Application of glycine in acute alcohol hallucinosis

Aliyev, Nadir A.; Aliyev, Zafar N.

doi:10.1002/hup.735

Cited by 14 publications

(16 citation statements)

References 13 publications

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“…Blockade of GlyT-1 also interferes with compulsive alcohol consumption and relapse [103]. The effect of GlyT-1 inhibitor has been attributed to reducing the alcohol-induced DA response in the NA and restoring the altered balance between the glutamatergic and glycinergic signaling function [104]. Similarly, GlyT-1 inhibitor blocks nicotine cue potentiated reinstatement and elevates NMDA signaling [105].…”

Section: Effect Of Nt69l On Nicotine-and Alcohol-induced Biochemical mentioning

confidence: 99%

Novel Therapy for Nicotine Addiction in Alcohol Dependent Rats

Boules¹,

Stennett²,

Muhktar³

et al. 2013

J Addict Res Ther

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IntroductionNicotine and alcohol addiction are frequently co-morbid problems [1]. The co-dependence of nicotine and alcohol addiction complicates treatment and is often associated with significant morbidity and mortality. Prevalence of smoking in alcoholics is as high as 90% compared to 30% for the general population [2] and alcohol consumption is associated with high nicotine use [3,4]. Co-morbid cigarette smoking and alcoholism has been associated with higher rates of depression in comparison with non-alcoholic smokers [5] and increased cravings for nicotine in comparison with non alcohol dependent smokers [6]. Additionally, smoker alcoholics are more likely to die from smoking related diseases rather than directly from an alcohol related medical condition [7]. Pharmacotherapeutic options for the treatment of alcohol and tobacco co-dependence are limited. Thus, there is a critical need for the development of novel drugs implementing new therapeutic targets.Neurotensin (NT) is a neuropeptide that is closely associated with, and modulates dopamine (DA) [8], acetylcholine (ACh), glutamate, and γ-aminobutyric acid (GABA) neurotransmission, all of which are involved in addiction and reward pathways. Local administration of NT in the prefrontal cortex (PFC) increases extracellular levels of ACh and GABA [9]. Similar data were obtained with the extracranial injection of the NT agonist NT69L [10], a compound that was developed in our laboratory. NT also enhances GABAergic activity in rat hippocampus [11] and reduces glutamatergic neurotransmission in dorsolateral striatum [12]. However, NT must be administered centrally to have an effect because it is easily degraded by peptidases. Our laboratory has developed many NT agonists that can be administered extracranially and mimic the central effects of NT. The most studied of these agonists is NT69L, which binds with equal affinity to the two well-characterized NT receptors, subtype 1 (NTS1) and subtype 2 (NTS2). Our work with NT69L shows that it blocks nicotine-induced sensitization and nicotine self-administration [13][14][15].In addition to its role in animal models for nicotine addiction, the NT system has been strongly implicated in the neurochemical and behavioral effects of alcohol use [16,17]. Chronic administration of NT69L reduces alcohol preference and consumption in mice through modulation of the NTS1 [18]. Biochemically, NT69L normalizes the nicotine-induced changes in DA [19], the neurotransmitter that promotes the motivational process for both nicotine and alcohol, and the alcohol-induced increase in DA and glutamate in the striatum [20]. Additionally, NT modulates other neurotransmitters implicated in alcohol use disorder (AUD). It causes neurochemical changes similar to acamprosate (the calcium salt of acetylhomotaurine), which is one of three FDA-approved drugs to treat AUD. Administration of acamprosate or NT69L increases extracellular concentration of DA in striatum [10,11] and both acamprosate and NT69L modulate glutamate [21,22].Considering the behav...

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Section: Effect Of Nt69l On Nicotine-and Alcohol-induced Biochemical mentioning

confidence: 99%

Novel Therapy for Nicotine Addiction in Alcohol Dependent Rats

Boules¹,

Stennett²,

Muhktar³

et al. 2013

J Addict Res Ther

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“…AIPD is often described as a “rare complication” [1] of alcohol use disorders. Despite this description, it was noted that the number of persons’ diagnosed with alcohol psychosis has escalated by four times in certain countries [2] and for patients diagnosed with AIPD there is 68% risk of re-admission [3]. There is a 37% co-morbidity of AIPD with other mental disorders [4] and a 5–30% risk that patients with AIPD will develop a chronic schizophrenia-like syndrome [5].…”

Section: Introductionmentioning

confidence: 99%

“…There are inconsistent reports regarding the outcome of this disorder [2, 5]. Some authors [2, 5] noted that AIPD may become prolonged and schizophrenia-like symptoms may develop.…”

Section: Introductionmentioning

confidence: 99%

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Cognitive changes in alcohol-induced psychotic disorder

et al. 2017

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AimsThis study aimed to explore the neuro-cognitive deficits of alcohol-induced psychotic disorder as compared to the cognitive deficits of uncomplicated alcohol dependence.MethodsParticipants were recruited from the acute psychiatric admission wards of the Department of Psychiatry, University of Stellenbosch and Stikland and Tygerberg Academic Hospitals in the Western-Cape, South Africa. Participants who met DSM IV TR criteria (American Psychiatric Association. Diagnostic and statistical manual of mental disorders. American Psychiatric Association, Washington, DC, 2000) for Alcohol Dependence and for alcohol-induced psychotic disorder, respectively, were included. Participants who met criteria for another current DSM IV TR Axis I disorder were excluded. A structured interview was done prior to neuropsychological assessment to ascertain current mental state and to obtain relevant demographic detail and history. Neuropsychological assessments were performed and supervised by clinical psychologists at either Tygerberg or Stikland Hospital.ResultsThe groups were matched demographically with similar period of abstinence prior to assessment. The alcohol-induced psychotic disorder group experienced first psychotic symptoms at age 35. The results reflected statistically significant differences on tasks measuring immediate memory; recall upon delay; exaggeration of memory difficulty and abstract thinking.ConclusionThis study concurs with earlier literature that some cognitive deficits are greater in alcohol-induced psychotic disorder compared to uncomplicated alcohol dependence.

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“…No studies have been performed on the pharmacotherapy of alcohol psychosis and there is no established therapy. A few case series have been published [1,5,10,13,15] . We performed a retrospective chart analysis to study the effects of neuroleptic treatment in patients with alcohol hallucinosis.…”

mentioning

confidence: 98%