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The regulation of gene expression in the brain reward regions is known to contribute to the pathogenesis and persistence of drug addiction. Increasing evidence suggests that the regulation of gene transcription is mediated by epigenetic mechanisms that alter the chromatin structure at specific gene promoters. To better understand the involvement of(More)
OBJECTIVE To examine the causative relationship between aberrant histone acetylation changes and cocaine-induced reward. METHODS Male Sprague-Dawley rats (n=160) were tested by conditioned place preference (CPP) procedure, to evaluate the effects of inhibitors of histone deacetylase (HDAC) and histone acetyltransferase (HAT) on the conditioned effects of(More)
We investigated the role of histone H3 phosphoacetylation in the nucleus accumbens (NAc) in heroin-conditioned place preference paradigm. Heroin could dose-dependently increase histone H3 phosphoacetylation specifically in the NAc and could enhance heroin place preference. Injection of trichostatin A into the NAc significantly augmented heroin-induced(More)
Impaired inflammatory functions may be critical factors in the mechanisms of severe CNS disorders classified as the human immunodeficiency virus-1 (HIV-1)-associated dementia (HAD). Evidence indicates that a viral gene product, the transactivator of transcription protein (Tat), can markedly contribute to these events. We herein report that sulfated(More)
In order to substantiate the concept that cocaine behavioral effects may be influenced by histone modification, rats were trained to self-administer cocaine intravenously (0.75 mg/(kginjection)), and were systemically pretreated with sodium butyrate (NaBu), a potent histone deacetylase inhibitor, before the test session during the maintenance phase. The(More)
Human immunodeficiency virus (HIV)-1 infection of the central nervous system occurs in the vast majority of HIV-infected patients. HIV-associated dementia (HAD) represents the most severe form of HIV-related neuropsychiatric impairment. The pathogenesis of HAD is mediated by disruption of neuronal cell signal pathways, which ultimately triggers neuronal(More)
Pristimerin, a naturally occurring quinonemethide triterpenoid compound, is known to exert a variety of pharmacological activities. In the present study, we investigated the molecular actions of pristimerin against LPS-induced inflammatory responses in human monocytic THP-1 cells. The results showed that pristimerin inhibited the production of TNF-α and(More)
Several lines of evidence suggest the non-cholinergic functions of acetylcholinesterase (AChE) in promoting neurite outgrowth of cultured neurons and in inducing the postsynaptic specializations of developing neuromuscular junctions. In order to support the hypothesis, a cholinergic synapse-forming cell line NG108-15 was over-expressed with chick AChE by(More)
Familial appearance of Wolff-Parkinson-White (WPW) syndrome is rare and displays an autosomal dominant inheritance. Here we report a Chinese kindred of WPW syndrome whose unique clinical features consist of a high risk of sudden cardiac death due to atrial fibrillation, causing a rapid antegrade conduct over the accessory pathway. The mutation in the PRKAG2(More)
AIM To investigate the effects of sulfated polymannuroguluronate (SPMG), a novel candidate anti-AIDS drug in Phase II clinical trial, on Tat-induced release of proinflammatory cytokines (i.e., TNFalpha, IL-1beta and IL-6) and its related mechanism. METHODS The effects of SPMG on Tat induced TNFalpha (4 h), IL-1beta and IL-6 (6 h) secretion in THP-1 cells(More)
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