Acute Ethanol Impairs Spatial Memory But Not Stimulus/Response Memory in the Rat

Matthews, Douglas B.; Simson, Peter E.; Best, Phillip J.

doi:10.1111/j.1530-0277.1995.tb00965.x

Cited by 97 publications

(46 citation statements)

References 16 publications

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“…While many reports have suggested the dorsal hippocampus as the main site for modulation of memory (59,63), accumulating evidence have proposed that NAc or other sites of the brain may be involved in memory processes (7). According to the present data, the pre-training or pre-test injection of ethanol could decrease the step-through latency in a dose-dependent manner when animals were tested following 24 h. Other investigations have similarly shown that the pre-training ethanol inhibits the acquisition of memory in different paradigms such as inhibitory avoidance (7,8), working (9) and spatial memory (10)(11)(12).Our findings also showed that administration of the same dose of ethanol before retention, reverses the ethanol-induced amnesia. This phenomenon, called ethanol statedependent learning, has previously been studied in our laboratory (6)(7)(8) and by others as well.…”

Section: Discussionsupporting

confidence: 47%

“…Both ethanol and nicotine can potentially activate the mesolimbic dopaminergic system projecting from the ventral tegmental area to the nucleus accumbens, hippocampus, amygdala and the prefrontal cortex. These drugs have therefore an important role in reward and rewardrelated learning (3).The impairing effects of ethanol on learning and memory have been well-established in different experimental models (4)(5)(6)including the inhibitory avoidance (7,8), working (9) and spatial memory (10)(11)(12). In agreement with some earlier reports (4,13,14), we noticed that ethanol, when administered both pre-and post-training, can impair inhibitory avoidance memory in a state-dependent manner, and the effect is reversible by pre-test ethanol treatment.…”

Section: Introductionmentioning

confidence: 99%

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Activation of the Nitric-Oxide System in Nucleus Accumbens Inhibits the Nicotine Reversal Effects upon Ethanol-Induced Amnesia

Raoufi¹,

Moshfegh²,

Piri³

et al. 2016

Journal of Advanced Medical Sciences and Applied Technologies

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The present study investigated the possible involvement of the nucleus accumbens' (NAc) nitric oxide system in nicotine's reversal effect upon ethanol-induced amnesia. The hypothesis was tested through ethanol state-dependent memory assessment in adult male Wistar rats. Bilateral chronic cannulae were implanted in the NAc and the animals were trained in a step-through type inhibitory avoidance memory task. The step-through latency was examined 24 h after animals' training. The pre-training or pre-test intraperitoneal (i.p.) injection of ethanol (0.9 g/kg) decreased the step-through latency, indicating an amnesic effect of the drug. Meanwhile, the pre-test administration of ethanol (0.6 and 0.9 g/kg) could reverse the pre-training ethanol (0.9 g/kg)-induced amnesia, suggesting a state-dependent effect. Similar to ethanol, the pre-test intra-NAc microinjection of nicotine (0.25 and 0.5 µg/rat) alone or nicotine (0.1, 0.25 and 0.5 µg/mouse, intra-NAc) in combination with an ineffective dose of ethanol (0.3 g/kg) could significantly reverse the (pre-training) ethanol-induced memory impairment. The ethanol (0.9 g/kg)-induced amnesia was similarly prevented following the pre-test intra-NAc administration of a nitric oxide synthase (NOS) inhibitor, L-NAME (0.4 and 0.8 µg/rat). Of note, the co-administration of L-NAME (0.04 and 0.08 µg/rat, intra-NAc) with an ineffective dose of nicotine (0.1 µg/rat, intra-NAc) could significantly potentiate the memoryimproving effect of nicotine on ethanol-induced amnesia and resembled the effects of pretest administration of a higher dose of nicotine. Furthermore, while the pre-test intra-NAc injection of L-NAME impaired the memory retrieval by itself, the pre-test intra-NAc administration of L-arginine, a nitric oxide precursor (0.3 and 0.6 µg/rat, intra-NAc), did not exert any effect either alone or in combination with an effective dose of nicotine (0.5 µg/rat, intra-NAc) on pre-training ethanol-induced memory impairment. Our findings indicated a possible role of the nucleus accumbens' nitric oxide system in the improving effects of nicotine on ethanol-induced amnesia and the related state-dependent learning.

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Section: Discussionsupporting

confidence: 47%

Section: Introductionmentioning

confidence: 99%

Activation of the Nitric-Oxide System in Nucleus Accumbens Inhibits the Nicotine Reversal Effects upon Ethanol-Induced Amnesia

Raoufi¹,

Moshfegh²,

Piri³

et al. 2016

Journal of Advanced Medical Sciences and Applied Technologies

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“…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: 97%

“…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%

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).…”

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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

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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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Acute Ethanol Impairs Spatial Memory But Not Stimulus/Response Memory in the Rat

Cited by 97 publications

References 16 publications

Activation of the Nitric-Oxide System in Nucleus Accumbens Inhibits the Nicotine Reversal Effects upon Ethanol-Induced Amnesia

Activation of the Nitric-Oxide System in Nucleus Accumbens Inhibits the Nicotine Reversal Effects upon Ethanol-Induced Amnesia

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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Acute Ethanol Impairs Spatial Memory But Not Stimulus/Response Memory in the Rat

Cited by 97 publications

References 16 publications

Activation of the Nitric-Oxide System in Nucleus Accumbens Inhibits the Nicotine Reversal Effects upon Ethanol-Induced Amnesia

Activation of the Nitric-Oxide System in Nucleus Accumbens Inhibits the Nicotine Reversal Effects upon Ethanol-Induced Amnesia

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