Structural-functional and metabolic changes in the nervous system in low- and high-excitable rats deprived of paradoxical sleep

Studying of the influence of 24-hour deprivation of paradoxical sleep phase (PSPh) on rats with different genetically determined levels of excitability of the nervous system allowed to establish: 1) significant changes in functional state of the central part of the nervous system responsible for elaboration and preservation of defensive conditioned reflexes; 2) considerable lowering of functional state of the peripheral nervous system expressed both in a decrease of tibial nerve excitability thresholds and in changing of morpho-tinctorial characteristics of the studied nerve receptor parameters. The degree of the observed effects of PSPh deprivation is dependent on animal line belonging.     

EEG Spectral Analysis of Relaxation Techniques

The acute central nervous system effects of relaxation techniques (RT) have not been systematically studied. We conducted a controlled, randomized study of the central nervous system effects of RT using spectral analysis of EEG activity. Thirty-six subjects were randomized to either RT or a music comparison condition. After listening to an RT audiotape or music audiotapes daily for 6 weeks, the acute central nervous system effects of RT and music were measured using power spectral analysis of alpha and theta EEG activity in all cortical regions. RT produced significantly greater increases in theta activity in multiple cortical regions compared to the music condition. These findings are consistent with widespread reductions in cortical arousal during RT. They extend previous findings and suggest that theta, and not alpha, EEG may be the most reliable marker of the central nervous system effects of RT. These findings demonstrate that RT produce greater reductions in central nervous system activity than a credible comparison condition. The findings suggest that RT represent a hypoactive central nervous system state that may be similar to Stage 1 sleep and that RT may exert their therapeutic effects, in part, through cerebral energy conservation/restoration.     

Brain function and higher nervous activity

Some actual problems of higher nervous activity have been analysed on the peculiarities of brain states in the course of different types of conditioning and reactivity of the nervous structures which depend on the brain state have been considered. A concept of brain state as a specific mechanism of each temporal connection forming during the learning process has been formulated for the first time. The authors suggest that the brain represents the dynamic system with changeable structure which reveals itself in multitude nervous set constellation during various types of activity. This concept is presented to be the theoretical basis for integral evaluation of functional capacities of central nervous system.     

The peripheral nervous system and the pathogenesis of prion diseases

Prion diseases are inevitably fatal neurodegenerative conditions which affect humans and a wide variety of animals. Unlike other protein aggregation diseases such as Alzheimer's, Parkinson's, and polyglutamine repeat diseases, prion diseases are unique in that they are transmissible. Therefore, prion diseases are also called transmissible spongiform encephalopathies. A number of prion diseases are caused by peripheral uptake of the infectious agent. In order to reach their target, the central nervous system, prions enter their host, accumulate and replicate in lymphoid organs, and eventually spread to the central nervous system via peripheral nerves. Once the agent has reached the central nervous system, disease progression is rapid, resulting in neurodegeneration and death. In this article, we review the state of knowledge on the routes of neuroinvasion used by the infectious agent in order to gain access to the central nervous system upon entry into extracerebral sites.     

一氧化氮与神经血管单元的关联性及相关药物研究进展

一氧化氮（NO）作为一种重要的信号分子,对中枢神经系统具有重要影响。神经血管单元是近年来提出的从整体上描述中枢神经 系统的新概念,NO对中枢系统的作用是多层次多角度的,NO与神经血管单元这个整体及其各组成单元均密切相关。综述NO及其合成酶 的功能,在中枢神经系统疾病中NO与神经血管单元的相互作用关系及以NO信号通路为靶点的相关药物研究进展。     

Cholesterol metabolism in the brain

The central nervous system accounts for only 2% of the whole body mass but contains almost a quarter of the unesterified cholesterol present in the whole individual. This sterol is largely present in two pools comprised of the cholesterol in the plasma membranes of glial cells and neurons and the cholesterol present in the specialized membranes of myelin. From 0.02% (human) to 0.4% (mouse) of the cholesterol in these pools turns over each day so that the absolute flux of sterol across the brain is only approximately 0.9% as rapid as the turnover of cholesterol in the whole body of these respective species. The input of cholesterol into the central nervous system comes almost entirely from in situ synthesis, and there is currently little evidence for the net transfer of sterol from the plasma into the brain of the fetus, newborn or adult. In the steady state in the adult, an equivalent amount of cholesterol must move out of the brain and this output is partly accounted for by the formation and excretion of 24S-hydroxycholesterol. This cholesterol turnover across the brain is increased in neurodegenerative disorders such as Alzheimer's disease and Niemann-Pick type C disease. Indirect evidence suggests that large amounts of cholesterol also turn over among the glial cells and neurons within the central nervous system during brain growth and neuron repair and remodelling. This internal recycling of sterol may involve ligands such as apolipoproteins E and AI, and one or more membrane transport proteins such as members of the low density lipoprotein receptor family. Changes in cholesterol balance across the whole body may, in some way, cause alterations in sterol recycling and apolipoprotein E expression within the central nervous system, which, in turn, may affect neuron and myelin integrity. Further elucidation of the processes controlling these events is very important to understand a variety of neurodegenerative disorders.     

