共查询到20条相似文献,搜索用时 8 毫秒
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Function of GABAergic and glutamatergic neurons in the stomach 总被引:1,自引:1,他引:0
Tsai LH 《Journal of biomedical science》2005,12(2):255-266
-Aminobutyric acid (GABA) and L-glutamic acid (L-Glu) are transmitters of GABAergic and glutamatergic neurons in the enteric interneurons, targeting excitatory or inhibitory GABA receptors or glutamate receptors that modulate gastric motility and mucosal function. GABAergic and glutamatergic neuron immunoreactivity have been found in cholinergic enteric neurons in the stomach. GABA and L-Glu may also subserve hormonal and paracrine signaling. Disruption in gastrointestinal function following perturbation of enteric GABA receptors and glutamate receptors presents potential new target sites for drug development. 相似文献
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E. É. Kolesnikova 《Neurophysiology》2004,36(4):293-309
In this review, modern concepts on molecular mechanisms underlying reception of the oxygen level in natural O2-sensory structures and cellular in vitro models are considered and discussed.Neirofiziologiya/Neurophysiology, Vol.36, No.4, pp.330–347, July–August, 2004. 相似文献
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《Free radical research》2013,47(6):721-742
AbstractRegardless of the progress in therapeutic drugs and devices to treat heart failure (HF) during the last few years, the clinical outcome of this disease remains deleterious. Impaired left ventricular function leads to neurohumoral activation, altered local shear forces, and hypoxia, which might give rise to inflammatory processes within the vasculature. Among those, the imbalance of the redox equilibrium toward increased concentrations of reactive oxygen species (ROS) is particularly important, as it affects the integrity of vascular function. Apart from injured or dysfunctional cardiomyocytes, vascular dysfunction has been demonstrated to play a crucial role in the development and progression of HF, which makes it an interesting target for new HF therapies. The mechanisms that initiate vascular dysfunction in HF pathogenesis and the processes leading to oxidative stress are not yet fully elucidated. However, oxidative stress promotes a variety of redox-sensitive mechanisms contributing to vascular dysfunction in HF. Here, we will summarize the sources of ROS in the vasculature, elucidate the impact of oxidative stress on functional and structural vascular remodeling, and consider the link to vascular dysfunction. Furthermore, we will point out the importance of vascular dysfunction in HF and discuss therapeutic options. 相似文献
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NAAG peptidase inhibition reduces locomotor activity and some stereotypes in the PCP model of schizophrenia via group II mGluR 总被引:2,自引:0,他引:2
Olszewski RT Bukhari N Zhou J Kozikowski AP Wroblewski JT Shamimi-Noori S Wroblewska B Bzdega T Vicini S Barton FB Neale JH 《Journal of neurochemistry》2004,89(4):876-885
Phencyclidine (PCP) administration elicits positive and negative symptoms that resemble those of schizophrenia and is widely accepted as a model for the study of this human disorder. Group II metabotropic glutamate receptor (mGluR) agonists have been reported to reduce the behavioral and neurochemical effects of PCP. The peptide neurotransmitter, N-acetylaspartylglutamate (NAAG), is a selective group II agonist. We synthesized and characterized a urea-based NAAG analogue, ZJ43. This novel compound is a potent inhibitor of enzymes, glutamate carboxypeptidase II (K(i) = 0.8 nM) and III (K(i) = 23 nM) that deactivate NAAG following synaptic release. ZJ43 (100 microM) does not directly interact with NMDA receptors or metabotropic glutamate receptors. Administration of ZJ43 significantly reduced PCP-induced motor activation, falling while walking, stereotypic circling behavior, and head movements. To test the hypothesis that this effect of ZJ43 was mediated by increasing the activation of mGluR3 via increased levels of extracellular NAAG, the group II mGluR selective antagonist LY341495 was co-administered with ZJ43 prior to PCP treatment. This antagonist completely reversed the effects of ZJ43. Additionally, LY341495 alone increased PCP-induced motor activity and head movements suggesting that normal levels of NAAG act to moderate the effect of PCP on motor activation via a group II mGluR. These data support the view that NAAG peptidase inhibitors may represent a new therapeutic approach to some of the components of schizophrenia that are modeled by PCP. 相似文献
