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PubMedDate not supplied

Ultrastructure of the nervous system.

Within the nervous system, five cell types were studied by the electron microscope: the neuron, astrocyte, oligodendroglia, microglia and ependymal cells. The neurons are characterized by the Nissl substance within the perikaryon, the neurotubules and the neurofilaments. The three types of glial cells can be distinguished from one another. The astrocyte has relatively lucent cytoplasm and contains filaments which extend into long cytoplasmic processes. The oligodendroglia has electron-dense cytoplasm with thin extensions wedged between the cellular processes of the neuropil. The microglia cytoplasm is similar to the oligodendroglia but can be differentiated by the peculiar convoluted outline of the nuclear membrane and the clear space which separate the nucleus from the cytoplasm. The ependymal cell has characteristic microvilli and cilia at its ventricular surface. The cytoplasm contain parabasal bodies and tight junctions between adjacent cells. In the peripheral nerve, the axon and the myelin sheath are located within the Schwann cells. The terminal nerve endings from enlargements filled with synaptic vesicles. Electron microscopy of the nervous system is not only essential for research, but is also helpful in diagnosis of certain diseases.

Astrocytes↗
PubMed1998

Programmed cell death is a universal feature of embryonic and postnatal neuroproliferative regions throughout the central nervous system.

During central nervous system (CNS) development, programmed cell death (PCD) has been viewed traditionally as a fate reserved for differentiating neurons that are in the process of making synaptic connections. Recent studies in the embryonic cerebral cortex (Blaschke et al. [1996] Development 122:1165-1174), however, have shown that many neuroblasts in the proliferative ventricular zone undergo PCD as well and that this likely represents a novel form distinct from that found in regions of postmitotic neurons. To determine the commonality of this form of PCD throughout the CNS, the prevalence of dying cells identified by in situ end labeling plus (ISEL +; Blaschke et al. [1996]) was determined within populations of proliferating neuroblasts that were identified by rapid bromodeoxyuridine incorporation. Based on this approach, dying cells were observed to be a common feature of all proliferative neuroblast populations examined. In addition, when ISEL+ was combined with in situ hybridization for postmitotic neural gene-1 (png-1; Weiner and Chun [1997] J. Comp. Neurol. 381:130-142), which identifies newly postmitotic neurons, a positive correlation was found between the start of differentiation and the onset of PCD. These data indicate that PCD in neuroblast proliferative zones is a universal feature of nervous system development. Moreover, cell death represents a prominent cell fate that may be linked to mechanisms of differentiation.

Aging↗
PubMed1992

Neurotoxicity of dichlorvos: effect on antioxidant defense system in the rat central nervous system.

The effect of dichlorvos exposure (5 mg kg-1 body wt, ip) on lipid peroxidation and antioxidant defense system in different regions of the rat central nervous system was studied. In the present paper an inhibition of acetylcholinesterase activity was used as an index of dichlorvos neurotoxicity. We observed significant increases in the activities of the antioxidant enzymes superoxide dismutase (SOD) and catalase which were accompanied by a decrease in the values of lipid peroxidation. Dichlorvos exposure also resulted in a significant decrease in glutathione peroxidase activity. The decreased levels of both reduced and oxidized glutathione as observed on dichlorvos exposure affected the GSH/GSSG ratio. These results indicate that the enzymes SOD and catalase may enhance the disposal of potentially toxic radicals. Furthermore, the decrease in GSH levels may be a mechanism for the detoxification of dichlorvos in the brain.

Acetylcholinesterase↗
PubMed1994

Cerebrospinal fluid interleukin-6, prostaglandin E2 and autoantibodies in patients with neuropsychiatric systemic lupus erythematosus and central nervous system infections.