The effects of insulin on the central nervous system--focus on appetite regulation.

Appetite and satiety are subject to complex regulation, with neuroendocrine mechanisms playing an important role. The central nervous system is attracting increasing attention as a target tissue for many hormones such as leptin, PYY3-36, ghrelin, glucagon-like-peptide 1 and many others. Among its many well-known functions, insulin is also a potent anorexigenic hormone, and insulin receptors are widely distributed throughout the central nervous system. One way to advance our understanding of central nervous regulation of hunger and satiety in humans is to develop suitable neuroimaging techniques for use in various clinical and experimental conditions. Several studies have been performed using functional magnetic resonance imaging and positron emission tomography to identify areas of the brain that are differentially activated by alteration of the feeding state. These preliminary data are taking shape as a complex neuronal network involving the hypothalamus, thalamus, limbic and paralimbic areas including the insular cortex and the anterior cingulate gyrus and the orbitofrontal cortex. Continuous efforts to understand hormonal effects on these pathways may advance our understanding of human obesity.     

原发性中枢神经系统淋巴瘤治疗方案的探讨

原发性中枢神经系统淋巴瘤(Primary central nervous system lymphoma,PCNSL)是仅累及中枢神经系统而全身其他部位未发现的结外非霍奇金淋巴瘤,发病率较低,进展快,死亡率高,其主要原因是中枢神经系统是淋巴瘤细胞抵抗化疗药物的一个避难所,血脑屏障通透性升高为淋巴瘤发生转移的重要机制之一[1],但其通透性升高机制尚不明确。其治疗和预后的观念不断发生变化,因此探讨最佳的治疗方案是本文的重点。     

Receptor-Mediated Interaction Between the Sympathetic Nervous System and Immune System in Inflammation

The sympathetic nervous system plays a central role in establishing communication between the central nervous system and the immune system during inflammation. Inflammation activates the sympathetic nervous system, which causes release of the transmitters of the sympathetic nerv-ous system in the periphery. The transmitters of the sympathetic nervous system are the cate-cholamines noradrenaline and adrenaline and the purines ATP, adenosine, and inosine. Once these transmitters are released, they stimulate both presynaptic receptors on nerve terminals and post-synaptic receptors on immune cells. The receptors that are sensitive to catecholamines are termed adrenoceptors, whereas the receptors that bind purines are called purinoceptors. Stimulation of the presynaptic receptors exerts an autoregulatory effect on the release of transmitters. Ligation of the postsynaptic receptors on inflammatory cells modulates the inflammatory ac-tivities of these cells. The present review summarizes some of the most important aspects of the current state of knowledge about the interactions between the sympathetic nervous system and the immune system during inflammation with a special emphasis on the role of adreno and purinoceptors.     

Abnormal reaction to central nervous system injury in mice lacking glial fibrillary acidic protein and vimentin

In response to injury of the central nervous system, astrocytes become reactive and express high levels of the intermediate filament (IF) proteins glial fibrillary acidic protein (GFAP), vimentin, and nestin. We have shown that astrocytes in mice deficient for both GFAP and vimentin (GFAP-/-vim-/-) cannot form IFs even when nestin is expressed and are thus devoid of IFs in their reactive state. Here, we have studied the reaction to injury in the central nervous system in GFAP-/-, vimentin-/-, or GFAP-/-vim-/- mice. Glial scar formation appeared normal after spinal cord or brain lesions in GFAP-/- or vimentin-/- mice, but was impaired in GFAP-/-vim-/- mice that developed less dense scars frequently accompanied by bleeding. These results show that GFAP and vimentin are required for proper glial scar formation in the injured central nervous system and that some degree of functional overlap exists between these IF proteins.     

基于经血源性子宫内膜干细胞的中枢神经系统疾病治疗的研究进展

干细胞研究已成为当今生命科学领域中的前沿和热点问题,该研究为探讨胚胎发生、组织细胞分化以及基因表达调控等生物学问题提供了理想的模型,同时也为临床组织缺陷性疾病和遗传性疾病的细胞治疗和基因治疗开辟了新的手段。其中,经血源性子宫内膜干细胞(Menstrual blood-derived stem cells,MenSCs)来源丰富,具有多向分化潜能和较低的免疫排斥的特性,可以实现个体化治疗,是临床最具有应用优势的干细胞。脑与脊髓作为中枢神经系统,其损伤极为常见,致死率和致残率居各类创伤之首。与周围神经系统损伤相比,中枢神经受损后恢复较为困难,其治疗仍缺乏突破。而MenSCs的治疗有希望解决此难题,故结合近年来国内外对MenSCs的生物学特性及其对中枢神经系统疾病治疗的研究作一综述,从而为中枢神经系统疾病的治疗提供参考。     

