Enzymes that degrade phosphatidylinositol 4-phosphate and phosphatidylinositol 4,5-bisphosphate have different developmental profiles in chick brain

1990 ◽  
Vol 68 (4) ◽  
pp. 800-803 ◽  
Author(s):  
Frederick B. St.C. Palmer
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Specific Activity ◽  
Chick Brain ◽  
Phosphodiesterase Activity ◽  
Developmental Profiles ◽  
Key Words Brain Development ◽  
Specific Activities ◽  
Phosphatidylinositol 4 ◽  
Preferential Association

The activities and subcellular distributions of the hydrolases that degrade polyphosphoinositides were compared in the developing chick central nervous system. Specific activities increased 2- 3-fold and total activities increased 13-to 16-fold. Phosphatidylinositol 4-phosphate phosphatase is localized in membranes (78%), but is preferentially associated with nonmyelin membranes, since the increase in specific activity preceded myelination and proportions of membrane and soluble activities were constant during accumulation of myelin membranes. Phosphatidylinositol 4,5-bisphosphate phosphatase is largely soluble in embryonic (57%) and myelinated brain (50%). Although specific activity increased coincident with myelination, approximately equal increases in soluble and membrane activity indicate no preferential association with myelin membranes. Phosphatidylinositol 4,5-bisphosphate phosphodiesterase activity increased only in the early stages of myelination, but showed some preferential association with myelin membranes, since the proportion of soluble diesterase declined from 40 to 25%.Key words: brain, development, myelin, phosphodiesterase, phosphoinositide, phosphomonoesterase, phospholipids.

A radiotracer method for the measurement of central nervous system catecholamines in vivo

1978 ◽  
Vol 56 (3) ◽  
pp. 535-538 ◽  
Author(s):  
S. W. Tang ◽  
H. C. Stancer ◽  
J. J. Warsh
Keyword(s):  
Central Nervous System ◽  
Animal Model ◽  
Nervous System ◽  
Specific Activity ◽  
Brain Catecholamines ◽  
Radiotracer Method ◽  
New Strategy ◽  
The Central Nervous System ◽  
6 Hydroxydopamine

A new strategy for measurement of brain catecholamines was tested in an animal model. [3H]Norepinephrine was infused intravenously in rabbits to label the peripheral norepinephrine pools. The specific activity of urinary 3-methoxy-4-hydroxymandelic acid was consistently higher than that for 3-methoxy-4-hydroxyphenylglycol (MHPG). Central sympathectomy with 6-hydroxydopamine abolished this difference. Using the formula we propose, it is estimated that 30–50% of urinary MHPG originates from the central nervous system.

scholarly journals Central nervous system (CNS)–resident natural killer cells suppress Th17 responses and CNS autoimmune pathology

2010 ◽  
Vol 207 (9) ◽  
pp. 1907-1921 ◽  
Author(s):  
Junwei Hao ◽  
Ruolan Liu ◽  
Wenhua Piao ◽  
Qinghua Zhou ◽  
Timothy L. Vollmer ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Nk Cells ◽  
Natural Killer ◽  
Nk Cell ◽  
Specific Activity ◽  
Cns Inflammation ◽  
Selective Blockade ◽  
Autoimmune Pathology ◽  
Organ Specific

Natural killer (NK) cells of the innate immune system can profoundly impact the development of adaptive immune responses. Inflammatory and autoimmune responses in anatomical locations such as the central nervous system (CNS) differ substantially from those found in peripheral organs. We show in a mouse model of multiple sclerosis that NK cell enrichment results in disease amelioration, whereas selective blockade of NK cell homing to the CNS results in disease exacerbation. Importantly, the effects of NK cells on CNS pathology were dependent on the activity of CNS-resident, but not peripheral, NK cells. This activity of CNS-resident NK cells involved interactions with microglia and suppression of myelin-reactive Th17 cells. Our studies suggest an organ-specific activity of NK cells on the magnitude of CNS inflammation, providing potential new targets for therapeutic intervention.

scholarly journals Photoaffinity labelling of central-nervous-system myelin. Evidence for an endogenous type I cyclic AMP-dependent kinase phosphorylating the larger subunit of 2′,3′-cyclic nucleotide 3′-phosphodiesterase

1984 ◽  
Vol 221 (2) ◽  
pp. 361-368 ◽  
Author(s):  
J M Bradbury ◽  
R J Thompson
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Protein Kinase ◽  
Cyclic Amp ◽  
Cyclic Nucleotide ◽  
Type I ◽  
Phosphodiesterase Activity ◽  
Dependent Protein Kinase ◽  
Photoaffinity Labelling ◽  
Dependent Protein

Endogenous cyclic AMP-stimulated phosphorylation of a 49700-Mr Wolfgram protein component in rabbit central nervous system was investigated by using photoaffinity labelling and 2′,3′-cyclic nucleotide 3′-phosphodiesterase activity staining after electroblotting on to nitrocellulose paper. Photoaffinity labelling with 8′-azidoadenosine 3′,5′-cyclic monophosphate showed a cyclic AMP-binding protein that appeared to be intrinsic to the myelin membrane and appeared to represent the R-subunit of a type I cyclic AMP-dependent protein kinase. This photoaffinity-labelled protein was of larger apparent Mr than the protein showing cyclic AMP-stimulated phosphorylation. Blotting of one-dimensional sodium dodecyl sulphate/polyacrylamide-gel electrophoretograms followed by staining for 2′,3′-cyclic nucleotide 3′-phosphodiesterase activity showed two activity bands corresponding to the two components of the Wolfgram protein doublet. Cyclic AMP-stimulated protein phosphorylation corresponded to the upper component of this doublet. Electroblotting of two-dimensional non-equilibrium pH-gradient electrophoretograms also showed co-migration of cyclic AMP-stimulated protein phosphorylation with enzyme activity. It is proposed that central-nervous-system myelin contains an endogenous type I cyclic-AMP dependent protein kinase that phosphorylates the larger subunit of 2′,3′-cyclic nucleotide 3′-phosphodiesterase.