Cerebrospinal fluid (CSF) from patients with a variety of central nervous system (CNS) disorders was assayed for cytokines, prostaglandins, and autoantibodies. CSF interleukin-6 (IL-6) in patients with CNS infection (374.24 +/- 92.61 pg/mL) and neuropsychiatric systemic lupus erythematosus (NP-SLE) (71.40 +/- 5.89 pg/mL) were significantly higher than in patients with CNS inflammation (33.92 +/- 29.36 pg/mL) or controls (non-inflammatory CNS diseases) (4.35 +/- 3.00 pg/mL). Interleukin-1 beta, interferon alpha, and tumor necrosis factor alpha were undetectable in these samples: CSF prostaglandin E2 (PGE2) also exhibited similar patterns as IL-6. CSF immunoglobulin G (IgG) in patients with NP-SLE (8.84 +/- 1.80 mg/dL) was much higher than in patients with CNS infection (4.65 +/- 3.09 mg/dL), CNS inflammation (2.54 +/- 1.24 mg/dL), or controls (2.11 +/- 1.03 mg/dL). CSF autoantibodies against calf thymus antigens were present in patients with NP-SLE but not in patients with CNS infection as demonstrated by immunoblot. These results suggest that high IL-6 and PGE2 in CSF favors the diagnosis of CNS infection, while modestly elevated IL-6, high IgG, and autoantibodies against calf thymus antigens in CSF are the features of NP-SLE.

Autoantibodies↗
PubMed1998

Pharmacological interactions between magnesium ion and adenosine on monoaminergic system in the central nervous system.

The effects of magnesium ion (Mg2+), adenosine A1 and A2 receptor ligands on basal extracellular levels of striatal dopamine, hippocampal dopamine and serotonin were investigated by using in vivo microdialysis in freely moving rats. An increase in extracellular levels of Mg2+ ([Mg2+]o) reduced extracellular striatal and hippocampal monoamine levels, in a concentration dependent manner. The extracellular monoamine level was increased by perfusion with a non-selective adenosine receptor antagonist, caffeine, a selective adenosine A1 receptor antagonist, 8-cyclopentyl-1,3-dimethylxanthine (CPT), and an antiepileptic drug, carbamazepine, whereas adenosine, a selective adenosine A1 receptor agonist, 2-chloro-N6-cyclopentyladenosine (CCPA) reduced extracellular monoamine levels. The former and latter were reduced and enhanced by an increase in [Mg2+]o, respectively. Neither a selective adenosine A2 agonist, N6-[2-(3,5-dimethoxyphenyl)-2-(methylphenyl) ethyl]adenosine (PD125944), nor an antagonist, 3,7-dimethyl-1-propargylxanthine (DMPX), affected extracellular monoamine levels. Under the conditions of adenosine A1 receptor blockade by CPT, adenosine, PD125944 and carbamazepine increased extracellular monoamine levels, whereas caffeine and DMPX decreased them. These stimulatory effects of adenosine, PD125944 and carbamazepine were enhanced by an increase in [Mg2+], whereas the inhibitory effects of caffeine and DMPX were reduced by Mg2+, in a concentration dependent manner. It is concluded that an activation of adenosine A1 and A2 receptors decrease and increase extracellular levels of striatal dopamine, hippocampal dopamine and serotonin, respectively. These whereas the stimulatory effects of adenosine A2 receptor on extracellular levels of monoamine are masked by the inhibitory effects of adenosine A1 receptor. In addition, an increase in [Mg2+]o enhances and reduces the effects of adenosine receptor agonists and antagonists on extracellular monoamine levels, respectively.

Adenosine↗
PubMed1981

Neurochemical and morphological studies on the myelin of peripheral nervous system from Shiverer mutant mice: absence of basic proteins common to central nervous system.

Shiverer mouse is characterized by poor lamella formation and absence of major dense line in the CNS myelin. PNS of the Shiverer was normal with regard to myelin lamellar formation, immunohistochemical staining of the Schwann cells by S-100 protein, and the activity of 2',3'-cyclic nucleotide 3'-phosphohydrolase. Analysis of the purified myelin by SDS-polyacrylamide gel electrophoresis revealed that P1 and Pr, which are common to BP in CNS, and PM protein were missing, while P0 and P2 proteins were of the same level as the control.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMedDate not supplied

Hemodynamic effects of endothelin after systemic and central nervous system administration in the conscious rat.

