substance dependence/tyrosine

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An association study revealed substantial effects of dominance, epistasis and substance dependence co-morbidity on alcohol dependence symptom count.

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Alcohol dependence is a complex disease involving polygenes, environment and their interactions. Inadequate consideration of these interactions may have hampered the progress on genome-wide association studies of alcohol dependence. By using the dataset of the Study of Addiction: Genetics and

The roles of glial cell line-derived neurotrophic factor, tumor necrosis factor-alpha, and an inducer of these factors in drug dependence.

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There are few efficacious medications for drug dependence at present. Recent evidence has suggested that various cytokines are involved in the effects of abused drugs, suggesting that these factors play a role in drug dependence. In this article, the roles of glial cell line-derived neurotrophic

Tyrosine Hydroxylase Gene Polymorphisms Contribute to Opioid Dependence and Addiction by Affecting Promoter Region Function.

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Mounting evidence shows that drug dependence involves the complex interplay between genetics and the environment. Tyrosine hydroxylase (TH) is the rate-limiting enzyme in dopamine (DA) synthesis, which plays an essential role in the development of drug addiction. Noradrenergic dysfunction due to

Increase of MET gene copy number confers resistance to a monovalent MET antibody and establishes drug dependence.

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The relevant role in cancer played by the tyrosine kinase receptor encoded by the MET oncogene led to the development of specific inhibitors, some of which are now in advanced phases of clinical trials. Previous experience has shown that the main limit to the efficacy of most targeted treatments is

[The forecast of illicit drug use in adolescents with addictive behavior: personality traits and the level of genetic risk of substance dependence.]

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OBJECTIVE To clarify the psychological mechanism underlying the genetic risk of substance addiction at the first stage of drug use by adolescents. METHODS Genetic risk was evaluated by genotyping of 5 polymorphisms of the dopaminergic system genes (dopamine receptor D2 and D4 genes and tyrosine

[Learning/memory and drug dependence].

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We investigated the possible mechanisms of development of latent learning and morphine dependence by the methods of behavioral pharmacology and confirmed them by using mutant mice. The heterozygous mice for the tyrosine hydroxylase (TH) gene and for the cyclic AMP (cAMP) response element binding

Deletion of the fyn-kinase gene alters sensitivity to GABAergic drugs: dependence on beta2/beta3 GABAA receptor subunits.

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Tyrosine phosphorylation can modulate GABA(A) receptor function, and deletion of the fyn-kinase gene alters GABAergic function in olfactory bulb neurons, as reported by Kitazawa, Yagi, Miyakawa, Niki, and Kawai (J Neurophysiol 1998;79:137-142). Our goal was to determine whether fyn gene deletion

Developments in harmine pharmacology--implications for ayahuasca use and drug-dependence treatment.

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Ayahuasca is a hallucinogenic botanical mixture originating in the Amazon area where it is used ritually, but is now being taken globally. The 2 main constituents of ayahuasca are N,N-dimethyltryptamine (DMT), a hallucinogen, and harmine, a monoamine oxidase inhibitor (MAOI) which attenuates the

The neuropeptide galanin modulates behavioral and neurochemical signs of opiate withdrawal.

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Much research has focused on pathways leading to opiate addiction. Pathways opposing addiction are more difficult to study but may be critical in developing interventions to combat drug dependence and withdrawal. Galanin decreases firing of locus coeruleus neurons, an effect hypothesized to decrease

Gene transcription alterations associated with decrease of ethanol intake induced by naltrexone in the brain of Wistar rats.

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Preclinical and clinical studies suggest that the administration of the opioid antagonist naltrexone decreases the intake of ethanol. However, the neuroplastic adaptations in the brain associated to reduction of ethanol consumption remains to be elucidated. The aim of the study was to identify gene

CB1 receptor blockade decreases ethanol intake and associated neurochemical changes in fawn-hooded rats.

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BACKGROUND This study was undertaken to identify the neurochemical changes underlying the attenuation of voluntary ethanol intake induced by the cannabinoid CB1 receptor antagonist AM251 in fawn-hooded rats. METHODS Rats were exposed to the 2-bottle-choice paradigm (ethanol 10% v/v or water) for 15

An-jun-ning, a traditional herbal formula, attenuates spontaneous withdrawal symptoms via modulation of the dopamine system in morphine-dependent rats.

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BACKGROUND The dopamine system, which is involved in drug dependence, can be damaged by opioid abuse. However, current clinical medicines cannot reverse these damages in the brain, which are believed to be a key reason for the high relapse rate after abstinence treatment. This study aimed to

[Localization of non-monoaminergic aromatic L-amino acid decarboxylase neurons (D-neurons) in the human striatum and their functional significance].

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It has recently been reported that the human corpus striatum, especially its ventral part, named as the nucleus accumbens, contains numerous non-monoaminergic aromatic L-amino acid decarboxylase (AADC; the second-step monoamine synthesizing enzyme) neurons (D-neurons). D-neurons are the neurons

[Human striatal D-neurons and their significance].

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It has recently been reported that the human striatum, especially its ventral part, the nucleus accumbens, contains numerous neurons immunoreactive for aromatic L-amino acid decarboxylase (AADC; the second-step monoamine synthesizing enzyme), but not for tyrosine hydroxylase (TH; the first-step

L-DOPA-induced dyskinesia is associated with regional increase of striatal dynorphin peptides as elucidated by imaging mass spectrometry.

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Opioid peptides are involved in various pathophysiological processes, including algesia, epilepsy, and drug dependence. A strong association between L-DOPA-induced dyskinesia (LID) and elevated prodynorphin mRNA levels has been established in both patients and in animal models of Parkinson's

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