Symbiotic Origin of Eukaryotic Nucleus: From Cell Body to Neo-Energide

2018 ◽  
pp. 39-66 ◽  
Author(s):  
František Baluška ◽  
Sherrie Lyons
Keyword(s):  
Cell Body ◽  
Eukaryotic Nucleus

Localization of DNA in chromatin using ESI and osmium ammine staining

1990 ◽  
Vol 48 (3) ◽  
pp. 116-117
Author(s):  
C.L. Woodcock ◽  
R.A. Horowitz ◽  
D. P. Bazett-Jones ◽  
A.L. Olins
Keyword(s):  
Spectroscopic Imaging ◽  
Energy Losses ◽  
Electron Spectroscopic Imaging ◽  
Feulgen Reaction ◽  
Specific Location ◽  
Eukaryotic Nucleus ◽  
Chromatin Fibers ◽  
Patiria Miniata ◽  
Model Structures

In the eukaryotic nucleus, DNA is packaged into nucleosomes, and the nucleosome chain folded into ‘30nm’ chromatin fibers. A number of different model structures, each with a specific location of nucleosomal and linker DNA have been proposed for the arrangment of nucleosomes within the fiber. We are exploring two strategies for testing the models by localizing DNA within chromatin: electron spectroscopic imaging (ESI) of phosphorus atoms, and osmium ammine (OSAM) staining, a method based on the DNA-specific Feulgen reaction.Sperm were obtained from Patiria miniata (starfish), fixed in 2% GA in 150mM NaCl, 15mM HEPES pH 8.0, and embedded In Lowiciyl K11M at -55C. For OSAM staining, sections 100nm to 150nm thick were treated as described, and stereo pairs recorded at 40,000x and 100KV using a Philips CM10 TEM. (The new osmium ammine-B stain is available from Polysciences Inc). Uranyl-lead (U-Pb) staining was as described. ESI was carried out on unstained, very thin (<30 nm) beveled sections at 80KV using a Zeiss EM902. Images were recorded at 20,000x and 30,000x with median energy losses of 110eV, 120eV and 160eV, and a window of 20eV.

Body Effect Measurement in DRAM Cell Transistor Using Memory Test System

2016 ◽  
Author(s):  
Ilwoo Jung ◽  
Byoungdeok Choi ◽  
Bonggu Sung ◽  
Daejung Kim ◽  
Ilgweon Kim ◽  
...  
Keyword(s):  
Conventional Method ◽  
Cell Body ◽  
Test System ◽  
Memory Test ◽  
Effect Measurement ◽  
Nondestructive Measurement ◽  
Individual Values ◽  
Body Effect ◽  
Sample Damage ◽  
Viable Method

Abstract Body effect is the key characteristic of DRAM cell transistor. Conventional method uses a TEG structure for body effect measurement. But this measurement is not accurate, because TEG structure has only several transistors and it is located outside of the DRAM die. This paper suggests a viable method for measuring DRAM cell transistor body effect. It uses a memory test system for fast, massive, nondestructive measurement. Newly developed method can measure 100,000 DRAM cell body effects in two minute, without sample damage. The test gives one median value and 100,000 individual values of body effects. Median value of measured body effects is equal to the TEG body effect. An individual DRAM cell body effect has a correlation with the fin height.

Metabotropic glutamate receptor dependent EPSP and EPSP-spike potentiation in area CA1 of the submerged rat hippocampal slice

1996 ◽  
Vol 76 (5) ◽  
pp. 3126-3135 ◽  
Author(s):  
N. A. Breakwell ◽  
M. J. Rowan ◽  
R. Anwyl
Keyword(s):  
Nmda Receptor ◽  
Receptor Antagonist ◽  
Cell Body ◽  
Metabotropic Glutamate Receptor ◽  
Long Term Potentiation ◽  
High Frequency Stimulation ◽  
Excitatory Postsynaptic Potential ◽  
Area Ca1 ◽  
Gabaa Receptor Antagonist

