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At least 307 records · Page 17Linked to original sources
PubMed1983

Peripheral nervous system myelin and Schwann cell glycoproteins: identification by lectin binding and partial purification of a peripheral nervous system myelin-specific 170,000 molecular weight glycoprotein.

Radioiodinated lectins were used to detect glycoproteins of peripheral nervous system (PNS) myelin (rat, human, bovine) and cultured rat Schwann cells. Proteins were resolved by sodium dodecyl sulfate-polyacrylamide slab gel electrophoresis and transferred to nitrocellulose filters. The filters were overlaid with radioiodinated lectins of known saccharide affinities. These included concanavalin A, Helix pomatia, Limulus polyphemus, Maclura pomifera, peanut, soybean, Ulex europaeus, and wheat germ agglutinins. Inclusion of the appropriate monosaccharide in the overlay solution (0.2 M) inhibited lectin binding to the nitrocellulose-fixed proteins. Fluorography permitted identification of 26 myelin glycoproteins and many more in Schwann cells. All lectins labeled a band present in myelin, but not Schwann cells, corresponding to the major PNS myelin protein, P0. Our attention focused on a high-molecular-weight myelin glycoprotein [apparent molecular weight (Mr) 170,000], which appeared abundant by Coomassie Blue staining and which was heavily labeled by all lectins except concanavalin A. A protein with approximately this Mr and lectin-binding pattern was present in human and bovine PNS myelin as well, but not detected in rat Schwann cells, CNS myelin, liver and fibroblast homogenates, or cultured bovine oligodendroglia. Hence this 170,000 Mr glycoprotein is apparently unique to PNS myelin.

Animals↗
PubMed1999

The cellular localization of the L-ornithine decarboxylase/polyamine system in normal and diseased central nervous systems.

Natural polyamines, spermidine and spermine, and their precursor putrescine, are of considerable importance for the developing and mature nervous system. They exhibit a number of neurophysiological and metabolic effects in the nervous system, including control of nucleic acid and protein synthesis, modulation of ionic channels and calcium-dependent transmitter release. The polyamine system is also known to be involved in various brain pathologic events (seizures, stroke, Alzheimer's disease and others). While cerebral polyamine concentrations and the activities of polyamine-metabolizing enzymes have been studied in great detail, much less is known about the cells that are responsible for cerebral polyamine synthesis and interconversion. With the present review the attempt is made to show how exact knowledge about the regional distribution and cellular localization of polyamines and the polyamine-synthesizing enzymatic machinery (and especially of L-ornithine decarboxylase) may help to better understand the functional interplay between polyamines and other endogenous agents (transmitters, receptors, growth factors neuroactive drugs etc.). Polyamines have been localized both in neurones and glial cells. However, the main cellular locus of the ODC is the neuron--both in the immature and adult central nervous system. Each period of normal brain development and ageing seems to have its own, characteristic temporo-spatial pattern of neuronal ODC expression. During strong functional activation (kindling, epileptic seizures, neural transplantation) astrocytes and other non-neuronal cells do also express ODC and other polyamine-metabolizing enzymes. Astroglial expression of ODC is accompanied by an increase in glial fibrillary acidic protein in these cells. This shift in the cellular mechanisms of polyamine metabolism is currently far from being understood. In human brain diseases (Alzheimer's disease, schizophrenia) certain neurones show an increased expression of ODC, the first and rate-limiting enzyme of polyamine metabolism. Since polyamines are structurally related to psychoactive drugs (neuroleptics, antidepressants) the polyamine system might be of importance as a putative target for drug intervention in psychiatry.

Animals↗
PubMed1982

Neuroimmunology. II: Antigenic specificity of the nervous system.

