scholarly journals Antibodies to synaptic vesicles purified from Narcine electric organ bind a subclass of mammalian nerve terminals.

1980 ◽  
Vol 87 (1) ◽  
pp. 104-113 ◽  
Author(s):  
J E Hooper ◽  
S S Carlson ◽  
R B Kelly
Keyword(s):  
Nervous System ◽  
Synaptic Vesicles ◽  
Chromaffin Cells ◽  
Molecular Layer ◽  
Electric Organ ◽  
Antigenic Determinants ◽  
Nerve Terminals ◽  
The Central Nervous System ◽  
Adrenal Chromaffin ◽  
Mammalian Nerve

Antibodies were raised in rabbits to synaptic vesicles purified to homogeneity from the electric organ of Narcine brasiliensis, a marine electric ray. These antibodies were shown by indirect immunofluorescence techniques to bind a wide variety of nerve terminals in the mammalian nervous system, both peripheral and central. The shared antigenic determinants are found in cholinergic terminals, including the neuromuscular junction, sympathetic ganglionic and parasympathetic postganglionic terminals, and in those synaptic areas of the hippocampus and cerebellum that stain with acetylcholinesterase. They are also found in some noncholinergic regions, including adrenergic sympathetic postganglionic terminals, the peptidergic terminals in the posterior pituitary, and adrenal chromaffin cells. They are, however, not found in many noncholinergic synapse-rich regions. Such regions include the molecular layer of the cerebellum and those laminae of the dentate gyrus that receive hippocampal associational and commissural input. We conclude that one or more of the relatively small number of antigenic determinants in pure electric fish synaptic vesicles have been conserved during evolution, and are found in some but not all nerve terminals of the mammalian nervous system. The pattern of antibody binding in the central nervous system suggests unexpected biochemical similarities between nerve terminals heretofore regarded as unrelated.

scholarly journals An antiserum specific for cholinergic synaptic vesicles from electric organ.

1980 ◽  
Vol 87 (1) ◽  
pp. 98-103 ◽  
Author(s):  
S S Carlson ◽  
R B Kelly
Keyword(s):  
Synaptic Vesicle ◽  
Synaptic Vesicles ◽  
Membrane Fraction ◽  
Motor Nerve ◽  
Buoyant Density ◽  
Electric Organ ◽  
Rabbit Serum ◽  
Antigenic Determinants ◽  
Nerve Terminals ◽  
Isopycnic Centrifugation

Rabbit antisera to highly purified synaptic vesicles from the electric organ of Narcine brasiliensis, an electric ray, reveal a unique population of synaptic vesicle antigens in addition to a population shared with other electric organ membranes. Synaptic vesicle antigens were detected by binding successively rabbit antivesicle serum and radioactive goat anti-rabbit serum. To remove antibodies directed against antigens common to synaptic vesicles and other electric organ fractions, the antivesicle serum was extensively preadsorbed against an electric organ membrane fraction that was essentially free of synaptic vesicles. The adsorbed serum retained 40% of its ability to bind to synaptic vesicles, suggesting that about half of the antigenic determinants are unique. Vesicle antigens were quantified with a radioimmunoassay (RIA) that utilized precipitation of antibody-antigen complexes with Staphylococcus aureus cells. By this assay, the vesicles, detected by their acetylcholine (ACh) content and the antigens detected by the RIA, have the same buoyant density after isopycnic centrifugation of crude membrane fractions on sucrose and glycerol density gradients. The ratio of ACh to antigenicity was constant across the vesicle peaks and was close to that observed for vesicles purified to homogeneity. Even though the vesicles make up only approximately 0.5% of the material in the original homogenate, the ratio of acetylcholine to vesicle antigenicity could still be measured and also was indistinguishable from that of pure vesicles. We conclude that synaptic vesicles contain unique antigenic determinants not present to any measurable extent in other fractions of the electric organ. Consequently, it is possible to raise a synaptic vesicle-specific antiserum that allows vesicles to be detected and quantified. These findings are consistent with earlier immunohistochemical observations of specific antibody binding to motor nerve terminals.

scholarly journals Further Investigations on the Function of the Electrical Organ of the Skate