1. We reexamined the important areas of conflict in (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid [(1S,3R)-ACPD]-induced potentiation of the field excitatory postsynaptic potential (EPSP) and, for the first time, investigated the role of mGluRs in EPSP-spike (E-S) coupling. 2. (1S,3R)-ACPD (10 microM) bath applied for 20 min consistently induced a long-lasting potentiation of the dendritic EPSP in area CA1 of submerged rat hippocampal slices, which was considerably faster in onset than described previously. 3. This effect was not associated with any change in presynaptic fiber volley but was dependent on both an intact CA3 connection, because removal of area CA3 blocked (1S,3R)-ACPD-induced potentiation, and also on functional N-methyl-D-aspartate (NMDA) receptors, because (1S,3R)-ACPD-induced potentiation was blocked by inclusion of the NMDA receptor antagonist D(-)-2-amino-5-phosphonopentanoic acid (AP5; 50 microM). 4. (1S,3R)-ACPD induced a long-lasting potentiation of the population spike (PS) amplitude that was consistently larger than that of the EPSP measured in the cell body area. This EPSP-PS (E-S) potentiation was blocked by inclusion of the gamma-aminobuturic acid-A (GABAA) receptor antagonist, picrotoxin (50 microM). 5. E-S potentiation induced by high-frequency stimulation (HFS), which was of the same magnitude as that induced by (1S,3R)-ACPD, was blocked by the mGluR-selective antagonist (+)-alpha-methyl-4-carboxyphenylglycine (+MCPG; 250 microM). +MCPG also blocked HFS-induced long-term potentiation (LTP) of the EPSP measured in the cell body. 6. These results suggest that (1S,3R)-ACPD-induced potentiation is NMDA receptor dependent, contrary to some previous findings, and provide further evidence that both synaptic and E-S potentiation induced by (1S,3R)-ACPD share common mechanisms of expression with HFS-induced LTP. The data emphasize the important role of mGluRs in induction of EPSP LTP and E-S potentiation.

scholarly journals Permanent central synaptic disconnection of proprioceptors after nerve injury and regeneration. I. Loss of VGLUT1/IA synapses on motoneurons

2011 ◽  
Vol 106 (5) ◽  
pp. 2450-2470 ◽  
Author(s):  
Francisco J. Alvarez ◽  
Haley E. Titus-Mitchell ◽  
Katie L. Bullinger ◽  
Michal Kraszpulski ◽  
Paul Nardelli ◽  
...  
Keyword(s):  
Peripheral Nerve ◽  
Nerve Injury ◽  
Cell Body ◽  
Peripheral Nerve Injury ◽  
Motor Coordination ◽  
Electrophysiological Study ◽  
Peripheral Nerve Injuries ◽  
Nerve Injuries ◽  
Ia Afferent ◽  
Axon Collaterals

Motor and sensory proprioceptive axons reinnervate muscles after peripheral nerve transections followed by microsurgical reattachment; nevertheless, motor coordination remains abnormal and stretch reflexes absent. We analyzed the possibility that permanent losses of central IA afferent synapses, as a consequence of peripheral nerve injury, are responsible for this deficit. VGLUT1 was used as a marker of proprioceptive synapses on rat motoneurons. After nerve injuries synapses are stripped from motoneurons, but while other excitatory and inhibitory inputs eventually recover, VGLUT1 synapses are permanently lost on the cell body (75–95% synaptic losses) and on the proximal 100 μm of dendrite (50% loss). Lost VGLUT1 synapses did not recover, even many months after muscle reinnervation. Interestingly, VGLUT1 density in more distal dendrites did not change. To investigate whether losses are due to VGLUT1 downregulation in injured IA afferents or to complete synaptic disassembly and regression of IA ventral projections, we studied the central trajectories and synaptic varicosities of axon collaterals from control and regenerated afferents with IA-like responses to stretch that were intracellularly filled with neurobiotin. VGLUT1 was present in all synaptic varicosities, identified with the synaptic marker SV2, of control and regenerated afferents. However, regenerated afferents lacked axon collaterals and synapses in lamina IX. In conjunction with the companion electrophysiological study [Bullinger KL, Nardelli P, Pinter MJ, Alvarez FJ, Cope TC. J Neurophysiol (August 10, 2011). doi:10.1152/jn.01097.2010], we conclude that peripheral nerve injuries cause a permanent retraction of IA afferent synaptic varicosities from lamina IX and disconnection with motoneurons that is not recovered after peripheral regeneration and reinnervation of muscle by sensory and motor axons.

