Effect of NMDA antagonists, an NMDA agonist, and serotonin depletion on acute tolerance to ethanol

Khanna, J. M.; Morato, Gina Struffaldi; Kalant, H.

doi:10.1016/s0091-3057(01)00773-0

Cited by 37 publications

(40 citation statements)

References 35 publications

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“…Together, these 2 sets of data add evidence to the hypothesis that the decline in ethanol-related social impairment from 5 to 30 minutes after administration in the younger animals (P28, P35) reflects a rapid emergence of acute tolerance at these ages. This hypothesis was further examined in Experiment 3 by evaluating expression of acute tolerance, as indexed by an increasing dissociation between ethanol levels in blood or brain and a more rapid decline in ethanol-induced impairment following a given dose of ethanol (Khanna et al, 2002;Radlow, 1994). Therefore, the relationship between BrECs and degree of social impairment was assessed in individual animals at P28, P35, P42, and P70 during the early recovery period following acute ethanol challenge.…”

Section: Experiments 3 Acute Tolerance To Ethanol-induced Social Impamentioning

confidence: 99%

“…For instance, to the extent that acute tolerance is a linear process with time, this tolerance can be indexed by the increasing dissociation between BEC and ethanol-induced impairment following a given dose of ethanol, with ethanolinduced impairment declining more rapidly than BECs (Khanna et al, 2002;Radlow, 1994). There is experimental evidence, however, that acute tolerance to some ethanol effects emerges extremely rapidly and may be seen within minutes following ethanol administration in both electrophysiological (Palmer et al, 1992;Pearson et al, 1997;Sorensen et al, 1980) and behavioral studies Gill and Deitrich, 1998).…”

Section: Introductionmentioning

confidence: 99%

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Ontogeny of Acute Tolerance to Ethanol‐Induced Social Inhibition in Sprague–Dawley Rats

Varlinskaya

Spear

2006

Alcoholism Clin & Exp Res

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Background-Adolescent rats are less sensitive than adults to a number of acute effects of ethanol, including ethanol-induced social inhibition. Adolescent insensitivity to the suppressing effects of ethanol on social interactions could be related in part to age differences in compensatory responses, including acute tolerance, that serve to counteract these inhibitory effects of ethanol. The present study explored ontogenetic development of acute tolerance within 30 minutes after administration of a relatively low ethanol dose, using ethanol-induced social impairment as the target response measure.

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Section: Experiments 3 Acute Tolerance To Ethanol-induced Social Impamentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Ontogeny of Acute Tolerance to Ethanol‐Induced Social Inhibition in Sprague–Dawley Rats

Varlinskaya

Spear

2006

Alcoholism Clin & Exp Res

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“…This effectively reduces peak levels and accelerates elimination rates [45]. The pharmacodynamic changes are secondary to neuroreceptor effects at serotonergic, stimulatory (such as NMDA), and inhibitory (such as GABA) receptors [46,47]. The changes that occur at neuroreceptors are complex and involve a blunted physiologic response from escalating ethanol doses.…”

Section: Tolerancementioning

confidence: 99%

The clinical significance of variations in ethanol toxicokinetics

2007

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Introduction: Many variables affect the interpretation of an isolated ethanol level in an acutely intoxicated patient. This review demonstrates the significant variability in metabolism and elimination of ethanol, how it can differ between individuals, and the clinical importance of these variables.Discussion: Isolated ethanol values in a clinical scenario are only a snapshot of a dynamic process. The individual pharmacokinetic differences of people make it extremely difficult to estimate ethanol elimination rates or calculate previous ethanol concentrations at the time of an accident because of medical-legal reasons. Not only are the techniques used in measuring ethanol concentrations in bodily fluids (blood, serum, breath, and urine) not equivalent, but also the units used to report ethanol concentrations are often misinterpreted. Acute and chronic tolerance and social adaptive changes make interpreting this isolated ethanol level extremely difficult. The purpose of this review is to enable the clinician to appropriately interpret ethanol concentrations. Conclusion:The clinical evaluation of a patient's inebriation is always more reliable than an isolated ethanol level for determining disposition. Only an estimation of a current serum ethanol level can be made if the blood draw was performed hours earlier. This review is clinically important because it shows the clinically significant variability in metabolism and elimination of ethanol and how it can differ between individuals. It will also describe different ways to measure ethanol concentrations and how to compare them. Finally, the interpretation of isolated ethanol levels will be discussed.