Antigenic specificity of the nervous system refers to a property conveyed by unique cell surface structures that are present on different classes of nervous system tissue. These structures are of major importance for the study of nervous system structure and function, and can play a central role in determining patterns of nervous system injury. Thus, the major classes of nervous system cells are identified by structures that are unique to them: neurons by the presence of tetanus toxin receptors on their surface and oligodendrocytes by the presence of surface galactocerebroside, for example. With the advent of hybridoma technology, a large number of monoclonal antibodies are being identified which have increased by several orders of magnitude the ability to define subclasses of nervous system tissue according to unique antigens. In addition, surface antigens of nervous system tissue may determine the specificity of nervous system injury by (1) functioning as receptors for viruses or (2) being the targets of autoimmune responses. Patterns of viral injury to the nervous system are often extraordinarily selective (e.g., poliovirus tropism for motor neurons), and nervous system viral tropism is due is some instances to the interaction of a virus with a unique surface antigen on neural cells. The specificity of injury in autoimmune disease (such as that against the acetylcholine receptor in myasthenia gravis) likewise must be explained by an immune response against unique antigenic determinants on the tissue being damaged. Some antigens are known to be shared between nervous system and other tissues or between nervous system and infectious agents such as bacteria or viruses. The presence of shared antigenic structures between the nervous system and infectious agents creates the possibility that an immune response generated against a virus may concurrently damage normal nervous system tissue.

Antigens↗
PubMed1989

Central nervous system AIDS.

The retrovirus that causes the acquired immunodeficiency syndrome (AIDS) has two targets: the immune system and the nervous system. Central nervous system (CNS) manifestations of AIDS are protean. This review describes the opportunistic infections and malignancies that affect the nervous system in AIDS, and discusses the syndromes resulting from primary infection of the CNS by the AIDS virus. Possible mechanisms of CNS injury are cited as well as potential predictors of neurologic expression of AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed2000

The peroxynitrite scavenger uric acid prevents inflammatory cell invasion into the central nervous system in experimental allergic encephalomyelitis through maintenance of blood-central nervous system barrier integrity.

Uric acid (UA), a product of purine metabolism, is a known scavenger of peroxynitrite (ONOO(-)), which has been implicated in the pathogenesis of multiple sclerosis and experimental allergic encephalomyelitis (EAE). To determine whether the known therapeutic action of UA in EAE is mediated through its capacity to inactivate ONOO(-) or some other immunoregulatory phenomenon, the effects of UA on Ag presentation, T cell reactivity, Ab production, and evidence of CNS inflammation were assessed. The inclusion of physiological levels of UA in culture effectively inhibited ONOO(-)-mediated oxidation as well as tyrosine nitration, which has been associated with damage in EAE and multiple sclerosis, but had no inhibitory effect on the T cell-proliferative response to myelin basic protein (MBP) or on APC function. In addition, UA treatment was found to have no notable effect on the development of the immune response to MBP in vivo, as measured by the production of MBP-specific Ab and the induction of MBP-specific T cells. The appearance of cells expressing mRNA for inducible NO synthase in the circulation of MBP-immunized mice was also unaffected by UA treatment. However, in UA-treated animals, the blood-CNS barrier breakdown normally associated with EAE did not occur, and inducible NO synthase-positive cells most often failed to reach CNS tissue. These findings are consistent with the notion that UA is therapeutic in EAE by inactivating ONOO(-), or a related molecule, which is produced by activated monocytes and contributes to both enhanced blood-CNS barrier permeability as well as CNS tissue pathology.

Animals↗
PubMed1975

Use of the analytical electron microscope (AEM) in cytochemical studies of the central nervous system.

Central nervous tissues (median eminence and arcuate nucleus) were studied by means of energy dispersive x-ray analysis using electron optical systems (analytical electron microscopy). These studies were conducted after the tissue had been treated specifically for localized biogenic amines (BA). The results indicate that not only is the BA cytochemical reaction highly specific, and that BAs can be localized intraneuronally in areas not previously identified, but also that the analytical electron microscope is a very valuable and potentially powerful tool in the studies of inclusion bodies and organelles in the central nervous system and other tissues. Thus, the nonspecific density production by osmium tetroxide can be elucidated from the specific BA reaction plus other areas of the nervous system containing density producing heavy metals, i.e., iron are readily identifiable.

Adrenal Medulla↗
PubMed2002

Smad10 is required for formation of the frog nervous system.