The effects of endothelin-1 (ET-1) administered i.v. or intracerebroventricularly (i.c.v.) on arterial pressure (MAP), heart rate and cardiac output were studied in the conscious rat. Systemic injection of ET-1 (0.1 to 1 nmol/kg i.v.) increased dose-dependently MAP and decreased heart rate. The doses of 0.3 and 1 nmol/kg produced initially transient hypotension and tachycardia which were accompanied by a decrease in total peripheral resistance index (TPRI). Cardiac output was significantly reduced and TPRI increased during the pressor response to 0.3 and 1 nmol/kg ET-1. ET-1 i.c.v. (30 pmol/kg) produced a profound pressor and vasoconstrictor response which was followed by cardiovascular collapse and death within 20 min after i.c.v. injection. Low doses (1 to 10 pmol/kg) of ET-1 i.c.v. had no effect on the cardiovascular system. The present data are in accordance with the studies demonstrating biphasic blood pressure and heart rate responses to i.v. ET-1 in the rat. Profound cardiac depressor and peripheral vasoconstrictor responses were found to accompany the pressor phase. Our results also showed for the first time direct central pressor and vasoconstrictor effects of ET-1 insinuating that endothelin might be a neuropeptide participating in the central cardiovascular control.

Animals↗
PubMed2002

Effects of systemic and central nervous system localized inflammation on the contributions of metabolic precursors to the L-kynurenine and quinolinic acid pools in brain.

L-Kynurenine and quinolinic acid are neuroactive L-tryptophan-kynurenine pathway metabolites of potential importance in pathogenesis and treatment of neurologic disease. To identify precursors of these metabolites in brain, [(2)H(3) ]-L-kynurenine was infused subcutaneously by osmotic pump into three groups of gerbils: controls, CNS-localized immune-activated, and systemically immune-activated. The specific activity of L-kynurenine and quinolinate in blood, brain and systemic tissues at equilibrium was then quantified by mass spectrometry and the results applied to a model of metabolism to differentiate the relative contributions of various metabolic precursors. In control gerbils, 22% of L-kynurenine in brain was derived via local synthesis from L-tryptophan/formylkynurenine versus 78% from L-kynurenine from blood. Quinolinate in brain was derived from several sources, including: local tissue L-tryptophan/formylkynurenine (10%), blood L-kynurenine (35%), blood 3-hydroxykynurenine/3-hydroxyanthranilate (7%), and blood quinolinate (48%). After systemic immune-activation, however, L-kynurenine in brain was derived exclusively from blood, whereas quinolinate in brain was derived from three sources: blood L-kynurenine (52%), blood 3-hydroxykynurenine or 3-hydroxyanthranilate (8%), and blood quinolinate (40%). During CNS-localized immune activation, > 98% of both L-kynurenine and quinolinate were derived via local synthesis in brain. Thus, immune activation and its site determine the sources from which L-kynurenine and quinolinate are synthesized in brain. Successful therapeutic modulation of their concentrations must take into account the metabolic and compartment sources.

Animals↗
PubMed1991

[Fundamental and applied studies of AIDS of the nervous system. A new stage in the study of slow infections of the nervous system].

Problems of the etiology, pathogenesis, classification, clinical manifestations, diagnosis and treatment of neuro-AIDS are analyzed. The causes of the origin and mechanisms of the development of multiple sclerosis and lateral amyotrophic sclerosis, attributable presumably to slow infections are discussed from the standpoint of the retroviral etiology. In the author's opinion, it is more probable in the first case.

Acquired Immunodeficiency Syndrome↗
PubMed1990

[Current status of research of a lymphatic system in the nervous system: initial trials with cerebral lymphography].

After having recognized the existence of post-mortem intra-cerebral circulation of a coloring substance with lymphatic resorption, the author is continuing his research by injecting a product sharing the same characteristics: Iotrolan. Brain X-rays show brain circulation from the cortex to the ventricular cavities and from the spinal cord to the bulbar area and to the cerebellum. One question deserves to be asked: what is this circulation?

Animals↗