1889 ◽  
Vol 1 (1) ◽  
pp. 74-74 ◽  
Author(s):  
Burdon Sanderson ◽  
F. Gotch
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Electromotive Force ◽  
Electric Organ ◽  
Physiological Laboratory ◽  
The Central Nervous System ◽  
Work Done ◽  
The Way

During the month of September, 1888, we availed ourselves of the facilities afforded by the Laboratory for the purpose of continuing the investigations began by us the year before, of the function of the electrical organ of the skate. In the record of the work done by us in 1887 at St. Andrews, published in the Journal of Physiology, vol. ix, p. 137, we indicated several new lines of investigation which we hoped to pursue if the opportunity offered. Two of these indications we have now been able to fulfil satisfactorily, namely, those relating to the electromotive force of the shock, and to the way in which the function of the electric organ is controlled and influenced by the central nervous system. In the first of these inquiries, we used apparatus which was brought from the Oxford Physiological Laboratory, and temporarily fitted up in the room at Plymouth, which is set apart for physiological researches, and which we found well adapted for this purpose. For the second, a large number of experiments and consequently a considerable number of fish were requisite. Forty skates of various species (Raia Batis, R. clavata, R. microcellata, and R. maculata) were supplied to us and used in our researches, of which the result will shortly be ready for publication.We desire to express in the strongest terms our appreciation of the advantages afforded by the Laboratory for physiological researches. We would also record our personal obligation to the Director for his uniform courtesy and untiring zeal in obtaining for us, in spite of considerable difficulties, the material required for our work.

Acute Hypoxia Induces Enkephalin Production and Release in an Adrenergic Cell Line Model of Neonatal Chromaffin Cell Responses to Hypoxic Stress

2018 ◽  
Vol 35 (11) ◽  
pp. 1100-1106
Author(s):  
Alexa Calero ◽  
Hazel Villanueva ◽  
Priyadarshani Giri ◽  
Arthur Tischler ◽  
James Powers ◽  
...  
Keyword(s):  
Nervous System ◽  
Adrenal Medulla ◽  
Chromaffin Cells ◽  
Acute Hypoxia ◽  
Enzyme Linked Immunosorbent Assay ◽  
Messenger Ribonucleic Acid ◽  
Objective Prior ◽  
A Cell ◽  
The Central Nervous System ◽  
Heart Contractility

Objective Prior to maturation of the human sympathetic nervous system, the neonatal adrenal medulla senses and responds to hypoxia. In addition to catecholamine release, the adrenal medulla synthesizes and stores opioid peptides, notably enkephalin (ENK). However, it is not known whether acute hypoxia evokes adrenal ENK production and release, as seen in the central nervous system (CNS). We hypothesize that acute hypoxia stimulates synthesis and release of ENK in chromaffin cells. Study Design Cultures of adrenergic mouse pheochromocytoma cells (MPC) 10/9/96CR were incubated in 10% oxygen (O2) at intervals of up to 60 minutes. ENK content and release were measured by Met-ENK enzyme-linked immunosorbent assay (ELISA). ENK messenger ribonucleic acid (mRNA) was analyzed by quantitative reverse-transcriptase polymerase chain reaction (PCR). Results Incubation of MPC 10/9 cells in 10% O2 evoked rapid release of epinephrine and of Met-ENK which increased approximately twofold in 15 minutes. Reduced [O2] also induced an overall increase (14%) in cellular ENK peptide content within 60 minutes. Acute hypoxia-stimulated release of Met-ENK was accompanied by increased mRNAENK expression in MPC 10/9s, a cell culture model of adrenergic chromaffin cells. Conclusion We speculate that the ability of reduced [O2] to evoke ENK release from chromaffin cells may influence blood pressure regulation and heart contractility, thereby providing an adaptive survival advantage during neonatal asphyxia.