Monofocal origin of telencephalic oligodendrocytes in the anterior entopeduncular area of the chick embryo

Development ◽  
2001 ◽  
Vol 128 (10) ◽  
pp. 1757-1769 ◽  
Author(s):  
C. Olivier ◽  
I. Cobos ◽  
E.M. Perez Villegas ◽  
N. Spassky ◽  
B. Zalc ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Chick Embryo ◽  
Embryonic Development ◽  
Progenitor Cells ◽  
Oligodendrocyte Progenitor Cells ◽  
Chick Brain ◽  
The Central Nervous System ◽  
The Brain

Oligodendrocytes are the myelin-forming cells in the central nervous system. In the brain, oligodendrocyte precursors arise in multiple restricted foci, distributed along the caudorostral axis of the ventricular neuroepithelium. In chick embryonic hind-, mid- and caudal forebrain, oligodendrocytes have a basoventral origin, while in the rostral fore-brain oligodendrocytes emerge from alar territories (Perez Villegas, E. M., Olivier, C., Spassky, N., Poncet, C., Cochard, P., Zalc, B., Thomas, J. L. and Martinez, S. (1999) Dev. Biol. 216, 98–113). To investigate the respective territories colonized by oligodendrocyte progenitor cells that originate from either the basoventral or alar foci, we have created a series of quail-chick chimeras. Homotopic chimeras demonstrate clearly that, during embryonic development, oligodendrocyte progenitors that emerge from the alar anterior entopeduncular area migrate tangentially to invade the entire telencephalon, whereas those from the basal rhombomeric foci show a restricted rostrocaudal distribution and colonize only their rhombomere of origin. Heterotopic chimeras indicate that differences in the migratory properties of oligodendroglial cells do not depend on their basoventral or alar ventricular origin. Irrespective of their origin (basal or alar), oligodendrocytes migrate only short distances in the hindbrain and long distances in the prosencephalon. Furthermore, we provide evidence that, in the developing chick brain, all telencephalic oligodendrocytes originate from the anterior entopeduncular area and that the prominent role of anterior entopeduncular area in telencephalic oligodendrogenesis is conserved between birds and mammals.

Inhibition of the complement anaphylatoxin activities in the central nervous system disorders

2021 ◽  
Vol 21 (2) ◽  
pp. 37-52
Author(s):  
Kseniya A. Nekrasova ◽  
Alexander M. Ischenko ◽  
Alexander V. Trofimov
Keyword(s):  
Traumatic Brain Injury ◽  
Central Nervous System ◽  
Nervous System ◽  
Brain Injury ◽  
Specific Activity ◽  
Craniocerebral Trauma ◽  
Epidemiological Data ◽  
Cerebrovascular Diseases ◽  
The Central Nervous System

The review is devoted to inhibition of the complement anaphylatoxin activities in diseases of the central nervous system. Here we present epidemiological data on the prevalence of cerebrovascular diseases, in particular, ischemic stroke and craniocerebral trauma. The mechanisms of complement activation and complement-mediated pathology in the central nervous system are considered in detail. Clinical data confirming the role of the complement system in the pathogenesis of stroke and of traumatic brain injury secondary injury are presented. We also summarize the results of in vivo specific activity studies of the complement anaphylatoxin inhibitors using animal models of stroke and traumatic brain injury. Briefly described is the present state of the art in developing drugs that target the effector compounds of the complement cascade.

scholarly journals Regulation by cytidine nucleotides of the acylation of sn-[14C]glycerol 3-phosphate. Regional and subcellular distribution of the enzymes responsible for phosphatidic acid synthesis de novo in the central nervous system of the rat

1973 ◽  
Vol 132 (3) ◽  
pp. 381-394 ◽  
Author(s):  
F. Possmayer ◽  
B. Meiners ◽  
J. B. Mudd
Keyword(s):  
Central Nervous System ◽  
Endoplasmic Reticulum ◽  
Nervous System ◽  
Phosphatidic Acid ◽  
Subcellular Distribution ◽  
De Novo ◽  
Specific Activity ◽  
Reductase Activity ◽  
Brain Lipids ◽  
The Central Nervous System

1. The regional and subcellular distribution of the incorporation of sn-[14C]glycerol 3-phosphate into rat brain lipids in vitro was investigated and compared with the relative specific activity of various chemical and enzyme markers. The similarity between the subcellular distribution of this incorporation and of NADPH-cytochrome c reductase activity indicated that the synthesis of phosphatidic acid via this route correlated with the presence of endoplasmic reticulum. 2. Experiments in which various amounts of the microsomal fraction were added to fixed amounts of nuclear, myelin, nerve-ending and mitochondrial preparations clearly demonstrated that the endoplasmic-reticulum contamination of these fractions was entirely responsible for the incorporation of sn-[14C]glycerol 3-phosphate. 3. The presence of CMP or CTP inhibited the incorporation of sn-[14C]glycerol 3-phosphate into the whole homogenate. Similar effects were observed with individual fractions, except for the mitochondria. With the mitochondrial fraction the effect of these cytidine nucleotides varied with the preparation, stimulating in some preparations and inhibiting with other preparations. The presence of CDP-choline stimulated the incorporation into the whole homogenate and to a lesser extent into the subcellular fractions. 4. These results indicate that the various organelles of the central nervous system are more dependent on endoplasmic reticulum for the production of glycerolipids de novo than has previously been appreciated.

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