The adrenal paraneurone: tubulin organization

1984 ◽  
Vol 62 (5) ◽  
pp. 502-511 ◽  
Author(s):  
M. F. Bader ◽  
F. Bernier-Valentin ◽  
B. Rousset ◽  
D. Aunis
Keyword(s):  
Cell Body ◽  
Intracellular Transport ◽  
Cultured Cells ◽  
Specific Binding ◽  
Secretory Granules ◽  
Immunofluorescent Staining ◽  
Chromaffin Granules ◽  
Two Dimensional Gel Electrophoresis ◽  
Granule Membrane

When chromaffin cells from the bovine adrenal medulla are maintained in culture, they develop neuritelike processes which end with growth-cone-like structures. Chromaffin granules were found to migrate from the cell body to the neurite endings. Thus, the intracellular transport of secretory granules, existing in vivo, seems to occur in an exaggerated way in the cultured cells. These cells offer an excellent model for studying the mechanism of transport, particularly the role of microtubules. By immunofluorescent staining, we observed that tubulin antibodies decorate a complex network visible along the neurites. Colchicine treatment induced the disappearance of this network followed by a return of granules in the cell body and a retraction of neurites. To test the presence of tubulin in the chromaffin granule membrane, we used two-dimensional gel electrophoresis and a radioimmunoassay. Our results indicate that tubulin is not a significant component of chromaffin granules. However, binding experiments show that granule membranes are able to bind tubulin through high affinity binding sites. These results show that microtubules appear involved in neurite formation and probably in granule transport. Tubulin is not an integral constituent of the granule membrane, but is present as a result of a reversible specific binding. This insertion of tubulin into the membrane might represent a step in the association between microtubules and secretory granules.

scholarly journals Progressive and spatially differentiated stability of microtubules in developing neuronal cells.

1989 ◽  
Vol 109 (1) ◽  
pp. 253-263 ◽  
Author(s):  
S S Lim ◽  
P J Sammak ◽  
G G Borisy
Keyword(s):  
Cell Body ◽  
Growth Cone ◽  
Cellular Differentiation ◽  
Progressive Increase ◽  
Fluorescence Recovery ◽  
Plastic Properties ◽  
Intracellular Location ◽  
Laser Microbeam ◽  
Neuronal Cytoskeleton ◽  
The Stability

The establishment of neural circuits requires both stable and plastic properties in the neuronal cytoskeleton. In this study we show that properties of stability and lability reside in microtubules and these are governed by cellular differentiation and intracellular location. After culture for 3, 7, and 14 d in nerve growth factor-containing medium, PC-12 cells were microinjected with X-rhodamine-labeled tubulin. 8-24 h later, cells were photobleached with a laser microbeam at the cell body, neurite shaft, and growth cone. Replacement of fluorescence in bleached zones was monitored by digital video microscopy. In 3-d cultures, fluorescence recovery in all regions occurred by 26 +/- 17 min. Similarly, in older cultures, complete fluorescence recovery at the cell body and growth cone occurred by 10-30 min. However, in neurite shafts, fluorescence recovery was markedly slower (71 +/- 48 min for 7-d and 201 +/- 94 min for 14-d cultures). This progressive increase in the stability of microtubules in the neurite shafts correlated with an increase of acetylated microtubules. Acetylated microtubules were present specifically in the neurite shaft and not in the regions of fast microtubule turnover, the cell body and growth cone. During the recovery of fluorescence, bleached zones did not move with respect to the cell body. We conclude that the microtubule component of the neuronal cytoskeleton is differentially dynamic but stationary.

scholarly journals Contribution of whole-cell optimization via cell body rolling to polarization of T cells

2006 ◽  
Vol 3 (3) ◽  
pp. 209-219 ◽  
Author(s):  
Sergey N Arkhipov ◽  
Ivan V Maly
Keyword(s):  
T Cells ◽  
Cell Body ◽  
Whole Cell ◽  
Body Rolling
Sign in / Sign up

Export Citation Format

Share Document