Up-regulation of NMDA receptor subunits in rat brain following chronic ethanol treatment

Kalluri, Haviryaji S. G.; Mehta, Abhishek; Ticku, Maharaj K.

doi:10.1016/s0169-328x(98)00112-0

Cited by 177 publications

(132 citation statements)

References 21 publications

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“…Some previous reports support this viewpoint. For example, chronic ethanol treatment, which induces amnesia (Brioni et al 1989), up-regulates the expression of the NMDA receptor in vitro and in vivo (Henniger et al 2003;Kalluri et al 1998). Memory behavior is impaired in the Rett syndrome mice model even though hippocampal NR2B expression is increased (Asaka et al 2006).…”

Section: Discussionmentioning

confidence: 99%

Accumulated hippocampal formaldehyde induces age-dependent memory decline

Tong

Han

Luo

et al. 2012

AGE

187

151

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Aging is an important factor in memory decline in aged animals and humans and in Alzheimer's disease and is associated with the impairment of hippocampal long-term potentiation (LTP) and downregulation of NR1/NR2B expression. Gaseous formaldehyde exposure is known to induce animal memory loss and human cognitive decline; however, it is unclear whether the concentrations of endogenous formaldehyde are elevated in the hippocampus and how excess formaldehyde affects LTP and memory formation during the aging process. In the present study, we report that hippocampal formaldehyde accumulated in memorydeteriorating diseases such as age-related dementia. Spatial memory performance was gradually impaired in normal Sprague-Dawley rats by persistent intraperitoneal injection with formaldehyde. Furthermore, excess formaldehyde treatment suppressed the hippocampal LTP formation by blocking N-methyl-D-aspartate (NMDA) receptor. Chronic excess formaldehyde treatment over a period of 30 days markedly decreased the viability of the hippocampus and down-regulated the expression of the NR1 and NR2B subunits of the NMDA receptor. Our results indicate that excess endogenous formaldehyde is a critical factor in memory loss in age-related memory-deteriorating diseases.

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Section: Discussionmentioning

confidence: 99%

Accumulated hippocampal formaldehyde induces age-dependent memory decline

Tong

Han

Luo

et al. 2012

AGE

187

151

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“…Chronic alcohol treatment in vivo is known to up regulate NMDA receptor number with a concomitant increase in NMDA R1 polypeptide levels in several different regions of the brain (Trevisan et al1994;Snell et al, 1996a;Kalluri et al, 1998). Therefore we examined, by Western blotting, the effect of chronic alcohol exposure on the NMDA R1 polypeptide levels in hippocampus and cerebral cortex of mice.…”

Section: Discussionmentioning

confidence: 99%

“…Supplementing the alcohol containing liquid diet with regular rodent chow did not alter known effects of chronic alcohol exposure such as alcohol-mediated increase in (i) hepatic cytochrome P450 2E1 (Cyp 2E1) enzyme activity and apoprotein levels (Forkert et al, 1991), and (ii) polypeptide levels of the NMDA R1 receptor subunit in hippocampus and cerebral cortex (Trevisan et al, 1994;Snell et al, 1996a;Kalluri et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

Supplementing the liquid alcohol diet with chow enhances alcohol intake in C57 BL/6 mice

Anji

2008

Drug and Alcohol Dependence

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Background-Administration of alcohol-containing liquid diet is associated with body weight loss in rodents.Aim-of this study was to modify the alcohol-containing liquid diet paradigm to reduce the body weight loss in mice during the alcohol treatment period.Methods-Two sets of animals (Chow and No Chow groups) were exposed to chronic alcohol with a step-wise increase of alcohol in the diet. One set of control and alcohol exposed animals (Chow group) received chow during alcohol treatment. Food intake and body weight was measured every 24h. Level of intoxication was determined by measuring blood alcohol levels. Alcohol dependence of mice was determined by handling-induced convulsions (HIC) scoring. Chronic alcohol-mediated effects on brain and liver were examined.Results-Body weight loss was attenuated in chronic alcohol exposed mice in Chow group as compared to No Chow group. Chow group mice consumed higher amounts of alcohol diet resulting in higher blood alcohol levels. Brain NMDAR1 protein levels and liver Cyp2E1 levels were significantly enhanced in chronic alcohol-exposed mice in Chow and No Chow groups suggesting that known medical consequences of alcohol are not interfered with in our modified alcohol treatment paradigm. HIC in Chow and No Chow group mice peaked between 3h and 5h after alcohol withdrawal. However, the severity of alcohol withdrawal was greater in Chow group mice.Conclusions-Supplementing alcohol diet with chow not only attenuated body weight loss associated with alcohol intake in mice but also resulted in higher consumption of alcohol diet and higher blood alcohol levels. KeywordsC57 BL/6 mice; chronic alcohol treatment; handling-induced convulsions; NMDA R1 subunit; Cyp 2E1 enzyme activity

