Ethanol inhibition of NMDA-induced responses and acute tolerance to the inhibition in rat rostral ventrolateral medulla in vivo: Involvement of cAMP-dependent protein kinases

Lin, Hsun-Hsun; Chang, Shinn‐Jen; Shie, Hui-Jhan; Lai, Chih-Chia

doi:10.1016/j.neuropharm.2006.05.018

Cited by 23 publications

(24 citation statements)

References 30 publications

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“…Furthermore, the observation that a high concentration of ethanol (60 mM) did not occlude NAc LTD is consistent with the idea that such concentrations of ethanol can induce dopamine release (Brodie et al, 1990(Brodie et al, , 1999 and DARPP-32 phosphorylation directly (Maldve et al, 2002). Both of these effects therefore increase Ser897-NR1 phosphorylation and thereby decrease ethanol sensitivity of NMDA receptors (Maldve et al, 2002;Zhang et al, 2005;Lin et al, 2006). Therefore, the observation of NAc LTD in the presence of a high concentration of ethanol, which is occluded by D1 receptor inhibition, is consistent with prior observations.…”

Section: Ethanol Occludes Ltd In the Nucleus Accumbenssupporting

confidence: 85%

“…Our lab and others previously observed that activation of D1 receptors strongly suppressed the inhibitory effects of ethanol on NMDA receptor-mediated synaptic transmission dependent on activation of DARPP-32 and phosphorylation of Ser897 of the NR1 subunit (Maldve et al, 2002;Zhang et al, 2005;Lin et al, 2006; but also see Xu and Woodward, 2006).…”

Section: Ethanol Occludes Ltd In the Nucleus Accumbensmentioning

confidence: 71%

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In Vivo Chronic Intermittent Ethanol Exposure Reverses the Polarity of Synaptic Plasticity in the Nucleus Accumbens Shell

Jeanes

Buske

Morrisett³

2010

J Pharmacol Exp Ther

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Glutamatergic synaptic plasticity in the nucleus accumbens (NAc) is implicated in response to sensitization to psychomotor-stimulating agents, yet ethanol effects here are undefined. We studied the acute in vitro and in vivo effects of ethanol in medium spiny neurons from the shell NAc subregion of slices of C57BL/6 mice by using whole-cell voltage-clamp recordings of ␣-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid (AMPA) excitatory postsynaptic current (EPSCs). Synaptic conditioning (low-frequency stimulation with concurrent postsynaptic depolarization) reliably depressed AMPA EPSCs by nearly 30%; this accumbal long-term depression (LTD) was blocked by a nonselective N-methyl-D-aspartate (NMDA) receptor antagonist (DL-2-amino-5-phosphonovaleric acid) and a selective NMDA receptor 2B antagonist [R-(R*,S*)-␣-(4-hydroxyphenyl)-␤-methyl-4-(phenylmethyl)-1-piperidine propanol]. Acute ethanol exposure inhibited the depression of AMPA EPSCs differentially with increasing concentrations, but this inhibitory action of ethanol was occluded by a D1-selective dopamine receptor agonist. Ethanol dependence was elicited in C57BL/6 mice by two separate 4-day bouts of chronic intermittent ethanol (CIE) vapor exposure. When assessed 24 h after a single bout of in vivo CIE vapor exposure, NAc LTD was absent, and instead NMDA receptor-dependent synaptic potentiation [long-term potentiation (LTP)] was reliably observed. It is noteworthy that both LTP and LTD were completely absent after an extended withdrawal (72 h) after a single 3-day CIE vapor bout. These observations demonstrate that 1) accumbal synaptic depression is mediated by NR2B receptors, 2) accumbal synaptic depression is highly sensitive to both acute and chronic ethanol exposure, and 3) alterations in this synaptic process may constitute a neural adaptation that contributes to the induction and/or expression of ethanol dependence.

