Effect of CGP39551 administration on the kindling of ethanol-withdrawal seizures

Ripley, Tamzin; Dunworth, Sarah J.; Stephens, David

doi:10.1007/s00213-002-1138-7

Cited by 12 publications

(7 citation statements)

References 33 publications

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“…This theory of kindling seizure activity was subsequently supported by several clinical investigations (Booth and Blow 1993;Brown et al 1988;Lechtenberg and Worner 1990, 1991Worner 1996). Work in rats showing that repeated withdrawals from chronic alcohol facilitate inferior collicular kindling afforded critical support for the kindling hypothesis (McCown and Breese 1990), as did other animal studies that demonstrated enhanced seizure susceptibility following repeated withdrawals (Baker and Cannon 1979;Becker and Hale 1993;Becker et al 1997Becker et al , 1998Clemmesen and Hemmingsen 1984;Kokka et al 1993;Maier and Pohorecky 1989;Meert and Huysmans 1994;Ripley et al 2002;Stephens et al 2001;Ulrichsen et al 1995Ulrichsen et al , 1998. This concept of "kindling" of seizure activity following repeated detoxifications has been a major advance, as it provided an appreciation of the necessity of progressive adaptive change preceding withdrawal-induced seizure activity in alcoholics.…”

Section: Concept Of Kindling Seizure Susceptibility With Repeated Witmentioning

confidence: 81%

Conceptual framework for the etiology of alcoholism: a ?kindling?/stress hypothesis

2004

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Rationale-The rationale for proposing the "kindling"/stress hypothesis is to provide a conceptual basis for the insidious development and maintenance of alcohol abuse.Objective and results-An objective of the hypothesis is to emphasize how continued alcohol abuse is linked to progressive neural adaptation. Work has shown that repeated withdrawals from chronic low levels of alcohol sensitize ("kindle") anxiety-like behavior ("anxiety") in rats, a finding consistent with multiple withdrawal kindling of seizure activity. Additionally, stress substitutes for initial cycles of the multiple withdrawal protocol to sensitize withdrawal-induced anxiety, which is indicative that stress is capable of facilitating neuroadaptive processes related to withdrawal. The persistence of adaptation caused by stress and multiple withdrawals is revealed by the appearance of withdrawal-induced anxiety following a future re-exposure to a single 5-day period of alcohol. This persisting adaptation also permits stress to induce anxiety during a period of abstinence-a response not observed in animals without previous exposure to alcohol. Furthermore, stress interacts with repeated withdrawals to enhance voluntary alcohol drinking. Results of other preclinical and clinical studies reported in the literature are integrated with these investigations in support of the proposed hypothesis.Conclusions-The "kindling"/stress hypothesis is based on the premise that repeated withdrawals from cycles of chronic alcohol exposure contribute to a progressive development of persisting adaptive change that sensitizes withdrawal-induced anxiety and allows stress to evoke symptoms associated with negative affect during abstinence. Thus, these consequences of repeated withdrawals account for the evolution of major characteristics of alcoholism, which include worsened acute withdrawal symptoms and increased stress-induced negative affect during abstinence, both of which enhance the likelihood of relapse-and with relapse an inability to limit an abusive pattern of alcohol intake. The "kindling"/stress hypothesis provides a clear strategy for future studies to explore the advancing neural adaptation proposed to contribute to the pathogenesis of alcoholism.

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Section: Concept Of Kindling Seizure Susceptibility With Repeated Witmentioning

confidence: 81%

Conceptual framework for the etiology of alcoholism: a ?kindling?/stress hypothesis

2004

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“…This procedure has been proven to be an effective and reliable method for producing functional dependence to ethanol (De Witte et al, 2003; Kliethermes et al, 2004; Nowak et al, 2006; Ripley et al, 2002). Briefly, mice were given a priming dose of ethanol (2 g/kg body wt, i.p.)…”

Section: Methodsmentioning

confidence: 99%

“…with ethanol, (b) ethanol exposure, (c) SR141716A treatment, and (d) vehicle administration. Mice were tested for severity of HIC 8 h following withdrawal from ethanol as previously described (Ripley et al, 2002). Briefly, animals were first lifted by the tail and body tremor and convulsions were assessed.…”

Section: Methodsmentioning

confidence: 99%

Genetic and pharmacological manipulations of the CB₁ receptor alter ethanol preference and dependence in ethanol preferring and nonpreferring mice

