An ultrastructural study of serially sectioned renshaw cells. I. Architecture of the cell body, axon hillock, initial axon segment and proximal dendrites

1982 ◽  
Vol 235 (1) ◽  
pp. 1-15 ◽  
Author(s):  
Per-A˚ke Lagerba¨ck ◽  
Lars-Olof Ronnevi
Keyword(s):  
Cell Body ◽  
Ultrastructural Study ◽  
Renshaw Cells ◽  
Initial Axon Segment ◽  
Axon Hillock

Altered excitability of goldfish mauthner cell following axotomy. I. Characterization and correlations with somatic and axonal morphological reactions

1986 ◽  
Vol 55 (6) ◽  
pp. 1424-1439 ◽  
Author(s):  
M. J. Titmus ◽  
D. S. Faber ◽  
S. J. Zottoli
Keyword(s):  
Cell Body ◽  
Initial Segment ◽  
Membrane Properties ◽  
Resting Potential ◽  
M Cells ◽  
M Cell ◽  
Spike Amplitude ◽  
Axon Hillock ◽  
The Mean ◽  
Lateral Dendrite

Axonal transection 7-10 mm distal to the cell body of the goldfish Mauthner (M) cell induced alterations in its excitability; namely, the antidromic spike recorded in the soma was converted from a single-component axon-hillock response to a larger amplitude, two-component impulse. The mean spike amplitude of the axotomized cells was approximately 50% greater (59.6 +/- 15.1 mV, n = 94) than that in controls (39.4 +/- 6.3 mV, n = 73). The onset of the induced increase in spike amplitude occurs at approximately 20 days postaxotomy, and the transition to a reactive spike is complete by approximately 30-35 days. Eighty-three percent of the M-cells axotomized for more than 30 days were physiologically reactive as judged by their large spike amplitudes and/or the presence of an additional spike component. Concomitant with the enhanced spike amplitudes, there was a depression of excitability in the initial segment-axon hillock region of the axotomized cells. This depression was suggested by a decrease in the initial segment (IS) spike height (from 39.4 +/- 6.3 mV, n = 73, in controls to 27.5 +/- 5.6 mV, n = 13, in axotomized cells), a decrease in its maximum rate of rise (from 153.6 +/- 24 V/s, n = 15, to 112.5 +/- 30 V/s, n = 29), and frequent failure of antidromic invasion into the initial segment and axon hillock. These changes in excitability could not be attributed to alterations in passive membrane properties, since the mean resting potential (77.8 +/- 5.2 mV, n = 37, control; 76.9 +/- 7.8 mV, n = 87, axotomized) and input resistance (170 +/- 21.3 K omega, n = 13, control; 176 +/- 26.6 K omega, n = 21, axotomized) were not altered significantly by axotomy. Threshold voltage was also unaffected (13.4 +/- 3.2 mV, n = 11, control; 11.9 +/- 2.5 mV, n = 11, axotomized). Sequential recordings of spike amplitudes from the axon hillock, soma, and lateral dendrite suggest that the generator of the axotomy-induced component is localized to the normally passive soma and proximal dendrite. In addition, the presumed soma-dendritic In addition, the presumed soma-dendritic component contributes very little if anything to the action potentials recorded in the axon. The onset and occurrence of alterations in excitability and cell body morphology (chromatolysis and nuclear associated changes) were compared in different M-cell populations and in the same identified M-cells. The comparisons suggested that these two events tend to occur in parallel.(ABSTRACT TRUNCATED AT 400 WORDS)

An ultrastructural study of serially sectioned Renshaw cells. II. Synaptic types

1982 ◽  
Vol 246 (2) ◽  
pp. 181-192 ◽  
Author(s):  
Per-Åke Lagerbäck ◽  
Lars-Olof Ronnevi
Keyword(s):  
Ultrastructural Study ◽  
Renshaw Cells

scholarly journals Identification of Active Membrane Areas in the Giant Neuron of Aplysia

1962 ◽  
Vol 45 (6) ◽  
pp. 1099-1115 ◽  
Author(s):  
L. Tauc
Keyword(s):  
Giant Cell ◽  
Cell Body ◽  
Giant Neuron ◽  
Active Membrane ◽  
Axon Hillock ◽  
Different Parts ◽  
Extracellular Potentials

Intracellular and extracellular potentials were simultaneously recorded from the soma and different parts of the axon of the giant cell of Aplysia. Evidence was obtained that for all modes of stimulation the spike originates in the axon at some distance from the cell body. The conduction of the spike is blocked at a distance of 200 to 300 µ from the soma for the antidromic spike, closer to the soma for an orthodromic spike. This event is recorded in the soma as a small or A spike. After some delay, a spike is initiated in the resting part of the axon and in the axon hillock; the soma is invaded only afterwards. The response of these three parts of the neuron is recorded in the soma as the big or S spike.

