Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Nervous System”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 109 records · Page 6Linked to original sources
PubMed1995

Effects of chronic NO synthase inhibition in rats on renin-angiotensin system and sympathetic nervous system.

This study was designed to assess the role of renin and of the sympathoadrenal system in the maintenance of the hypertension induced by chronic nitric oxide synthase (NOS) inhibition in rats kept on a normal (RS) or a low-sodium (LS) diet. With the administration of NG-nitro-L-arginine methyl ester (L-NAME) in drinking water (0.4 milligrams) for 6 wk, mean intra-arterial blood pressure rose to a similar extent to 201 mmHg in the RS and 184 mmHg in the LS animals. Simultaneously, plasma norepinephrine was increased to 838 and 527 pg/ml and epinephrine to 2,041 and 1,341 pg/ml in RS and LS, respectively. Plasma neuropeptide Y levels did not change. Plasma renin activity rose to 21 ng.ml-1.h-1 in RS but remained at 44 ng.ml-1.h-1 in the LS. Both losartan (10 mg/kg) and phentolamine (0.1 mg/kg) intravenous bolus injections reduced blood pressure considerably in the L-NAME hypertensive animals. Whole brain NOS activity was reduced by 84%. Hypertension induced by chronic NOS inhibition in LS as well as in RS fed rats seems to be sustained by an interaction of several mechanisms, including the activation of the sympathetic nervous system and the renin-angiotensin system.

Amino Acid Oxidoreductases↗
PubMed1999

Systemic and central nervous system correction of lysosomal storage in mucopolysaccharidosis type VII mice.

Mucopolysaccharidosis (MPS) type VII patients lack functional beta-glucuronidase, leading to systemic and central nervous system dysfunction. In this study we tested whether recombinant adenovirus that encodes beta-glucuronidase (Adbetagluc), delivered intravenously and into the brain parenchyma of MPS type VII mice, could provide long-term transgene expression and correction of lysosomal distension. We also tested whether systemic treatment with the immunosuppressive anti-CD40 ligand antibody, MR-1, affected transgene expression. We found substantial plasma beta-glucuronidase activity for over 9 weeks after gene transfer in the MR-1- treated group, with subsequent decline in activity corresponding to a delayed anti-beta-glucuronidase antibody response. At 16 weeks, near wild-type amounts of beta-glucuronidase activity and striking reduction of lysosomal pathology were detected in livers from mice that had received either MR-1 cotreatment or control antibody. In the lung and kidney, beta-glucuronidase activity was markedly higher for the MR-1-treated group. beta-Glucuronidase activity in the brain persisted independently of MR-1 treatment. Activity was intense in the injected hemisphere and was also evident in the noninjected cortex and striatum, with dramatic improvements in storage deposits in areas of both hemispheres. These results indicate that prolonged enzyme expression from transgenes delivered to deficient liver and brain can mediate pervasive correction and illustrate the potential for gene therapy of MPS and other lysosomal storage diseases.

Adenoviridae↗
PubMed1998

Potential role of apoE in structural plasticity in the nervous system; implications for disorders of the central nervous system.

Apolipoprotein E (apoE) is a well characterized 299 amino acid protein that participates in the regulation of plasma cholesterol and lipid metabolism. In humans, apoE has three major protein isoforms: E2 (cys(112), cys(158)); E3 (cys(112), arg(158)); and E4 (arg(112), arg(158)) that are encoded for by a single gene on chromosome 19. Genetic studies have shown that apoE4 is a risk factor for Alzheimer's disease (AD) as well as for poor outcome following certain injuries to the central nervous system (CNS). These genetic data, as well as other data reviewed herein, suggest that apoE may play an important role in the nervous system under certain conditions. This review focuses on studies demonstrating that apoE can modulate neuronal structure and the potential implication of these findings for its role following CNS injury, in AD, and in other neurodegenerative diseases.

Journal Article↗
PubMed1985

Apolipoprotein E associated with astrocytic glia of the central nervous system and with nonmyelinating glia of the peripheral nervous system.

