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Arterial pressure is rapidly and precisely readjusted by various reflexes. They are described from the anatomical and functional level. The most important is the medullary baroreflex. In spite of the complexity of their nervous connections and the numerous mediator substances involved, the cardiac vagal center and the sympathetic vasomotor centers are today better understood. The role of the brain is not purely reflex because it may also respond to biochemical variations (anoxia, circulating angiotensin). Finally, we shall describe the central mechanisms which play a role in situations as orthostatism, physical effort or stress. In relation to stress, we shall discuss the influence of suprabulbar structures on the baroreflexe and this will allow a description of three connected centers at different levels controlling arterial blood pressure via nervous mechanisms (i.e. diencephalic, medullary and spinal centers).
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A purpose of the study was determination of the relationships between the brain levels of neuro-mediators: noradrenaline (NA), dopamine (DA), 5-hydroxytryptamine (5-HT) and gamma-aminobutyric acid (GABA) and the development of tolerance to the sedative and anticonvulsive action of Nitrazepam. It was found that during tolerance development the GABA level increased in the cerebral tissue and changes appeared in the activity state of the serotoninergic system.
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Abnormalities of the nervous system are common occurrences among congenital defects and have been reported in most ruminant species. From a clinical standpoint, the signs of such defects create difficulty in arriving at an antemortem etiology through historical and physical examination alone. By first localizing clinical signs to their point of origin in the nervous system, however, a narrower differential list can be generated so that the clinician can pursue a definitive diagnosis. This article categorizes defects of the ruminant nervous system by location of salient clinical signs into dysfunction of one of more of the following regions: cerebrum, cerebellum,and spinal cord. A brief review of some of the more recognized etiologies of these defects is also provided. It is important to make every attempt to determine the cause of nervous system defects because of the impact that an inherited condition would have on a breeding program and for prevention of defects caused by infectious or toxic teratogen exposure.
Serologic studies were performed on 25 patients with systemic lupus erythematosus (SLE) during 29 acute episodes of central nervous system (CNS) disease. Increased anti-DNA antibody and decreased total serum hemolytic complement activity were observed only in those patients with associated extra-CNS disease manifestations. Patients with isolated CNS disease were otherwise in apparent clinical and serological remission regarding these two indices. No special association of cold-reactive IgM antilymphocyte antibodies was demonstrable in patients with ongoing CNS injury. Of special interest was an increased incidence of anti-Sm antibodies in the patients with CNS dysfunction relative to that in a large group of patients without neuropsychiatric disease. The incidence of anti-RNP was not increased. The data do not support direct involvement in SLE brain injury of either DNA/anti-DNA complexes or of lymphocytotoxic antibodies cross-reactive with brain cells, but do suggest an association of anti-Sm with CNS disease in this disorder.
Neuronal death during nervous system development, a widely observed phenomenon, occurs through unknown mechanisms. Recent evidence suggests an active, destructive process requiring new gene expression. Sulfated glycoprotein-2 (SGP-2), a secretory product of testicular Sertoli cells has been shown to up-regulate in several nonneural tissues undergoing programmed cell death and in several types of neuronal degeneration. In order to determine if this message up-regulates in neurons undergoing developmentally determined cell death, we have studied the expression of SGP-2 mRNA in the developing and adult rat central nervous system (CNS) with in situ hybridization. We also report on the expression of this message in nonneural tissues from several regions of the developing embryo. The developing and adult rat central nervous system as well as widely varied tissues in the rat embryo express SGP-2 mRNA in a pattern that does not correlate with regions undergoing developmental cell death. In the nervous system, SGP-2 mRNA is expressed in neuronal populations including motor neurons, cortical neurons, and hypothalamic neurons at ages when the period of developmental cell death has passed. In a nonneural tissue (palatal shelve epithelium) for which a developmental cell death period has been described, SGP-2 mRNA was not present in the region where cell death occurs. We conclude that SGP-2 mRNA expression cannot be correlated with programmed cell death in neural or nonneural tissues. The results of this study as well as recently reported SGP-2 homologies indicate a possible role for this protein in secretion and lipid transport.
The mature enteric nervous system (ENS) is characterized by a degree of neuronal phenotypic diversity and independence of central nervous system control unequaled by any other region of the peripheral nervous system. Studies that have utilized the immunocytochemical demonstration of neurofilament protein and explanation of primordial gut with subsequent growth in culture have indicated that the neural crest precursors of enteric neurons are already committed to the neuronal lineage when they colonize the bowel; however, neuronal phenotypic expression occurs within the gut itself. It is likely that precursors able to give rise to each type of neuron found in the mature ENS are present among the earliest neural crest émigrés to reach the bowel. In mice a proximodistal wave of neuronal phenotypic expression occurs that does not appear to reflect the descent of neuronal precursors. This observation, the known plasticity of developing neural crest-derived neurons, and the demonstration of a persistent population of proliferating neuroblasts in the gut raise the possibility that enteric neuronal phenotypic expression is influenced by the enteric microenvironment.