Hashimoto encephalopathy: a case study

The impact of thyroid hormones upon the proper function of central nervous system has been known for many years. The neurological symptoms and psychiatric disturbances may occur both in case of hypo- as well as hyperthyreosis. The encephalopathy Hashimoto (EH) described in this paper is a rare illness which occurs in case of patients suffering from the autoimmunological thyroid disease and increased level of antibodies in serum without any connections to the thyroid function. It is characterised by a variety of neurological symptoms and psychotic disturbances, acute state, high re-occurrence and good reaction to glicocorticosteroid treatment. Although we face encephalopathy Hashimoto extremely rarely in the clinical practice one should remember about it during the diagnostic process because when it is a long lasting untreated illness it may lead to the irreversible changes in the central nervous system.     

The molecular basis of herpes simplex virus pathogenicity

The key features of herpes simplex viruses are cell destruction with considerable pathology, particularly in productive infections of the central nervous system, and ability to remain latent in sensory and autonomic neurons of the peripheral nervous system. In cells in culture, approximately half of the 74 known different genes of the virus are not essential for viral replication. For the most part, these genes are required for efficient viral replication in experimental animal models. Mutations in a small number of viral genes have been shown to decrease the ability of the virus to access the central nervous system or in ability to multiply efficiently. These genes play a key role in defining the pathogenic properties of the virus. Current evidence suggests that viral gene expression is not required for initiation and maintenance of the latent state. Latency reflects the capacity of the cell to specifically and transiently repress viral gene expression.     

Effects of peptides: a cross-listing of peptides and their central actions published in the journal Peptides from 1994 through 1998.

Effects of peptides on the central nervous system are presented in two ways so as to provide a cross-listing. In the first table, the peptides are listed alphabetically. In the second table, the central nervous system effects are arranged alphabetically. No longer can there be any doubt that peptides affect the central nervous system, sometimes in several ways.     

Aminergic neurons: State control and plasticity in three model systems

Aminergic neurons have particular functions in many systems, and in this review their role is discussed and compared in three systems: those parts of the central nervous system controlling sleep and waking in the cat; the superior cervical ganglion; and the isolated nervous system of Aplysia.In the cat the aminergic neurons are most important in a waking state during which time external information is received, processed, and can be retrieved, and during which time habituation and sensitization occur. Aminergic neurons appear to have similar roles in state control in plasticity in both the Aplysianervous system and the superior cervical ganglion. The striking similarities in the role of aminergic neurons in these three systems support the speculation that aminergic neurons have uniquely important roles in regulation of the plastic properties of neurons.     

The visna virus long terminal repeat directs expression of a reporter gene in activated macrophages, lymphocytes, and the central nervous systems of transgenic mice.

Visna virus is a lentivirus which causes a slow progressive disease involving the immune system and the central nervous system. To determine the role of the viral long terminal repeat (LTR) in targeting the virus to specific host cells and tissues, transgenic mice were constructed which contained the visna virus LTR directing expression of the bacterial gene encoding chloramphenicol acetyltransferase (CAT). Analysis of the transgenic mouse tissues for CAT activity revealed that the viral LTR was responsible, in part, for the tropism of visna virus for macrophages and the central nervous system. Expression of the LTR required the macrophage to be in an activated state both in vivo and in vitro. Thioglycolate activation of peritoneal macrophages in vivo and 12-O-tetradecanoylphorbol 13-acetate treatment in vitro induced expression of the visna virus LTR. Lymphocytes from the spleens of the transgenic mice expressed CAT activity, suggesting that visna virus was able to replicate in lymphocytes, as did human immunodeficiency virus and simian immunodeficiency virus. These studies demonstrated that the lentivirus LTR was responsible, in part, for cell and tissue tropism in vivo.     

The gill withdrawal reflex is suppressed in sexually active Aplysia

In Aplysia, the central nervous system and peripheral nervous system interact and form an integrated system that mediates adaptive gill withdrawal reflex behaviours evoked by tactile stimulation of the siphon. The central nervous system (CNS) exerts suppressive and facilitatory control over the peripheral nervous system (PNS) in the mediation of these behaviours. We found that the CNS's suppressive control over the PNS was increased significantly in animals engaged in sexual activity as either a male or female. In control animals, the evoked gill withdrawal reflex met a minimal response amplitude criterion, while in sexually active animals the reflex did not meet this criterion. At the neuronal level, the increased CNS suppressive control was manifested as a decrease in excitatory input to the central gill motor neurons.