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细胞自噬是细胞在面对内外部环境压力的情况下, 为了自身的稳定而采取的一种降解内部及外来入侵物质的机制。SNARE(Soluble N-ethylmaleimide-sensitive factor attachment protein receptors)假说指出SNARE蛋白在细胞物质运输以及特异性膜融合过程中具有重要作用, 揭示了细胞正常生理活动有序进行的分子机制。由于细胞自噬涉及从自噬体的形成到自噬体溶酶体的融合等诸多膜融合的过程, 因此, 文章对近年来SNARE蛋白在调控细胞自噬过程的研究进展进行了综述。 相似文献
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Ben-Shachar D 《Journal of neurochemistry》2002,83(6):1241-1251
Mitochondria are not only the principal source of high energy intermediates, but play an important role in intracellular calcium buffering, are main producers of reactive oxygen species, and are the source of pro- and antiapoptotic key factors. Moreover, the mitochondria are of a ubiquitous nature and the respiratory chain has a dual genetic basis, i.e. the mitochondrial and the nuclear DNAs. Thus mitochondrial impairment could provide an explanation for the tremendous heterogeneity of clinical and pathological manifestations in schizophrenia. This article reviews several independent lines of evidence that suggest an involvement of mitochondrial dysfunction in schizophrenia. Among them are altered cerebral energy metabolism, mitochondrial hypoplasia, dysfunction of the oxidative phosphorylation system and altered mitochondrial related gene expression. In addition, the interaction between dopamine, a predominant etiological factor in schizophrenia, and mitochondrial respiration is considered as a possible mechanism underlying the hyper- and hypo-activity cycling in schizophrenia. Understanding the role of mitochondria in schizophrenia may encourage novel treatment approaches, the identification of candidate genes and new insights into the pathophysiology and etiology of the disorder. 相似文献
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In parasites, host specificity may result either from restricted dispersal capacity or from fixed coevolutionary host-parasite adaptations. Knowledge of those proximal mechanisms leading to particular host specificity is fundamental to understand host-parasite interactions and potential coevolution of parasites and hosts. The relative importance of these two mechanisms was quantified through infection and cross-infection experiments using mites and bats as a model. Monospecific pools of parasitic mites (Spinturnix myoti and S. andegavinus) were subjected either to individual bats belonging to their traditional, native bat host species, or to another substitute host species within the same bat genus (Myotis). The two parasite species reacted differently to these treatments. S. myoti exhibited a clear preference for, and had a higher fitness on, its native host, Myotis myotis. In contrast, S. andegavinus showed no host choice, although its fitness was higher on its native host M. daubentoni. The causal mechanisms mediating host specificity can apparently differ within closely related host-parasite systems. 相似文献
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V. E. Golimbet 《Molecular Biology》2008,42(5):738-746
Cognitive deficit is a key feature of schizophrenia. Genetic factors are thought to contribute to cognitive disturbances in schizophrenic patients. However, the role of specific genes in the development of cognitive deficit remains elusive. The review considers the current studies on the association between gene polymorphisms and cognitive dysfunction in schizophrenics. Main attention is drawn to the consistently reproducible association between the COMT polymorphism Val158Met and cognitive traits, which has a biological and neuropsychological support. The association studies with the genes for the dopamine and serotonin receptors, brain-derived neurotrophic factor, dysbindin, DISC1, D-amino acid oxidase, and D-amino acid oxidase activator are reviewed as well. 相似文献