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Section: Ethanol Occludes Ltd In the Nucleus Accumbenssupporting

confidence: 85%

Section: Ethanol Occludes Ltd In the Nucleus Accumbensmentioning

confidence: 71%

In Vivo Chronic Intermittent Ethanol Exposure Reverses the Polarity of Synaptic Plasticity in the Nucleus Accumbens Shell

Jeanes

Buske

Morrisett³

2010

J Pharmacol Exp Ther

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“…Finally, to fully understand the acute actions of ethanol and how these change across different time courses of ethanol consumption, it will be important to assess changes downstream from these receptors. Again, there is substantial precedence for investigating these cellular processes (Lin et al, 2006;Choi et al, 2008;Hellmann et al, 2009;Wu et al, 2011). …”

Section: Future Directionsmentioning

confidence: 99%

Assessing ethanol's actions in the suprachiasmatic circadian clock using in vivo and in vitro approaches

Prosser

Glass

2015

Alcohol

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Research over the past decade has demonstrated substantial interactions between the circadian system and the processes through which alcohol affects behavior and physiology. Here we summarize the results of our collaborative efforts focused on this intersection. Using a combination of in vivo and in vitro approaches, we have shown that ethanol affects many aspects of the mammalian circadian system, both acutely as well as after chronic administration. Conversely, we have shown circadian influences on ethanol consumption. Importantly, we are beginning to delve into the cellular mechanisms associated with these effects. We are also starting to form a picture of the neuroanatomical bases for many of these actions. Finally, we put our current findings into perspective by suggesting new avenues of inquiry for our future efforts.

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“…Expression assays using alcoholic rats indicated apoptotic genes could be up-or down-regulated upon ethanol exposure (McBride et al 2005), but this could also be part of a chronic rather than acute response. The cAMP/PKA signaling pathway is often connected to ethanol sensitivity (Mailliard and Diamond 2004;Lin et al 2006;Newton and Messing 2006). A candidate from eth-2 (GB13577) encodes adenosine deaminase, an enzyme involved in purine metabolism.…”

Section: Ethanol Absorption and Metabolismmentioning

confidence: 99%

Identification of Quantitative Trait Loci and Candidate Genes Influencing Ethanol Sensitivity in Honey Bees

Ammons

Hunt

2008

Behav Genet

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Invertebrate models have greatly furthered our understanding of ethanol sensitivity and alcohol addiction. The honey bee (Apis mellifera), a widely used behavioral model, is valuable for comparative studies. A quantitative trait locus (QTL) mapping experiment was designed to identify QTL and genes influencing ethanol vapor sensitivity. A backcross mating between ethanol-sensitive and resistant lines resulted in worker offspring that were tested for sensitivity to the sedative effects of alcohol. A linkage map was constructed with over 500 amplified fragment length polymorphism (AFLP) and sequence-tagged site (STS) markers. Four QTL were identified from three linkage groups with log of odds ratio (LOD) scores of 2.28, 2.26, 2.23, and 2.02. DNA from markers within and near QTL were cloned and sequenced, and this data was utilized to integrate our map with the physical honey bee genome. Many candidate genes were identified that influence synaptic transmission, neuronal growth, and detoxification. Others affect lipid synthesis, apoptosis, alcohol metabolism, cAMP signaling, and electron transport. These results are relevant because they present the first search for QTL that affect resistance to acute ethanol exposure in an invertebrate, could be useful for comparative genomic purposes, and lend credence to the use of honey bees as biomedical models of alcohol metabolism and sensitivity.

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Ethanol inhibition of NMDA-induced responses and acute tolerance to the inhibition in rat rostral ventrolateral medulla in vivo: Involvement of cAMP-dependent protein kinases

Cited by 23 publications

References 30 publications

In Vivo Chronic Intermittent Ethanol Exposure Reverses the Polarity of Synaptic Plasticity in the Nucleus Accumbens Shell

In Vivo Chronic Intermittent Ethanol Exposure Reverses the Polarity of Synaptic Plasticity in the Nucleus Accumbens Shell

Assessing ethanol's actions in the suprachiasmatic circadian clock using in vivo and in vitro approaches

Identification of Quantitative Trait Loci and Candidate Genes Influencing Ethanol Sensitivity in Honey Bees

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