Ethanol, memory, and hippocampal function: A review of recent findings

White, Aaron M.; Matthews, Douglas B.; Best, Phillip J.

doi:10.1002/(sici)1098-1063(2000)10:1<88::aid-hipo10>3.0.co;2-l

Cited by 229 publications

(109 citation statements)

References 99 publications

(123 reference statements)

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“…Nicotine acts primarily at nACh receptors, whereas ethanol acts on a wide variety of targets that include nAChRs (Bowers et al 2005;Escher and Mittleman 2004;Larsson et al 2002;Melia et al 1996;Meyerhoff et al 2006;Wehner et al 2004;White et al 2000). Thus, ethanol may directly interact with nicotine by altering nAChR function; in support, ethanol stabilizes the open state of nAChRs, producing a twofold leftward shift in the acetylcholine response curve (Forman and Zhou 1999).…”

Section: Discussionmentioning

confidence: 99%

“…Thus, ethanol may directly interact with nicotine by altering nAChR function; in support, ethanol stabilizes the open state of nAChRs, producing a twofold leftward shift in the acetylcholine response curve (Forman and Zhou 1999). Ethanol also acts on many other receptors, including GABA A and glutamatergic NMDA receptors (for review see White et al 2000), and nAChRs have been shown to modulate both GABAergic and glutamatergic function (Alkondon and Albuquerque 2001;Gray et al 1996). Thus, ethanol and nicotine may interact by modulating GABAergic and glutamatergic function.…”

Section: Discussionmentioning

confidence: 99%

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Interactive effects of ethanol and nicotine on learning in C57BL/6J mice depend on both dose and duration of treatment

Gulick

Gould

2007

Psychopharmacology

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Objective and rationale-Alcohol and nicotine are commonly co-abused; one possible explanation for co-abuse is that each drug ameliorates the aversive effects of the other. Both drugs have dose-dependent effects on learning and memory. Thus, this study examined the interactive effects of acute ethanol and acute, chronic, or withdrawal from chronic nicotine on fear conditioning in C57BL/6J mice.Materials and methods-Conditioning consisted of auditory conditioned stimulus-foot-shock unconditioned stimulus pairings. For acute studies, saline or ethanol, then saline or nicotine was administered before training, and saline or nicotine was also administered before testing. For chronic and withdrawal studies, saline or nicotine was administered chronically, and ethanol or saline was administered before training.Results-Acute nicotine (0.09 mg/kg) reversed ethanol-induced deficits (1.0 and 1.5 g/kg) in contextual and cued fear conditioning, whereas a low dose of ethanol (0.25 g/kg) reversed nicotine (6.3 mg kg −1 day −1 ) withdrawal-induced deficits in contextual conditioning. Tolerance developed for the effects of nicotine on ethanol-induced deficits in conditioning and cross-tolerance between chronic nicotine and acute ethanol was seen for the enhancing effects of ethanol on conditioning.Conclusions-The complex and sometimes polar actions of ethanol and nicotine on behavior may contribute to co-abuse of these drugs. Specifically, smoking may initially reduce the aversive effects of ethanol, but tolerance develops for this effect. In addition, low doses of alcohol may lessen nicotine withdrawal symptoms.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Interactive effects of ethanol and nicotine on learning in C57BL/6J mice depend on both dose and duration of treatment

Gulick

Gould

2007

Psychopharmacology

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“…whole-cell currents | null mutant mice A lcohol-induced memory deficits have been well documented in humans, as well as animal studies (1). Long-term potentiation (LTP) is widely accepted as a cellular mechanism underlying learning and memory in the hippocampus, as well as other brain regions (2), and is dependent upon NMDA receptor (NMDAR) activation (3).…”

mentioning

confidence: 99%

Alcohol inhibition of the NMDA receptor function, long-term potentiation, and fear learning requires striatal-enriched protein tyrosine phosphatase