The plasma protein apolipoprotein (apo) E is an important determinant of lipid transport and metabolism in mammals. In the present study, immunocytochemistry has been used to identify apo E in specific cells of the central and peripheral nervous systems of the rat. Light microscopic examination revealed that all astrocytes, including specialized astrocytic cells (Bergmann glia of the cerebellum, tanycytes of the third ventricle, pituicytes of the neurohypophysis, and Müller cells of the retina), possessed significant concentrations of apo E. In all of the major subdivisions of the central nervous system, the perinuclear region of astrocytic cells, as well as their cell processes that end on basement membranes at either the pial surface or along blood vessels, were found to be rich in apo E. Extracellular apo E was present along many of these same surfaces. The impression that apo E is secreted by astrocytic cells was confirmed by electron microscopic immunocytochemical studies, which demonstrated the presence of apo E in the Golgi apparatus. Apo E was not present in neurons, oligodendroglia, microglia, ependymal cells, and choroidal cells. In the peripheral nervous system, apo E was present within the glia surrounding sensory and motor neurons; satellite cells of the dorsal root ganglia and superior cervical sympathetic ganglion as well as the enteric glia of the intestinal ganglia were reactive. Apo E was also present within the non-myelinating Schwann cells but not within the myelinating Schwann cells of peripheral nerves. These results suggest that apo E has an important, previously unsuspected role in the physiology of nervous tissue.

Animals↗
PubMed1987

Metal toxicity in the central nervous system.

The nervous system is the principal target for a number of metals. Inorganic compounds of aluminum, arsenic, lead, lithium, manganese, mercury, and thallium are well known for their neurological and behavioral effects in humans. The alkyl derivatives of certain metals--lead, mercury and tin--are specially neurotoxic. Concern over human exposure and in some cases, outbreaks of poisoning, have stimulated research into the toxic action of these metals. A number of interesting hypotheses have been proposed for the mechanism of lead toxicity on the nervous system. Lead is known to be a potent inhibitor of heme synthesis. A reduction in heme-containing enzymes could compromise energy metabolism. Lead may affect brain function by interference with neurotransmitters such as gamma-amino-isobutyric acid. There is mounting evidence that lead interferes with membrane transport and binding of calcium ions. Methylmercury produces focal damage to specific areas in the adult brain. One hypothesis proposes that certain cells are susceptible because they cannot repair the initial damage to the protein sythesis machinery. The developing nervous system is especially susceptible to damage by methylmercury. It has been discovered that microtubules are destroyed by this form of mercury and this effect may explain the inhibition of cell division and cell migration, processes that occur only in the developmental stages. These and other hypotheses will stimulate considerable experimental challenges in the future.

Animals↗
PubMed1980

Acute renovascular hypertension in conscious dogs. Interaction of the renin-angiotensin system and sympathetic nervous system in systemic hemodynamics and regional blood flow responses.

The effects of acute renovascular hypertension on the sympathetic nervous system, regional blood flow and cardiac function were studied in conscious dogs submitted to renal artery occlusion by inflation of a cuff implanted previously around one renal artery. We then compared the alterations in plasma renin and catecholamine levels and in the various hemodynamic parameters induced by those maneuvers in intact dogs, to those in dogs pretreated with alpha- and beta-adrenergic receptor blockers. Subsequently, the converting enzyme inhibitor teprotide was administered to inhibit angiotensin formation in both experiments. Our results suggest that both the renin-angiotensin system and the sympathetic system contribute to the rise in blood pressure. The hemodynamic changes and alterations in regional blood flows accompanying this acute hypertension appear to be due mostly to the increase in plasma angiotensin, since prior adrenoceptor blockade only attenuated their magnitude but did not alter their direction. However, angiotensin-induced coronary vasoconstriction was observed only in adrenergically blocked but not intact animals, probably because of the protective effect of baroreceptor-mediated reflex sympathetic coronary vasodilation.

Acute Disease↗
PubMed2000

Nicotinic systems in central nervous systems disease: degenerative disorders and beyond.

