Effects of ethanol on nonspatial working memory and attention in rats.

Givens, Bennet; McMahon, Kathleèn

doi:10.1037/0735-7044.111.2.275

Cited by 62 publications

(46 citation statements)

References 33 publications

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“…Ethanol inhibited persistent activity and spike firing in the slice cocultures and reduced PFC firing in vivo. The concentrations of ethanol that produced these effects (17-100 mM; ϳ0.08 -0.4% blood alcohol concentration) are similar to those that alter PFC-mediated behaviors including working memory, error detection (Melchior et al, 1993;Givens and McMahon, 1997;Ridderinkhof et al, 2002;Rossetti et al, 2002), and EEG responses after stimulation of the frontal cortex in humans (Kahkonen et al, 2003). Ethanol's inhibition of persistent activity in the slice cocultures appeared to involve synaptic sites of action, as even high concentrations of ethanol had little effect on firing evoked by direct current injection.…”

Section: Discussionmentioning

confidence: 84%

Ethanol Inhibits Persistent Activity in Prefrontal Cortical Neurons

Tu¹,

Kroener²,

Abernathy³

et al. 2007

J. Neurosci.

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Section: Discussionmentioning

confidence: 84%

Ethanol Inhibits Persistent Activity in Prefrontal Cortical Neurons

Tu¹,

Kroener²,

Abernathy³

et al. 2007

J. Neurosci.

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“…The amnesic effects of alcohol are proposed to be mediated by an effect on the hippocampus and hippocampal circuitry (Anisman, 1972;Gibson, 1985;Ryabinin, 1998;Givens et al, 2000;. This is supported by work demonstrating alcohol-induced impairments in normal hippocampal function (Blitzer et al, 1990;Givens, 1995;Givens and McMahon, 1995) and impairments of memory by acute alcohol in hippocampal-dependent tasks in rats (Givens and McMahon, 1997;Shimizu et al, 1998).…”

Section: Introductionmentioning

confidence: 85%

“…However, studies that demonstrate alcohol-induced impairment of hippocampus-dependent learning and memory without affecting hippocampus-independent processes (Matthews et al, 1995;Melia et al, 1996;Givens and McMahon, 1997) have only shown this with the use of context-related cues or operant tasks. Whether alcohol impairs learning about an explicit cue when that learning is made hippocampusdependent has not yet been investigated.…”

Section: Introductionmentioning

confidence: 95%

“…Furthermore, physiological evidence on the effects of alcohol on the hippocampus reports that alcohol impairs hippocampal function, particularly long-term potentiation (Lovinger et al, 1989(Lovinger et al, , 1990Blitzer et al, 1990;Givens, 1995;. If alcohol reduces the capacity for synaptic plasticity in the hippocampus and impairs performance in hippocampus-dependent tasks (Givens, 1995;Matthews et al, 1995;Givens and McMahon, 1997), it would be difficult to see how alcohol would restore hippocampal function during tests for recall in a classical conditioning paradigm.…”

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confidence: 97%

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Alcohol‐induced memory impairment in trace fear conditioning: A hippocampus‐specific effect

Weitemier

Ryabinin

2003

Hippocampus

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It has been hypothesized that the amnesic effects of alcohol are through selective disruption of hippocampal function. Delay and trace fear conditioning are useful paradigms to investigate hippocampal-dependent and independent forms of memory. With delay fear conditioning, learning of explicit cues does not depend on normal hippocampal function, whereas learning explicit cues in trace fear conditioning does. In both delay and trace fear conditioning, the hippocampus is involved in learning to contextual cues, but it may not be entirely necessary. The present study investigates the effects of alcohol on the acquisition of delay and trace fear conditioning in mice, using freezing as a measure of learning. Male C57BL/6J mice were injected with 0.8 or 1.6 g/kg of 20% v/v alcohol and were immediately exposed to eight tone-footshock pairings in which the conditional stimulus (CS) either coterminated with a footshock unconditional stimulus (US) (delay conditioning) or was separated from the footshock by a 30-s trace interval (trace conditioning). During trace, but not delay fear conditioning, 0.8 g/kg alcohol impaired learning to a tone CS. This dose also impaired context-dependent learning in both procedures (although only slightly for trace fear conditioning). The 1.6 g/kg alcohol exerted a nonselective impairment on learning. The impairment by alcohol of learning to a tone CS when it is hippocampus-dependent, but not when it is hippocampus-independent provides further support for the hypothesis that alcohol exerts a selective effect on hippocampus-dependent learning.