Hicklin¹,

Radcliffe

et al. 2011

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

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Alcohol's deleterious effects on memory are well known. Acute alcohol-induced memory loss is thought to occur via inhibition of NMDA receptor (NMDAR)-dependent long-term potentiation in the hippocampus. We reported previously that ethanol inhibition of NMDAR function and long-term potentiation is correlated with a reduction in the phosphorylation of Tyr 1472 on the NR2B subunit and ethanol's inhibition of the NMDAR field excitatory postsynaptic potential was attenuated by a broad spectrum tyrosine phosphatase inhibitor. These data suggested that ethanol's inhibitory effect may involve protein tyrosine phosphatases. Here we demonstrate that the loss of striatal-enriched protein tyrosine phosphatase (STEP) renders NMDAR function, phosphorylation, and long-term potentiation, as well as fear conditioning, less sensitive to ethanol inhibition. Moreover, the ethanol inhibition was "rescued" when the active STEP protein was reintroduced into the cells. Taken together, our data suggest that STEP contributes to ethanol inhibition of NMDAR function via dephosphorylation of tyrosine sites on NR2B receptors and lend support to the hypothesis that STEP may be required for ethanol's amnesic effects.whole-cell currents | null mutant mice A lcohol-induced memory deficits have been well documented in humans, as well as animal studies (1). Long-term potentiation (LTP) is widely accepted as a cellular mechanism underlying learning and memory in the hippocampus, as well as other brain regions (2), and is dependent upon NMDA receptor (NMDAR) activation (3). Acute ethanol application in adult rodents inhibits NMDAR channel activity (4, 5). Ethanol's inhibitory effect on NMDARs is widely thought to underlie both the blockade of LTP and the acute amnesic effects of ethanol. Moreover, recent work suggests that ethanol's effect on the NMDAR may play a role in the addictive nature of ethanol (6, 7).NMDARs in the hippocampus consist of mainly NR1/NR2A, NR1/NR2B, and NR1/NR2A/NR2B receptor-subunit complexes (8). Although NR1 subunits are required to form an active ion channel, incorporation of the various NR2 subunits regulate NMDAR channel activity by altering the channel kinetics and mediating the differential effects of pharmacological agents, including alcohol (9-11). It has previously been shown that activation of members of the Src-family of kinases (SFKs) enhances NMDAR currents (12). Previous studies have demonstrated a correlation between ethanol inhibition of NMDAR function and dephosphorylation of tyrosine residues on the NR2A and NR2B subunits (13). In particular, ethanol was found to reduce the phosphorylation of a site on the NR2B subunit Tyr 1472 that has been shown to regulate endocytosis and function of NMDARs (14,15). Inhibition of protein tyrosine phosphatase activity using a nonspecific inhibitor, bpV(phen), significantly reduced ethanol inhibition of NMDAR field excitatory postsynaptic potentials (fEPSPs), suggesting that ethanol may inhibit NMDARs via activation of a tyrosine phosphatase (13). FerraniKile et al. indepe...

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“…Recent research using animal models has shown that alcohol profoundly suppresses the activity of pyramidal cells in the region of the hippocampus that has been associated with ability to form new explicit memories [7]. Much is known about the effects of alcohol on decrements in motor performance, and there is also compelling evidence to indicate that acute alcohol use impairs the performance of frontal lobe-mediated tasks such as those that require judgment and impulse control [8].…”

Section: Central Pattern Generators (Cpgs)mentioning

confidence: 99%

Role of the Expert Witness in Sleep-Related Violence Trials

Bornemann

2008

AMA Journal of Ethics

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Ethanol, memory, and hippocampal function: A review of recent findings

Cited by 229 publications

References 99 publications

Interactive effects of ethanol and nicotine on learning in C57BL/6J mice depend on both dose and duration of treatment

Interactive effects of ethanol and nicotine on learning in C57BL/6J mice depend on both dose and duration of treatment

Alcohol inhibition of the NMDA receptor function, long-term potentiation, and fear learning requires striatal-enriched protein tyrosine phosphatase

Role of the Expert Witness in Sleep-Related Violence Trials

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