The alcohol facilitation effect on memory: A dose-response study

Parker, Elizabeth S.; Morihisa, John M.; Wyatt, Richard Jed; Schwartz, Barbara L.; Weingartner, Herbert; Stillman, R. C.

doi:10.1007/bf00431763

Cited by 89 publications

(81 citation statements)

References 25 publications

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“…More recently, Parker, Birnbaum, Weingartner, Hartley, Stillman, and Wyatt (1980) and Parker, Morihisa, Wyatt, Schwartz, Weingartner, and Stillman (1981) found that subjects who viewed a series of scenic slides just before drinking alcohol later remembered the slides significantly better than did subjects who received a placebo. Parker et al (1981) concluded that this retrograde enhancement of memory is due to a facilitation of the trace consolidation process by the alcohol. Although their interpretation provides an explanation for the present data, the present results may also be explained easily by an interference mechanism: When recalling the practice list, the drugged subjects should have experienced much less retroactive interference than did the placebo subjects because the drugged subjects had learned so little of the postdrug material.…”

Section: Discussionmentioning

confidence: 98%

Diazepam and memory: Support for a duplex model of memory

1983

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In three experiments, the hypothesis that diazepam (Valium) selectively impairs the transfer of information from short-term to long-term memory was supported by differences between placebo and drugged subjects in effects of item difficulty, serial position (primacy-recency), and list length. In Experiment I, diazepam reduced recall in the primacy portion of the serial position function, but produced no performance difference in the recency component. Recall decreased in placebo subjects as item difficulty increased, but drugged subjects were relatively uaffected by manipulation of difficulty. In Experiments 2 and 3, subjects treated with diazepam exhibited smaller gains in immediate recall with increasing list length than placebo controls. Retrieval of words learned before drug administration was not impaired by diazepam; in fact, it was significantly enhanced relative to control performance. The results add further support to the distinction between short-and long-term memory.Since the 1960s, a dominant approach to learning and memory processes has been to divide memory into two components: a limited-capacity, short-term-memory (STM) store and a large-capacity, long-term-memory (LTM) store (see Atkinson & Shiffrin, 1968, 1971, and Waugh & Norman, 1965. Although there are a number of criticisms of the duplex model that have forced modifications of the theory (for a review, see Klatzky, 1980), it continues to be a comprehensive and useful approach to the analysis of human memory. The present paper is intended to illustrate the usefulness of the model in the growing area of cognitive psychopharmacology and also to illustrate how pharmacological manipulations can be utilized to investigate specific human memory processes.The literature on cognitive psychopharmacology contains many studies of drugs with similar and specific detrimental effects on memory (e .g., Birnbaum & Parker, 1977;Crow & Grove-White, 1973 ;Darley, Tinklenberg, Roth, Hollister, & Atkinson, 1973; Ghoneim & Mewaldt, 1975. Illustrative of these drugs is diazepam (Valium), until recently the most often prescribed drug in the world. The specific memory impairment produced by diazepam has been well demonstrated.This research was supported by NIMH Grant MH 35324. A portion of this paper was presented at the Psychonornic Society meeting in Minneapolis, November 12, 1982. We thank Nancy Fallis and Janis L. Berie for their assistance. Requests for reprints should be sent to Steven P. Mewaldt, Department of Psychology, Marshall University, Huntington, West Virginia 25701.For example, diazepam impairs acquisition of serial, paired-associate, and free-recall lists, but does not affect performance on a Brown-Peterson distractor task or a short memory span task, or, apparently, hinder retrieval of previously acquired information (see Clarke, Eccersley, Frisby, & Thornton, 1970; Dundee & Pandit, 1972; Ghoneim & Mewaldt, 1975 Hinrichs, Mewaldt, Ghoneim, & Berie, 1982). We have interpreted these data as suggesting that diazepam leaves STM and retrieval from LT...