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“…NMDARs are a major site of ethanol action, and dependence, tolerance, and withdrawal symptoms may be mediated in part by NMDARs. A prominent electrophysiological effect of acute ethanol is a decrease in current generated by NMDAR activation (Criswell and Breese, 2005;Criswell et al, 2003;Fadda and Rossetti, 1998;Kalluri et al, 1998;Lovinger, 2002;Lovinger et al, 1989;Nie et al, 1994;Roberto et al, 2004b;Tabakoff and Hoffman, 1996;Tsai and Coyle, 1998;Woodward, 2000;Yang et al, 1996). The sensitivity of NMDAR channels to ethanol is dependent on the NR2 subunit expressed: for example, NMDARs with NR1/2A and NR1/2B subunits are the most sensitive to ethanol (Allgaier, 2002;Lovinger, 1995;Mirshahi and Woodward, 1995).…”

Section: Discussionmentioning

confidence: 99%

“…NMDARs are important sites of ethanol action (Carter et al, 1995;Lovinger et al, 1989) and are thought to mediate, in part, ethanol dependence, tolerance, and withdrawal (Darstein et al, 2000;Eckardt et al, 1998;Kalluri et al, 1998;Krystal et al, 1998;Narita et al, 2000). It has been demonstrated that NR2A-and NR2B-containing NMDARs are the most sensitive to ethanol (Allgaier, 2002;Lovinger, 1995;Masood et al, 1994;Mirshahi and Woodward, 1995).…”

Section: Introductionmentioning

confidence: 99%

Chronic Ethanol Exposure and Protracted Abstinence Alter NMDA Receptors in Central Amygdala

Roberto

Bajo

Crawford

et al. 2005

Neuropsychopharmacol

108

115

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We recently reported that chronic ethanol treatment (CET) and early withdrawal (2-8 h) altered glutamatergic transmission at both preand postsynaptic sites in central nucleus of the amygdala (CeA). Acute ethanol (44 mM) inhibited the NMDA receptor (NMDAR)-mediated EPSCs (NMDA-EPSCs) more in CeA neurons from CET rats than from naïve rats and also decreased paired-pulse facilitation (PPF) of NMDA-EPSCs only in CET rats. To determine whether these CET effects persisted after prolonged withdrawal, we recorded intracellularly in rat CeA slices and measured mRNA and protein expression of CeA NMDAR subunits from CET rats and those withdrawn from ethanol for 1 or 2 weeks. At 1 week withdrawal, acute ethanol decreased evoked NMDA-EPSC amplitudes and NMDA currents induced by exogenous NMDA (B20%) equally to that in naïve rats, indicating that CET effects on postsynaptic mechanisms reversed 1 week after CET cessation. However, acute ethanol still decreased PPF of NMDA-EPSCs, indicating that the acute ethanolinduced increase in glutamate release in CeA seen in CET rats was still present at this time. CET also significantly increased mRNA levels of NR1 and NR2B NMDAR subunits compared to control rats. At 1 week withdrawal, mRNA levels for NR1 and NR2B subunits were significantly decreased. These changes reversed at 2 weeks withdrawal. In Western blots, a significant increase in protein for all three subunits occurred in CeA from CET rats, but not after 1 and 2 weeks of withdrawal. These data indicate that CET induces reversible neuroadaptations in synaptic function, gene expression, and protein composition of NMDAR at CeA synapses. Neuropsychopharmacology (2006) 31, 988-996.

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Up-regulation of NMDA receptor subunits in rat brain following chronic ethanol treatment

Cited by 177 publications

References 21 publications

Accumulated hippocampal formaldehyde induces age-dependent memory decline

Accumulated hippocampal formaldehyde induces age-dependent memory decline

Supplementing the liquid alcohol diet with chow enhances alcohol intake in C57 BL/6 mice

Chronic Ethanol Exposure and Protracted Abstinence Alter NMDA Receptors in Central Amygdala

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