Advances in the understanding of the structure, function, and distribution of central nervous system (CNS) nicotinic receptors has provided the impetus for new studies examining the role(s) that these receptors and associated processes may play in CNS functions. Further motivation has come from the realization that such receptors are changed in degenerative neurologic diseases such as Alzheimer's disease (AD) and Parkinson's disease (PD). Ongoing investigations of the molecular substructure of CNS nicotinic receptors and their pharmacology have begun to open up new possibilities for novel CNS therapeutics with nicotinic agents. Exploiting these possibilities will require understanding of the role(s) that these receptor systems play in human cognitive, behavioral, motor, and sensory functioning. Clues from careful studies of human cognition and behavior are beginning to emerge and will provide direction for studies of potentially therapeutic novel nicotinic agents. Modulation of these receptors with the ultimate goal of producing therapeutic benefits is the goal of these investigations and drug development. This paper will review studies from our laboratory and others that point to the importance of CNS nicotinic mechanisms in normal human cognitive and behavioral functioning as well as their role in disease states. In addition, this paper will examine potential clinical applications of nicotine and/or nicotinic agonists in a variety of CNS disorders with particular emphasis on structural brain disease including: movement disorders such as Parkinson's disease and Tourette's syndrome, cognitive/behavioral disorders such as Alzheimer's disease, attention deficit/hyperactivity disorder, and schizophrenia, and other more speculative applications. Important results from early therapeutic studies of nicotine and/or nicotinic agonists in these disease states are presented. For example, recent studies with nicotine and novel nicotinic agonists such as ABT-418 by our group in AD patients suggest that nicotinic stimulation can improve the acquisition and retention of verbal information and decrease errors. Preliminary results from a series of studies examining the acute and subchronic quantitative effects of nicotine on cognitive and motor functioning in Parkinson's disease suggest that acute nicotine administration and stimulation improves some aspects of cognitive and motor performance and may improve the processing speed of more complex tasks. The most likely near-term applications of novel nicotinic agonists in CNS disorders are likely to be in those disorders that are degenerative in nature, e.g. Parkinson's disease and Alzheimer's disease, or other movement disorders such as Tourette's syndrome. The most likely direct therapeutic role for nicotinic agonists is as augmentation therapy in combination with other agents rather than as monotherapy, except early in disease states or as a prophylactic or preventative treatment.

Animals↗
PubMed2001

The complement system in central nervous system diseases.

The activation of complement system is an important factor participating in inflammatory, neurodegenerative, and cerebrovascular diseases. Astrocytes and neurons are able to synthesize complement components. Myelin and oligodendrocyte (OLG) activate the classical pathway of complement in vitro in the absence of antibodies. Sublytic C5b-9 in the absence of cell death induces proto-oncogenes, activates cell cycle, and enhances cell survival in OLG. In addition, C5b-9 reverses the differentiation phenotype in OLG and enhances cell survival. beta amyloid protein is an activator of the complement system and neurons are susceptible to bystander complement mediated damage. These findings indicate that complement activation and membrane assembly of C5b-9 play an important role in pathogenesis of central nervous system (CNS) disorders.

Animals↗
PubMed2003

Gene transfer to the nervous system: prospects for novel treatments directed at diseases of the aging nervous system.

In the past 3 decades, gene therapy has moved from a theoretical construct to an active field of basic research, animal studies, and clinical trials. In this article, we describe the conceptual basis underlying the use of gene therapy for diseases of the aging nervous system, the principal techniques used for gene delivery, and review preclinical animal studies in 4 different classes of neurologic dysfunction: 1) focal neuronal degeneration in the central nervous system; 2) global neuronal dysfunction in the central nervous system; 3) degenerative disease affecting components of the peripheral nervous system; and 4) intractable focal pain. The full potential of this approach will not be established until the human trials are completed.

Aging↗
PubMed1987

The nervous system of Diplostomum pseudospathaceum Niewiadomska, 1984 (Trematoda, Diplostomatidae). III. Structure of the nervous system in the adult stage.

The nervous system of adult Diplostomum pseudospathaceum Niewiadomska, 1984 was studied using Koelle's (1951) method for revealing cholinesterase activity. The nervous system in the fore body grows but its pattern remains the same as in the metacercaria: three pairs of stems connected by numerous commissures and differentiated innervation of various organs in this part of the body. In the elongated hind body the nervous system develops according to another pattern: two pairs of stems connected by a number of commissures form a loose net surrounding the whole segment. The net is more dense at the body end around the genital opening and copulatory organs. A brief discussion of the development of the nervous system of D. pseudospathaceum from cercaria to adult stage is given.