Excitation and Inhibition of Spinal Motoneurons

1955 ◽  
Vol 184 (1) ◽  
pp. 223-232 ◽  
Author(s):  
Adele E. U. Edisen
Keyword(s):  
Spinal Cord ◽  
Cell Body ◽  
Eddy Currents ◽  
Time Lag ◽  
Myelinated Axon ◽  
Synaptic Delay ◽  
Conduction Time ◽  
Direct Stimulation ◽  
Initial Axon Segment ◽  
Needle Position

Spinal cord motoneurons of the cat were stimulated by a needle electrode and reflexly via dorsal root impulses. Responses to direct stimulation originated in dendrites, initial axon segment, or myelinated axon, but apparently not in the cell body. The sites were differentiated by latency changes of the response as needle position and stimulus strength are varied, by ability to follow repetitive stimulation, and by responses to asphyxia duration and anesthesia depth. Facilitatory afferent impulses increased the excitability of the motoneurons, whether the direct test stimulus was activating either dendrites or initial axon segment, but inhibitory afferent impulses decreased the direct response only when dendrites were being activated. Facilitation is therefore nonlocalized and can be accounted for by the usual eddy currents. Inhibition is interpreted as a partial depolarization and impedance decrease of the cell body, induced by afferents reaching it directly and resulting in a short circuiting of eddy currents from excited dendrites to initial axon segment. The central delay of the spinal cord monosynaptic response (about 0.8 msec.) is accounted for by conduction time in the afferent fibers (0.5 msec.), determined by antidromic stimulation of these and by the time lag of afferent conditioning effects, and in the motoneurons, 0.2–0.3 msec. It is thus doubtful if any true ‘synaptic delay’ exists. The long intramedullary afferent conduction time also fully accounts for the lag seen in afferent inhibition, in harmony with the existence of a direct inhibitory pathway.

Tumor Diagnosis

1982 ◽  
Vol 40 ◽  
pp. 262-265
Author(s):  
Bruce Mackay
Keyword(s):  
Electron Microscopy ◽  
Transmission Electron Microscopy ◽  
Differential Diagnosis ◽  
Light Microscopy ◽  
Clinical Examination ◽  
Ultrastructural Study ◽  
Diagnostic Procedures ◽  
Specific Diagnosis ◽  
Transmission Electron ◽  
Microscopic Diagnosis

The broadest application of transmission electron microscopy (EM) in diagnostic medicine is the identification of tumors that cannot be classified by routine light microscopy. EM is useful in the evaluation of approximately 10% of human neoplasms, but the extent of its contribution varies considerably. It may provide a specific diagnosis that can not be reached by other means, but in contrast, the information obtained from ultrastructural study of some 10% of tumors does not significantly add to that available from light microscopy. Most cases fall somewhere between these two extremes: EM may correct a light microscopic diagnosis, or serve to narrow a differential diagnosis by excluding some of the possibilities considered by light microscopy. It is particularly important to correlate the EM findings with data from light microscopy, clinical examination, and other diagnostic procedures.

Further Observations on the Virus of Epizootic Diarrhea of Infant Mice. An Electron Microscopic Study

1967 ◽  
Vol 25 ◽  
pp. 110-111
Author(s):  
W. G. Banfield ◽  
G. Kasnic ◽  
J. H. Blackwell
Keyword(s):  
Electron Microscope ◽  
Infected Cell ◽  
Microscopic Study ◽  
Intestinal Epithelium ◽  
Ultrastructural Study ◽  
Osmium Tetroxide ◽  
Lead Citrate ◽  
Electron Microscopic ◽  
Virus Particles ◽  
Infected Cells

An ultrastructural study of the intestinal epithelium of mice infected with the agent of epizootic diarrhea of infant mice (EDIM virus) was first performed by Adams and Kraft. We have extended their observations and have found developmental forms of the virus and associated structures not reported by them.Three-day-old NLM strain mice were infected with EDIM virus and killed 48 to 168 hours later. Specimens of bowel were fixed in glutaraldehyde, post fixed in osmium tetroxide and embedded in epon. Sections were stained with uranyl magnesium acetate followed by lead citrate and examined in an updated RCA EMU-3F electron microscope.The cells containing virus particles (infected) are at the tips of the villi and occur throughout the intestine from duodenum through colon. All developmental forms of the virus are present from 48 to 168 hours after infection. Figure 1 is of cells without virus particles and figure 2 is of an infected cell. The nucleus and cytoplasm of the infected cells appear clearer than the cells without virus particles.

Glycogen in guinea pig neutrophils: Ultrastructural study of neutrophils at the intradermal site of BCG injection

1983 ◽  
Vol 41 ◽  
pp. 726-727
Author(s):  
Corazon D. Bucana
Keyword(s):  
Bone Marrow ◽  
Guinea Pig ◽  
Electron Density ◽  
Peritoneal Cavity ◽  
Ultrastructural Study ◽  
Guinea Pigs ◽  
Random Distribution ◽  
Glycogen Content ◽  
Polymorphonuclear Neutrophils ◽  
Ultrastructural Studies

In the circulating blood of man and guinea pigs, glycogen occurs primarily in polymorphonuclear neutrophils and platelets. The amount of glycogen in neutrophils increases with time after the cells leave the bone marrow, and the distribution of glycogen in neutrophils changes from an apparently random distribution to large clumps when these cells move out of the circulation to the site of inflammation in the peritoneal cavity. The objective of this study was to further investigate changes in glycogen content and distribution in neutrophils. I chose an intradermal site because it allows study of neutrophils at various stages of extravasation.Initially, osmium ferrocyanide and osmium ferricyanide were used to fix glycogen in the neutrophils for ultrastructural studies. My findings confirmed previous reports that showed that glycogen is well preserved by both these fixatives and that osmium ferricyanide protects glycogen from solubilization by uranyl acetate.I found that osmium ferrocyanide similarly protected glycogen. My studies showed, however, that the electron density of mitochondria and other cytoplasmic organelles was lower in samples fixed with osmium ferrocyanide than in samples fixed with osmium ferricyanide.

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