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“…A series of studies have demonstrated that acute ethanol administration affects behaviors that have been shown to be dependent on the hippocampus (Matthews et al, 1995;Givens, 1996;Melia et al, 1996;Givens and McMahon, 1997). Furthermore, acute ethanol administration also alters the specificity of hippocampal pyramidal "place" cells (Matthews et al, 1996).…”

mentioning

confidence: 99%

Differential Regulation of GABA_A Receptor Gene Expression by Ethanol in the Rat Hippocampus Versus Cerebral Cortex

Matthews

Devaud

Fritschy

et al. 1998

Journal of Neurochemistry

103

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Abstract:Previous research has shown that chronic ethanol consumption dramatically alters GABAA receptor a, and a 4 subunit gene expression in the cerebral cortex and GABAA receptor a, and a6 subunit gene expression in the cerebellum. However, it is not yet known if chronic ethanol consumption produces similar alterations in GA-BAA receptor gene expression in other brain regions. One brain region of interest is the hippocampus because it has recently been shown that a subset of GABAA receptors in the hippocampus is responsive to pharmacologically relevant concentrations of ethanol. Therefore, we directly compared the effects of chronic ethanol consumption on GABAA receptor subunit gene expression in the hippocampus and cerebral cortex. Furthermore, we investigated whether the duration of ethanol consumption (14 or 40 days) would influence regulation of GABAA receptor gene expression in these two brain regions. Chronic ethanol consumption produced a significant increase in the level of GABAA receptor a4 subunit peptide in the hippocampus following 40 days but not 14 days. The relative expression of hippocampal GABAA receptor a1, a2, a3, /32/3, or Y2 was not altered by either period of chronic ethanol exposure. In marked contrast, chronic ethanol consumption for 40 days significantly increased the relative expression of cerebral cortical GABAA receptor a4 subunits and significantly decreased the relative expression of cerebral cortical GABAA receptor a, subunits. This finding is consistent with previous results following 14 days of chronic ethanol consumption. Hence, chronic ethanol consumption alters GABAA receptor gene expression in the hippocampus but in a different manner from that in either the cerebral cortex or the cerebellum. Furthermore, these alterations are dependent on the duration of ethanol exposure.

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Effects of ethanol on nonspatial working memory and attention in rats.

Cited by 62 publications

References 33 publications

Ethanol Inhibits Persistent Activity in Prefrontal Cortical Neurons

Ethanol Inhibits Persistent Activity in Prefrontal Cortical Neurons

Alcohol‐induced memory impairment in trace fear conditioning: A hippocampus‐specific effect

Differential Regulation of GABA_A Receptor Gene Expression by Ethanol in the Rat Hippocampus Versus Cerebral Cortex

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Effects of ethanol on nonspatial working memory and attention in rats.

Cited by 62 publications

References 33 publications

Ethanol Inhibits Persistent Activity in Prefrontal Cortical Neurons

Ethanol Inhibits Persistent Activity in Prefrontal Cortical Neurons

Alcohol‐induced memory impairment in trace fear conditioning: A hippocampus‐specific effect

Differential Regulation of GABAA Receptor Gene Expression by Ethanol in the Rat Hippocampus Versus Cerebral Cortex

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Differential Regulation of GABA_A Receptor Gene Expression by Ethanol in the Rat Hippocampus Versus Cerebral Cortex