Animals↗
PubMed1980

Nervous system abnormality and nervous disease in diabetes.

Symptomatic diabetic neuropathy is present only in a few percent of the total diabetic population. In contrast abnormalities of the various parts of the nervous system can be demonstrated very early using neurophysiological techniques. These abnormalities are reversible at first, but progressive with duration of diabetes. Similar nervous abnormalities are present in experimental diabetes in the rat. The earliest structural changes have been demonstrated to be a decreased calibre of the myelinated axons. An abnormality in the axonal transport of proteins is possibly the very first change to appear. These recent results have enabled us to propose a hypothesis concerning the sequence of events in the development of the peripheral nerve abnormalities.

Animals↗
PubMed2004

[Assessment of mass-scale primary prevention of nervous system defects].

Nervous system defects are one of the main reasons of neonate mortality in Poland. In reply to that fact a special program for prophylaxis of nervous system defects was established in 1998. It includes three activity fields for women at reproductive age. These are following: propagation of nourishment rich in vitamin B and folic acid, recommendation for the day-to-day taking of 0.4 mg folic acid, improvement of the nutritive food value by adding such nutrients as folic acid. The aim of this article is to evaluate the efficiency of the prophylaxis of the nervous system defects.

Adult↗
PubMed2002

Feeding and wounding responses in Hydra suggest functional and structural polarization of the tentacle nervous system.

The nervous system of Hydra, a freshwater cnidaria, occurs as dispersed, or diffuse, nerve net throughout the animal. It is widely accepted that in a diffuse nervous system an external stimulus is conducted in all directions over the net. Here I report observations that hydra tentacles respond to feeding and wounding stimuli in a unidirectional manner. Upon contact of a tentacle with a brine shrimp larva during feeding, tissue on the proximal side of the point of contact contracted strongly, whereas tissue on the distal side contracted only very weakly. Feeding a tentacle to which a second tentacle was grafted to the proximal end in the reversed orientation showed that unidirectional conduction, once initiated, was blocked by the reversal of polarity, demonstrating that the distal to proximal polarity of tissue is crucial for unidirectional conduction. Unidirectional conduction was obtained also by mechanically pinching the tissue. The response of tentacles devoid of neurons examined was bidirectional, demonstrating that the nervous system is responsible for the unidirectional responses. These observations suggest that polarized property of the nerve net in hydra tentacles is responsible for the unidirectional tentacle contraction.

Animals↗
PubMed1979

Immunocytochemical localization of rat peripheral nervous system myelin proteins: P2 protein is not a component of all peripheral nervous system myelin sheaths.

Specific antibodies have been developed against P1, P2, and P0 myelin proteins and were used to study the localization of these proteins in the rat peripheral nervous system. Both peripheral and central nervous system myelin sheaths contain P1 protein. P0 and P2 proteins are found exclusively in peripheral nervous system myelin sheaths. Antisera to P1 and P0 proteins stain all peripheral nervous system myelin sheaths uniformly. P2 protein is not a component of all peripheral nervous system myelin sheaths. In sheaths that do contain P2 protein, it is concentrated in the area of the Schmidt-Lanterman incisures.

Animals↗
PubMed2004

Successful treatment of systemic and central nervous system lymphomatoid granulomatosis with rituximab.

Lymphomatoid granulomatosis (LYG) is a rare lymphoproliferative disorder with a mortality rate approaching 60% in the first year. The median survival is 14 months from the time of diagnosis. Although a variety of chemotherapeutic regimens have been utilized, there is no standard treatment. Studies have shown that in most cases the malignant cells are B-cells, which induce massive infiltration of reactive T-lymphocytes in the background. The disease is therefore considered as a T-cell rich B-cell lymphoproliferative disorder. We report a case of LYG with pulmonary, hepatic, central and peripheral nervous system involvement that was successfully treated with the anti-CD20 (B-cell) monoclonal antibody, Rituximab.

Antibodies, Monoclonal↗