There are suggestions of the participation of nicotinic acetylcholine receptors (nAChRs), the acetylcholine degradation enzyme, acetylcholinesterase (AChE), and the acetylcholine synthesizing enzyme, choline acetyltransferase (ChAT), in the development of the nervous system. In this study, we aimed at comparing the development of some subunits of the nAChRs, AChE, and ChAT in the chick nervous system by standard immunohistochemical methods. The expression of all molecules investigated here appeared very early in ganglia (embryonic day 3.5-4), persisting into posthatching, except for ChAT, which is not detected after hatching in ganglia. A differential development was observed for nAChR subunits, with these receptors appearing around embryonic day 6 in some sites. The time-course of development of different nAChR subunits revealed several instances of transient expression (such as in the cerebellum), increasing expression (such as in the nucleus spiriformis lateralis), and diminishing expression into posthatching stages (such as in the oculomotor and throclear nuclei). Expression of AChE and ChAT also starts around embryonic day 6 in some structures and follows mainly increasing time-courses in the chick brain. The results of this study reveal a developmentally regulated expression of cholinergic system-related molecules in the chick nervous system and characterize differential time-courses of expression for nAChR subunits, AChE, and ChAT during development.
The central nervous system (CNS) is arguably one of the most complex systems in the universe. To understand the CNS, scientists have investigated a variety of molecules, including proteins, lipids, and various small molecules. However, one large class of molecules, noncoding RNAs (ncRNAs), has been relatively unexplored. ncRNAs function directly as structural, catalytic, or regulatory molecules rather than serving as templates for protein synthesis. The increasing variety of ncRNAs being identified in the CNS suggests a strong connection between the biogenesis, dynamics of action, and combinatorial regulatory potential of ncRNAs and the complexity of the CNS. In this review, we give an overview of the diversity and abundance of ncRNAs before delving into specific examples that illustrate their importance in the CNS. In particular, we cover recent evidence for the roles of microRNAs, small nucleolar RNAs, retrotransposons, the NRSE small modulatory RNA, and BC1/BC200 in the CNS. Finally, we speculate why ncRNAs are well adapted to improving organism-environment interactions.
OBJECTIVE: To define central nervous system infections of infants and children that occur as co-morbid or predisposing conditions of sepsis. DESIGN: Standard pediatric infectious disease references and the pertinent literature in English were reviewed from 1960 to 2002 to ascertain the previous methods and definitions utilized in clinical studies of the epidemiology and treatment of bacterial infections of the central nervous system. An accepted definition of bacterial meningitis defined by the Infectious Disease Society of America was reviewed and adapted to the previous clinical definitions. The information was formulated into a proposed standard for definite, probable, and possible bacterial infections of the central nervous system. RESULTS: The diagnosis of definite bacterial infection of the central nervous system, including bacterial meningitis, requires the isolation of the pathogen from the cerebrospinal fluid or other significant clinical site such as surgical tissue, an implanted device, or blood. Probable bacterial infection is defined by the association of a compatible clinical syndrome or cerebrospinal fluid changes associated with bacterial meningitis or other central nervous system infection, and confirmed as an anatomically defined infection by imaging or surgery, in association with positive blood cultures or bacterial antigen from cerebrospinal fluid. Possible bacterial meningitis may be defined as a compatible clinical syndrome with predefined cerebrospinal fluid changes in the absence of a confirmatory culture or antigen test from any site. CONCLUSIONS: Bacterial meningitis and other central nervous system bacterial infections can be defined as definite, probable, and possible with a combination of a defining compatible clinical syndrome and an anatomic definition by surgery or imaging, coupled with isolation of the organism, bacterial antigen, or other defining molecular component of the organism.
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Primary central nervous system lymphoma is a stage 1E non-Hodgkin's lymphoma confined to the nervous system. It is seen in immunocompetent and immunodeficient populations, the latter group associated with the Epstein-Barr virus. Primary central nervous system lymphoma can affect the brain, leptomeninges, spinal cord or eyes. The institution of high-dose methotrexate-based regimens and whole-brain radiation therapy has significantly increased survival, but neurotoxicity is high in patients over 60 years of age. Despite these advances, 50% of patients initially treated will relapse. Recent investigations include the use of rituximab (immunotherapy) and stem-cell transplantation, as well as regimens without whole-brain radiation therapy in the elderly. The optimal treatment regimen is yet to been determined.