Before the nervous system establishes its complex array of cell types and connections, multipotent cells are instructed to adopt a neural fate and an anterior-posterior pattern is established. In this report, we show that Smad10, a member of the Smad family of intracellular transducers of TGFbeta signaling, is required for formation of the nervous system. In addition, two types of molecules proposed as key to neural induction and patterning, bone morphogenetic protein (BMP) antagonists and fibroblast growth factor (FGF), require Smad10 for these activities. These data suggest that Smad10 may be a central mediator of the development of the frog nervous system.

Animals↗
PubMed1976

General pharmacological properties of a new non-opiate antitussive: zipeprol (3024 CERM). II. Actions on the cardiovascular system, intestinal transit and central nervous system.

The effects of 1-(2-methoxy-2-phenyl)-ethyl-4-(2-hydroxy-3-methoxy-3-phenyl)-propyl-piperazine-dihydrochloride (zipeprol, 3024 CERM, Respilene), a new nonopiate antitussive agent, have been studied on the cardiovascular system, intestinal function and the central nervous system. Most of these studies were performed comparatively with reference antitussives, particularly codeine, whose activites in these fields are the basis of its undesirable side effects. In the dog, zipeprol showed no hypotensive or cardiac-depressant activity. It did not alter pulmonary arterial pressure. An important antiarrhythmic action was apparent in studies on rhythm disturbances induced by ouabain and coronary ligation. Intestinal function, measured by the recording of peristaltic movements in the dog and the speed of intestinal transit in the rat, was not modified by the product. Zipeprol showed no characteristic action on the central nervous system. Analgesic activity was seen only at doses just below toxic levels. Finally in the rat and the mouse, no evidence of physical dependence was seen after prolonged treatment. This together with the absence of chemical similarity to the morphinics, leads to exclude the possibility of zipeprol treatment leading to addiction. The results of these studies allow zipeprol to be clearly distinguished from the opiate antitussives.

Animals↗
PubMed1998

Chagas' heart disease and the autonomic nervous system.

The autonomic nervous system is abnormal in patients with advanced Chagas' heart disease. Most researchers consider these autonomic abnormalities as primary, specific and irreversible. However, when and why these abnormalities appear in the natural history of Chagas' disease, is still the subject of intense controversy. Recent morphological and functional studies strongly suggest that the sympathetic and the parasympathetic abnormalities are preceded by myocardial damage and left ventricular dysfunction. Moreover, chagasic patients with cardiac failure benefit from drugs which antagonize neurohumoral activation. Consequently, the abnormalities of the autonomic nervous system of chagasic patients are very likely secondary and partially reversible.

Autonomic Nervous System↗
PubMed1992

The neurotoxic actions of ibotenic acid on cholinergic and opioid peptidergic systems in the central nervous system of the rat.

The neurotoxic effects produced by ibotenic acid (IA) induced chemical lesions of the central nervous system (CNS) cholinergic system were examined on the opioid peptidergic system in adult rats. Forebrain cholinergic systems were bilaterally lesioned by the infusion of IA (1 or 5 micrograms/site) into the nucleus basalis magnocellularis (NBM). One week after the injections, the animals were sacrificed, and activities of acetylcholinesterase (AChE), choline acetyltransferase (ChAT) and concentrations of beta-endorphin (beta-End) and Met-enkephalin (Met-Enk) were measured in different brain regions. Animals treated with IA showed a decrease in the activity of ChAT (-24%), AChE (-36%) and beta-End level (-33%) in the frontoparietal cortex (FC). For the first time we report that these changes were associated with a compensatory increase in the activity of ChAT (+27%), AChE (+25%), beta-End level (+66%) in the remaining part of the cortex, i.e. cortex devoid of frontal cortex (C-FC). Met-enkephalin level increased by 59% in the frontoparietal cortex and did not change in the cortex devoid of frontal cortex upon IA treatment. These results suggest that IA treatment results in changes in the activity of cortical ChAT and AChE, and beta-End level in the same direction. Injection of IA in the NBM did not cause a change in the activity of ChAT or AChE in other brain regions such as hippocampus, striatum or midbrain. In addition to cortex devoid of frontal cortex, midbrain also showed a significant increase in the beta-End level in the IA treated animals. However, pituitary beta-End decreased in the neurotoxin treated animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholinesterase↗