Timing-dependent reduction in ethanol sedation and drinking preference by NMDA receptor co-agonist d-serine

Lockridge, Amber; Romero, Gabriel E.; Harrington, Justin; Newland, Brett; Gong, Zi; Cameron, Andrew; Li, Yuan

doi:10.1016/j.alcohol.2011.11.004

Cited by 13 publications

(12 citation statements)

References 67 publications

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“…This study also showed that administration of d-serine prior to alcohol exposure prolonged the latency of the loss of righting reflex and shortened the duration of the reflex (Lockridge et al, 2012). Interestingly, a significant decrease in alcohol preference has been reported in mice treated with d-serine (Lockridge et al, 2012). Together, targeting NMDA receptor could be a potential therapeutic approach for treatment of AUD.…”

Section: Glutamate Receptors In Audmentioning

confidence: 74%

“…However, the effects of NMDA receptor agonists on alcohol intoxication have not been well studied yet. A study used d-serine as an agonist to overstimulate the NMDA receptors and counteract the alcohol intoxicating effects (Lockridge et al, 2012). This study also showed that administration of d-serine prior to alcohol exposure prolonged the latency of the loss of righting reflex and shortened the duration of the reflex (Lockridge et al, 2012).…”

Section: Glutamate Receptors In Audmentioning

confidence: 99%

“…A study used d-serine as an agonist to overstimulate the NMDA receptors and counteract the alcohol intoxicating effects (Lockridge et al, 2012). This study also showed that administration of d-serine prior to alcohol exposure prolonged the latency of the loss of righting reflex and shortened the duration of the reflex (Lockridge et al, 2012). Interestingly, a significant decrease in alcohol preference has been reported in mice treated with d-serine (Lockridge et al, 2012).…”

Section: Glutamate Receptors In Audmentioning

confidence: 99%

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Metabotropic and ionotropic glutamate receptors as potential targets for the treatment of alcohol use disorder

Goodwani

Saternos

Alasmari

et al. 2017

Neuroscience & Biobehavioral Reviews

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Emerging evidence indicates that dysfunctional glutamate neurotransmission is critical in the initiation and development of alcohol and drug dependence. Alcohol consumption induced downregulation of glutamate transporter 1 (GLT-1) as reported in previous studies from our laboratory. Glutamate is the major excitatory neurotransmitter in the brain, which acts via interactions with several glutamate receptors. Alcohol consumption interferes with the glutamatergic signal transmission by altering the functions of these receptors. Among the glutamatergic receptors involved in alcohol-drinking behavior are the metabotropic receptors such as mGluR1/5, mGluR2/3, and mGluR7, as well as the ionotropic receptors, NMDA and AMPA. Preclinical studies using agonists and antagonists implicate these glutamatergic receptors in the development of alcohol use disorder (AUD). Therefore, the purpose of this review is to discuss the neurocircuitry involving glutamate transmission in animals exposed to alcohol and further outline the role of metabotropic and ionotropic receptors in the regulation of alcohol-drinking behavior. This review provides ample information about the potential therapeutic role of glutamatergic receptors for the treatment of AUD.

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Section: Glutamate Receptors In Audmentioning

confidence: 74%

Section: Glutamate Receptors In Audmentioning

confidence: 99%

Section: Glutamate Receptors In Audmentioning

confidence: 99%

See 1 more Smart Citation

Metabotropic and ionotropic glutamate receptors as potential targets for the treatment of alcohol use disorder

Goodwani

Saternos

Alasmari

et al. 2017

Neuroscience & Biobehavioral Reviews

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“…The studies are unequivocal that NMDA and AMPA regulate 2BC drinking, and both competitive and non-competitive GluN antagonists reduce 2BC intake 13– 15 . For example, NMDA and AMPA infused into the lateral hypothalamus can both increase 2BC consumption 14 .…”

Section: Low-level Drinkingmentioning

confidence: 95%

Glutamate plasticity woven through the progression to alcohol use disorder: a multi-circuit perspective

2017

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Glutamate signaling in the brain is one of the most studied targets in the alcohol research field. Here, we report the current understanding of how the excitatory neurotransmitter glutamate, its receptors, and its transporters are involved in low, episodic, and heavy alcohol use. Specific animal behavior protocols can be used to assess these different drinking levels, including two-bottle choice, operant self-administration, drinking in the dark, the alcohol deprivation effect, intermittent access to alcohol, and chronic intermittent ethanol vapor inhalation. Importantly, these methods are not limited to a specific category, since they can be interchanged to assess different states in the development from low to heavy drinking. We encourage a circuit-based perspective beyond the classic mesolimbic-centric view, as multiple structures are dynamically engaged during the transition from positive- to negative-related reinforcement to drive alcohol drinking. During this shift from lower-level alcohol drinking to heavy alcohol use, there appears to be a shift from metabotropic glutamate receptor-dependent behaviors to N-methyl-D-aspartate receptor-related processes. Despite high efficacy of the glutamate-related pharmaceutical acamprosate in animal models of drinking, it is ineffective as treatment in the clinic. Therefore, research needs to focus on other promising glutamatergic compounds to reduce heavy drinking or mediate withdrawal symptoms or both.

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“…Ethanol affects many functions of the central nervous system and the peripheral nervous system, resulting in analgesia, sedation, hypnosis, memory disturbance, confusion, neurodegeneration, dependence and motor disturbance (Deitrich et al, 1989; Fadda and Rossetti, 1998; Lockridge et al, 2012). Recent studies have shown that the expression and/or activity of a variety of enzymes (Ou et al, 2010), neurotransmitter receptors (Krystal et al, 2003; Lockridge et al, 2012; Lovinger and White, 1991) and proteins (Lu et al, 2008), such as glyceraldehyde 3-phosphate dehydrogenase (Ou et al, 2010), monoamine oxidase B (Ou et al, 2011; Ou et al, 2010) and Kruppel-like factor 11 (Lu et al, 2008; Ou et al, 2011) are altered by ethanol.…”

Section: Introductionmentioning

confidence: 99%

Diabetes-Causing Gene, Kruppel-Like Factor 11, Modulates the Antinociceptive Response of Chronic Ethanol Intake

Udemgba

Wang

et al. 2014

Alcohol Clin Exp Res

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Background-Alcohol (ethanol) is an antinociceptive agent, working in part, by reducing sensitivity to painful stimuli. The transcription factor, Kruppel-like factor 11 (KLF11), a human diabetes-causing gene that also regulates the neurotransmitter-metabolic enzymes monoamine oxidase (MAOs), has recently been identified as an ethanol-inducible gene. However, its role in antinociception remains unknown. Consequently, we investigated the function of KLF11 in chronic ethanol-induced antinociception using a genetically engineered knockout mouse model.

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Timing-dependent reduction in ethanol sedation and drinking preference by NMDA receptor co-agonist d-serine

Cited by 13 publications

References 67 publications

Metabotropic and ionotropic glutamate receptors as potential targets for the treatment of alcohol use disorder

Metabotropic and ionotropic glutamate receptors as potential targets for the treatment of alcohol use disorder

Glutamate plasticity woven through the progression to alcohol use disorder: a multi-circuit perspective

Diabetes-Causing Gene, Kruppel-Like Factor 11, Modulates the Antinociceptive Response of Chronic Ethanol Intake

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