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浮游动物昼夜垂直迁移机理的主要假说及其研究进展 总被引:3,自引:0,他引:3
对有关浮游动物昼夜垂直迁移(DVM)机理的实验、假说以及理论模型方面的研究进.展进行了综述。昼夜垂直迁移通常指常规迁移(傍晚上升,拂晓下降),其行为过程不仅影响浮游动物的垂直分布,而且也间接地影响其水平分布及生活史特征,对浮游动物在一定水域的种群维持和补充具有重要的意义。与垂直迁移机理有关的假说主要有光驱动假说、逃避捕食者假说、能量和资源利用假说等,其中逃避捕食者假说已得到大量的实验证实。其理论模型研究一般在两个时间尺度上进行,一个是短期的行为机制研究,另一个从长期的生活史策略的角度考虑。随着实验技术的进步和理论及建模工具的发展,这两个时间尺度的研究正逐渐统一到一个框架下进行。 相似文献
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Mesarwi Omar A. Sharma Ellora V. Jun Jonathan C. Polotsky Vsevolod Y. 《Sleep and biological rhythms》2015,13(1):2-17
Sleep and Biological Rhythms - It has recently become clear that obstructive sleep apnea (OSA) is an independent risk factor for the development of metabolic syndrome, a disorder of defective... 相似文献
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Ke Ma Hongxiu Zhang Shiyuan Wang Huaxin Wang Yuan Wang Juhai Liu Xiaobin Song Zhenfei Dong Xiaochun Han Yanan Zhang Honglei Li Abdul Rahaman Shijun Wang Zulqarnain Baloch 《Journal of cellular and molecular medicine》2019,23(10):7021-7028
Depression is the most frequent psychiatric disorder in the world. Recent evidence has shown that stress‐induced GABAergic dysfunction in the nucleus accumbens (NAc) contributed to the pathophysiology of depression. However, the molecular mechanisms underlying these pathological changes remain unclear. In this study, mice were constantly treated with the chronic unpredictable mild stress (CUMS) till showing depression‐like behaviours expression. GABA synthesis, release and uptake in the NAc tissue were assessed by analysing the expression level of genes and proteins of Gad‐1, VGAT and GAT‐3 by qRT‐PCR and Western blotting. The miRNA/mRNA network regulating GABA was constructed based on the bioinformatics prediction software and further validated by dual‐luciferase reporter assay in vitro and qRT‐PCR in vivo, respectively. Our results showed that the expression level of GAT‐3, Gad‐1 and VGAT mRNA and protein significantly decreased in the NAc tissue from CUMS‐induced depression‐like mice than that of control mice. However, miRNA‐144‐3p, miRNA‐879‐5p, miR‐15b‐5p and miRNA‐582‐5p that directly down‐regulated the expression of Gad‐1, VGAT and GAT‐3 were increased. In the mRNA/miRNA regulatory GABA network, Gad‐1 and VGAT were directly regulated by binding seed sequence of miR‐144‐3p, and miR‐15b‐5p, miR‐879‐5p could be served negative post‐regulators by binding to the different sites of VGAT 3′‐UTR. Chronic stress causes the impaired GABA synthesis, release and uptake by up‐regulating miRNAs and down‐regulating mRNAs and proteins, which may reveal the molecular mechanisms for the decreased GABA concentrations in the NAc tissue of CUMS‐induced depression. 相似文献
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Molecular genetics of schizophrenia: past, present and future 总被引:3,自引:0,他引:3
Suman Prasad Prachi Semwal Smita Deshpande Triptish Bhatia V. LNimgaonkar B. K. Thelma 《Journal of biosciences》2002,27(1):35-52
Schizophrenia is a severe neuropsychiatric disorder with a polygenic mode of inheritance which is also governed by non-genetic
factors. Candidate genes identified on the basis of biochemical and pharmacological evidence are being tested for linkage
and association studies. Neurotransmitters, especially dopamine and serotonin have been widely implicated in its etiology.
Genome scan of all human chromosomes with closely spaced polymorphic markers is being used for linkage studies. The completion
and availability of the first draft of Human Genome Sequence has provided a treasure-trove that can be utilized to gain insight
into the so far inaccessible regions of the human genome. Significant technological advances for identification of single
nucleotide polymorphisms (SNPs) and use of microarrays have further strengthened research methodologies for genetic analysis
of complex traits. In this review, we summarize the evolution of schizophrenia genetics from the past to the present, current
trends and future direction of research. 相似文献