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Section: Discussionmentioning

confidence: 98%

Diazepam and memory: Support for a duplex model of memory

1983

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“…7. Numerous studies have established that at concentrations produced by the ingestion of one to two drinks (5-10 mM), EtOH causes paradoxical excitatory effects, including memory facilitation (43)(44)(45). Importantly, an increase in the spontaneous firing rate of single units in the dorsal hippocampus has been demonstrated after injection of low doses of EtOH into rats (46).…”

Section: Discussionmentioning

confidence: 99%

Alcohol potently inhibits the kainate receptor-dependent excitatory drive of hippocampal interneurons

Carta

Ariwodola²,

Weiner³

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

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Kainate receptors (KA-Rs) are members of the glutamate-gated family of ionotropic receptors, which also includes N-methyl-Daspartate (NMDA) and ␣-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) receptors. KA-Rs are important modulators of interneuron excitability in the CA1 region of the hippocampus. Activation of these receptors enhances interneuron firing, which robustly increases spontaneous inhibitory postsynaptic currents in pyramidal neurons. We report here that ethanol (EtOH) potently inhibits this KA-R-mediated effect at concentrations as low as those that can be achieved in blood after the ingestion of just 1-2 drinks (5-10 mM). Pressure application of kainate, in the presence of AMPA and NMDA receptor antagonists, evoked depolarizing responses in interneurons that triggered repetitive action potential firing. EtOH potently inhibited these responses to a degree that was sufficient to abolish action potential firing. This effect appears to be specific for KA-Rs, as EtOH did not affect action potential firing triggered by AMPA receptor-mediated depolarizing responses. Importantly, EtOH inhibited interneuron action potential firing in response to KA-R activation by synaptically released glutamate, suggesting that our findings are physiologically relevant. KA-R-dependent modulation of glutamate release onto pyramidal neurons was not affected by EtOH. Thus, EtOH increases excitability of pyramidal neurons indirectly by inhibiting the KA-R-dependent drive of ␥-aminobutyric acid (GABA)ergic interneurons. We postulate that this effect may explain, in part, some of the paradoxical excitatory actions of this widely abused substance. The excitatory actions of EtOH may be perceived as positive by some individuals, which could contribute to the development of alcoholism.K ainate receptors (KA-Rs) are glutamate-gated ion channels that play important roles in the regulation of hippocampal excitability. In mossy fiber-to-CA3 pyramidal neuron synapses, KA-Rs mediate synaptic currents and plasticity and modulate glutamate release presynaptically (reviewed in refs. 1 and 2). Although KA-Rs are also present in CA1 pyramidal neurons, these receptors are not activated synaptically (3, 4). In the CA1 region, however, KA-Rs inhibit glutamate release presynaptically (5-7) and also regulate action potential (AP)-dependent GABA release from interneurons; studies have shown that the frequency of AP-independent GABA release is either unaffected (8-10) or inhibited by KA-R activation (11). Activation of KA-Rs by micromolar concentrations of KA inhibits evoked ␥-aminobutyric acid type A (GABA A ) receptor (GABA A -R)-mediated inhibitory postsynaptic currents (eIPSCs) in CA1 pyramidal neurons (8,9,(12)(13)(14)(15). However, the precise mechanism and the physiological importance of this effect are a matter of controversy (reviewed in refs. 1 and 16). This effect was initially interpreted to indicate that activation of interneuronal KA-Rs exerts a disinhibitory effect on CA1 pyramidal neurons, but subsequent studies have challenge...

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“…One interesting result with respect to the recall memory literature is that a number of studies identified facilitative effects of alcohol on recall performance (Kalin, 1964;Lamberty, Beckwith, Petros, and Ross, 1990), recognition performance (Parker, Birnbaum, Weingartner, Hartley, Stillman, and Wyatt, 1980;Parker, Morihisa, Wyatt, Schwartz, Weingartner, and Stillman, 1981), and continuous processing (Carpenter and Ross, 1965). The alcohol doses in these studies ranged from .03 to 0.1%.…”

Section: Acute Effects Of Alcohol On Task Performancementioning

confidence: 99%