Glial response in the central nervous system of cats with feline infectious peritonitis

2016 ◽  
Vol 18 (12) ◽  
pp. 1023-1030 ◽  
Author(s):  
Leonardo P Mesquita ◽  
Aline S Hora ◽  
Adriana de Siqueira ◽  
Fernanda A Salvagni ◽  
Paulo E Brandão ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Ricinus Communis ◽  
Molecular Layer ◽  
Lectin Histochemistry ◽  
Vimentin Expression ◽  
Feline Infectious Peritonitis ◽  
The Central Nervous System ◽  
Microglial Response ◽  
Cns Lesions

Objectives The aim of the study was to evaluate central nervous system (CNS) lesions in non-effusive and effusive cases of feline infectious peritonitis (FIP) regarding aspects related to astrocytic and microglial reactions. Methods Five necropsied cats that were naturally infected with FIP virus, confirmed by reverse transcriptase polymerase chain reaction and immunohistochemistry, with different intensities of CNS lesions, were studied. Brain and cerebellum were evaluated by light microscopy and immunohistochemistry for glial fibrillary acidic protein (GFAP) and vimentin to assess astrocytic morphology, and lectin histochemistry for Ricinus communis agglutinin-I (RCA-I) to detect microglia was performed to evaluate the glial response in the CNS of cats with FIP. Results An important astrocytic response in many areas of the CNS of all cats, including the periventricular areas of lateral ventricles and fourth ventricle, the molecular layer of the cerebellum and cerebral cortex, was visualized. This astrocytic reactivity was associated with areas of granulomatous or pyogranulomatous vasculitis/perivasculitis in most cases, and it was characterized by multifocal to coalescing astrocytosis and astrogliosis with an increase in the expression of intermediate filaments, such as GFAP. However, astrocytes exhibited strong vimentin expression in neuroparenchyma with severe inflammatory and necrotic changes, but GFAP expression was mild or absent in these cases. A microglial response was present only in severe lesions, and RCA-I expression was detected primarily in gitter cells and resting microglia. Conclusions and relevance The present study indicates a strong astrocytic response, including the presence of many less differentiated vimentin-positive astrocytes and gitter cells positive for RCA-1 in severe lesions in the CNS of cats with FIP.

Gaseous Transmitter Regulation of Catecholamine Secretion by hypoxia in Murine Adrenal Chromaffin Cells

2021 ◽  
Author(s):  
Anna Gridina ◽  
Xiaoyu Su ◽  
Shakil A. Khan ◽  
Ying-Jie Peng ◽  
Benjamin L Wang ◽  
...  
Keyword(s):  
Nervous System ◽  
Protein Kinase ◽  
Guanylyl Cyclase ◽  
Chromaffin Cells ◽  
Soluble Guanylyl Cyclase ◽  
Protein Kinase G ◽  
Adrenal Chromaffin Cells ◽  
Wild Type ◽  
Genetic Deletion ◽  
Adrenal Chromaffin

Emerging evidence suggests that gaseous molecules, carbon monoxide (CO) and hydrogen sulfide (H2S) generated by heme oxygenase-(HO)-2 and cystathionine γ-lyase (CSE), respectively, function as transmitters in the nervous system. Present study examined the roles of CO and H2S in hypoxia-induced catecholamine (CA) release from adrenal medullary chromaffin cells (AMC). Studies were performed on AMC from adult (≥6 weeks of age) wild type (WT), HO-2 null, CSE null and HO-2/CSE double null mice of either gender. CA secretion was determined by carbon fiber amperometry and [Ca2+]i by microflurometry using Fura-2. HO-2- and CSE immunoreactivities were seen in WT AMC, which were absent in HO-2 and CSE null mice. Hypoxia (medium pO2 30-38 mmHg) evoked CA release and elevated [Ca2+]i. The magnitude of hypoxic response was greater in HO-2 null mice and in HO inhibitor treated WT AMC compared to controls. H2S levels were elevated in HO-2 null AMC. Either pharmacological inhibition or genetic deletion of CSE prevented the augmented hypoxic responses of HO-2 null AMC and H2S donor rescued AMC responses to hypoxia in HO-2/CSE double null mice. CORM-3, a CO donor, prevented the augmented hypoxic responses in WT and HO-2 null AMC. CO donor reduced H2S levels in WT AMC. The effects of CO donor were blocked by either ODQ or 8pCT, inhibitors of soluble guanylyl cyclase (SGC) or protein kinase G, respectively. These results suggest that HO-2-derived CO inhibits hypoxia-evoked CA secretion from adult murine AMC involving soluble guanylyl cyclase (SGC)-protein kinase G (PKG)-dependent regulation of CSE- derived H2S.

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