 99%

Acute Effects of Alcohol on Encoding and Consolidation of Memory for Emotional Stimuli

Weafer

Gallo

Wit

2016

J. Stud. Alcohol Drugs

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ABSTRACT. Objective: Acute doses of alcohol impair memory when administered before encoding of emotionally neutral stimuli but enhance memory when administered immediately after encoding, potentially by affecting memory consolidation. Here, we examined whether alcohol produces similar biphasic effects on memory for positive or negative emotional stimuli. Method: The current study examined memory for emotional stimuli after alcohol (0.8 g/kg) was administered either before stimulus viewing (encoding group; n = 20) or immediately following stimulus viewing (consolidation group; n = 20). A third group received placebo both before and after stimulus viewing (control group; n = 19). Participants viewed the stimuli on one day, and their retrieval was assessed exactly 48 hours later, when they performed a surprise cued recollection and recognition test of the stimuli in a drug-free state. Results: As in previous studies, alcohol administered before encoding impaired memory accuracy, whereas alcohol administered after encoding enhanced memory accuracy. Critically, alcohol effects on cued recollection depended on the valence of the emotional stimuli: Its memory-impairing effects during encoding were greatest for emotional stimuli, whereas its memory-enhancing effects during consolidation were greatest for emotionally neutral stimuli. Effects of alcohol on recognition were not related to stimulus valence. Conclusions: This study extends previous findings with memory for neutral stimuli, showing that alcohol differentially affects the encoding and consolidation of memory for emotional stimuli. These effects of alcohol on memory for emotionally salient material may contribute to the development of alcohol-related problems, perhaps by dampening memory for adverse consequences of alcohol consumption. (J. Stud. Alcohol Drugs, 77, 86-94, 2016)

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confidence: 99%

Acute Effects of Alcohol on Encoding and Consolidation of Memory for Emotional Stimuli

Weafer

Gallo

Wit

2016

J. Stud. Alcohol Drugs

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“…In addition, several studies have provided evidence that LTD in the nucleus accumbens and prefrontal cortex of rats plays a pivotal supportive role in drug addiction (Brebner et al, 2005;Van den Oever et al, 2008). It may be speculated that the enhancing effect of low-dose ethanol on LTD-like plasticity in the present study relates to detrimental effects of acute ethanol ingestion on memory formation and learning (Lister et al, 1991;Mattila et al, 1998;Zorumski et al, 2014). However, this remains to be tested in further experiments as memory or learning processes have not been studied here.…”

Section: Behavioral Significance Of the Present Findingsmentioning

confidence: 56%

Low Doses of Ethanol Enhance LTD-like Plasticity in Human Motor Cortex

Fuhl

Müller‐Dahlhaus

Lücke

et al. 2015

Neuropsychopharmacol

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Humans liberally use ethanol for its facilitating effects on social interactions but its effects on central nervous system function remain underexplored. We have recently described that very low doses of ethanol abolish long-term potentiation (LTP)-like plasticity in human cortex, most likely through enhancement of tonic inhibition [Lücke et al, 2014, Neuropsychopharmacology 39:1508. Here, we studied the effects of low-dose ethanol on long-term depression (LTD)-like plasticity. LTD-like plasticity was induced in human motor cortex by paired associative transcranial magnetic stimulation (PAS LTD ), and measured as decreases of motor evoked potential input-output curve (IO-curve). In addition, sedation was measured by decreases in saccade peak velocity (SPV). Ethanol in two low doses (EtOH o10mM , EtOH o20mM ) was compared to single oral doses of alprazolam (APZ, 1mg) a classical benzodiazepine, and zolpidem (ZLP, 10 mg), a non-benzodiazepine hypnotic, in a double-blinded randomized placebo-controlled crossover design in ten healthy human subjects. EtOH o10mM and EtOH o20mM but not APZ or ZLP enhanced the PAS LTD -induced LTD-like plasticity, while APZ and ZLP but not EtOH o10mM or EtOH o20mM decreased SPV. Non-sedating low doses of ethanol, easily reached during social drinking, enhance LTD-like plasticity in human cortex. This effect is most likely explained by the activation of extrasynaptic α4-subunit containing gammaaminobutyric type A receptors by low-dose EtOH, resulting in increased tonic inhibition. Findings may stimulate cellular research on the role of tonic inhibition in regulating excitability and plasticity of cortical neuronal networks.

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“…Numerous studies have identified primary molecular targets for acute alcohol action in the brain, including, but not restricted to potassium channels (Li et al, 2013;Bukiya et al, 2014), Glutamate and GABAergic synapses (Santhakumar et al, 2007;Zorumski et al, 2014) and synaptic scaffold proteins (Romero et al, , 2013. However, the neural basis of the long term effect of alcohol is not entirely clear.…”

Section: Introductionmentioning

confidence: 99%