Vinod

Yalamanchili

Thanos

et al. 2008

Synapse

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Recent studies have indicated a role for the endocannabinoid system in ethanol-related behaviors. This study examined the effect of pharmacological activation, blockade, and genetic deletion of the CB 1 receptors on ethanol-drinking behavior in ethanol preferring C57BL/6J (B6) and ethanol nonpreferring DBA/2J (D2) mice. The deletion of CB 1 receptor significantly reduced the ethanol preference. Although the stimulation of the CB 1 receptor by CP-55,940 markedly increased the ethanol preference, this effect was found to be greater in B6 than in D2 mice. The antagonism of CB 1 receptor function by SR141716A led to a significant reduction in voluntary ethanol preference in B6 than D2 mice. A significant lower hypothermic and greater sedative response to acute ethanol administration was observed in both the strains of CB 1 -/-mice than wild-type mice. Interestingly, genetic deletion and pharmacological blockade of the CB 1 receptor produced a marked reduction in severity of handling-induced convulsion in both the strains. The radioligand binding studies revealed significantly higher levels of CB 1 receptor-stimulated G-protein activation in the striatum of B6 compared to D2 mice. Innate differences in the CB 1 receptor function might be one of the contributing factors for higher ethanol drinking behavior. The antagonists of the CB 1 receptor may have therapeutic potential in the treatment of ethanol dependence.

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“…The ethanol inhalation paradigm was employed to evaluate the handling-induced convulsions (HIC). This procedure has been proven to be an effective and reliable method for producing functional dependence to ethanol (Ripley et al 2002;Kliethermes et al 2004;Nowak et al 2006). Briefly, mice were given a priming dose of ethanol (2 g/kg body wt, i.p.)…”

Section: Handling-induced Convulsionsmentioning

confidence: 99%

Manipulation of fatty acid amide hydrolase functional activity alters sensitivity and dependence to ethanol

Vinod

Sanguino

Yalamanchili

et al. 2007

Journal of Neurochemistry

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The aim of this study was to examine the role of fatty acid amide hydrolase (FAAH) on ethanol sensitivity, preference, and dependence. The deletion of FAAH gene or the inhibition of FAAH by carbamoyl‐biphenyl‐3‐yl‐cyclohexylcarbamate (URB597) (0.1 mg/kg) markedly increased the preference for ethanol. The study further reveals that URB597 specifically acts through FAAH and that cannabinoid‐1 (CB1) receptor is critical for N‐arachidonoyl ethanolamide (AEA) mediated ethanol‐reinforced behavior as revealed by lack of URB597 effect in both FAAH and CB1−/− mice compared with vehicle‐treated −/− mice. The FAAH −/− mice displayed a lower sensitivity to hypothermic and sedative effects to acute ethanol challenge. The FAAH −/− mice also exhibited a reduction in the severity of handling‐induced convulsions following withdrawal from chronic ethanol exposure. The CB1 receptor and proenkephalin gene expressions, and CB1 receptor and μ‐opioid (MO) receptor‐mediated G‐protein activation were found to be significantly lower in the caudate‐putamen, nucleus accumbens core and shell of FAAH −/− than +/+ mice. Interestingly, the MO receptor‐stimulated G‐protein signaling was greater in the striatum of FAAH −/− than +/+ mice following voluntary ethanol consumption. These findings suggest that an elevation in the AEA content and its action on the limbic CB1 receptor and MO receptor might contribute to ethanol‐reinforced behavior. Treatment with drugs that decrease AEA tone might prove useful in reducing excessive ethanol consumption.

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Effect of CGP39551 administration on the kindling of ethanol-withdrawal seizures

Abstract: Treatment with an NMDA receptor-competitive antagonist potentiated the ethanol-withdrawal syndrome in animals with previous experience of ethanol withdrawal.

Cited by 12 publications

References 33 publications

Conceptual framework for the etiology of alcoholism: a ?kindling?/stress hypothesis

Conceptual framework for the etiology of alcoholism: a ?kindling?/stress hypothesis

Genetic and pharmacological manipulations of the CB₁ receptor alter ethanol preference and dependence in ethanol preferring and nonpreferring mice

Manipulation of fatty acid amide hydrolase functional activity alters sensitivity and dependence to ethanol

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Effect of CGP39551 administration on the kindling of ethanol-withdrawal seizures

Abstract: Treatment with an NMDA receptor-competitive antagonist potentiated the ethanol-withdrawal syndrome in animals with previous experience of ethanol withdrawal.

Cited by 12 publications

References 33 publications

Conceptual framework for the etiology of alcoholism: a ?kindling?/stress hypothesis

Conceptual framework for the etiology of alcoholism: a ?kindling?/stress hypothesis

Genetic and pharmacological manipulations of the CB1 receptor alter ethanol preference and dependence in ethanol preferring and nonpreferring mice

Manipulation of fatty acid amide hydrolase functional activity alters sensitivity and dependence to ethanol

Contact Info

Product

Resources

About

Genetic and pharmacological manipulations of the CB₁ receptor alter ethanol preference and dependence in ethanol preferring and nonpreferring mice