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“…Functional (pharmacodynamic) alcohol tolerance manifests itself in three different forms: chronic (Tabakoff et al, 1986), rapid (Khanna et al, 2002), or acute (Mellanby, 1919). Acute functional tolerance (AFT) refers to the tolerance that is manifested during a single session of alcohol drinking (Mellanby, 1919), and it can start to develop within minutes after an individual starts to imbibe alcohol.…”

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confidence: 99%

Genomic Insights into Acute Alcohol Tolerance

Saba²,

Kechris³

et al. 2008

J Pharmacol Exp Ther

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Alcohol "sensitivity" has been proposed as a predictive factor for development of alcohol dependence (Schuckit et al., 2005). Most measures of alcohol sensitivity in humans and animals include a component that can be ascribed to acute functional tolerance (AFT). AFT is a form of tolerance that develops within a single period of alcohol exposure and has a genetic component. We used microarray technology as well as quantitative trait locus analysis of phenotypic and gene expression data across 30 BXD recombinant inbred strains of mice, 20 inbred strains of mice, and two replicate lines of mice selectively bred for differences in AFT, to identify differentially expressed candidate genes that contribute to predisposition to AFT. Eight candidate genes were identified by our statistical and filtering methods. The location of brain expression of these genes was mapped using the Allen Brain Atlas (http://www.brainmap.org), and the transcript location and molecular pathway analysis indicated that brain structures and biochemical pathways implicated in long-term potentiation and memory might also participate in the generation of acute functional alcohol tolerance.The term ethanol (alcohol) tolerance refers to a decreased behavioral response to a given dose of alcohol after prior experience with alcohol or the need for a greater dose of ethanol to produce a given level of effect. Alcohol tolerance is an important diagnostic criterion for alcohol dependence in the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) (American Psychiatric Association, 1994).Functional (pharmacodynamic) alcohol tolerance manifests itself in three different forms: chronic (Tabakoff et al., 1986), rapid (Khanna et al., 2002), or acute (Mellanby, 1919. Acute functional tolerance (AFT) refers to the tolerance that is manifested during a single session of alcohol drinking (Mellanby, 1919), and it can start to develop within minutes after an individual starts to imbibe alcohol. The phenomenon of AFT was initially described by Mellanby (1919) through experiments that showed that humans display a greater degree of intoxication at a given blood alcohol concentration on the rising phase of the blood alcohol curve than at the same alcohol concentration on the falling phase of the blood alcohol curve. Acute functional alcohol tolerance is a neuronal resistance to alcohol effects (Tabakoff et al., 1986); however, its molecular mechanism is still not well characterized.Sons of alcoholics (SOA) are three to five times more likely to develop alcohol dependence than sons of nonalcoholics (Cotton, 1979). SOA also display less alcohol intoxication when measurements are made at least 1 h after drinking alcohol. The low level of response to alcohol has been found to predict future alcohol dependence (Schuckit et al., 2005), and both men and women with no prior history of alcohol dependence, but with a positive family history of alcohol dependence, display a lower response to alcohol than those with no family history of alcohol dependence (Schuck...

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Effect of NMDA antagonists, an NMDA agonist, and serotonin depletion on acute tolerance to ethanol

Cited by 37 publications

References 35 publications

Ontogeny of Acute Tolerance to Ethanol‐Induced Social Inhibition in Sprague–Dawley Rats

Ontogeny of Acute Tolerance to Ethanol‐Induced Social Inhibition in Sprague–Dawley Rats

The clinical significance of variations in ethanol toxicokinetics

Genomic Insights into Acute Alcohol Tolerance

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