The morphology of the sensory neuron in the cockroach femoral tactile spine

1993 ◽  
Vol 69 (3) ◽  
pp. 669-673 ◽  
Author(s):  
A. S. French ◽  
A. R. Klimaszewski ◽  
L. L. Stockbridge
Keyword(s):  
Action Potential ◽  
Sensory Neuron ◽  
Cell Body ◽  
Computer Software ◽  
Neuronal Cell ◽  
Neuronal Morphology ◽  
Neuronal Cell Body ◽  
Intracellular Recordings ◽  
Neuronal Nucleus ◽  
Spine Structure

1. The cockroach femoral tactile spine contains a single bipolar sensory neuron. The mechanosensitive dendrite in the wall of the spine leads through the spine lumen to a cell body, and then to an axon that proceeds proximally along the femur. The ultrastructure of the sensory ending has been examined before with electron microscopy. However, the morphology of the complete neuron and its relationship to the general spine structure have not been described before. 2. The tactile spine neuron has been extensively used in electrophysiological studies, including intracellular recordings. Action-potential amplitudes and thresholds were variable and inversely related in intracellular recordings, which could be caused by variability in the location of the action-potential initiation region, the position of the recording electrode, or the neuronal morphology. Attempts to observe the complete neuronal morphology by dye injection were hampered by the opaque and autofluorescent cuticle surrounding the neuron. 3. We examined 10 tactile spine neurons, and their surrounding structures, by taking serial 1-micron sections through the base of the spine, normal to its long axis. The sections were examined with light microscopy, digitized by tracing onto a graphics tablet, and then reassembled with the use of computer software. Reconstructions were made of the borders of the spine cuticle, neuron, neuronal nucleus, glial wrappings, and the main trachea in the spine lumen. 4. There was considerable variability in the size and shape of the neuronal cell body, although the sensory dendrite and axon had more consistent morphologies.(ABSTRACT TRUNCATED AT 250 WORDS)

Separation of a process from the neuronal cell body using a thin aluminum foil separator

1998 ◽  
Vol 2 (4) ◽  
pp. 352-356 ◽  
Author(s):  
Kosuke Noda ◽  
Keita Jimbo ◽  
Kazuo Suzuki ◽  
Kentaro Yoda
Keyword(s):  
Cell Body ◽  
Neuronal Cell ◽  
Aluminum Foil ◽  
Neuronal Cell Body ◽  
Thin Aluminum ◽  
Thin Aluminum Foil

scholarly journals Differences in splicing defects between the grey and white matter in myotonic dystrophy type 1

2019 ◽  
Author(s):  
Masamitsu Nishi ◽  
Takashi Kimura ◽  
Mitsuru Furuta ◽  
Koichi Suenaga ◽  
Tsuyoshi Matsumura ◽  
...  
Keyword(s):  
White Matter ◽  
Myotonic Dystrophy ◽  
Cell Body ◽  
Neuronal Cell ◽  
Neuronal Cell Body ◽  
Myotonic Dystrophy Type 1 ◽  
Myotonic Dystrophy Type ◽  
And Control ◽  
The Brain

AbstractMyotonic dystrophy type 1 (DM1) is a multi-system disorder caused by CTG repeats in the myotonic dystrophy protein kinase (DMPK) gene. This leads to sequestration of the splicing factor, muscleblind-like 2 (MBNL2), and aberrant splicing, mainly in the central nervous system. We investigated the splicing patterns of MBNL1/2 and genes controlled by MBNL2 in several regions of the brain and between the grey matter (GM) and white matter (WM) in DM1 patients using RT-PCR. Compared with the control, the percentage of spliced-in parameter (PSI) for most of the examined exons were significantly altered in most of the brain regions of DM1 patients, except for the cerebellum. The splicing of many genes was differently regulated between the GM and WM in both DM1 and control. The level of change in PSI between DM1 and control was higher in the GM than in the WM. The differences in alternative splicing between the GM and WM may be related to the effect of DM1 on the WM of the brain. We hypothesize that in DM1, aberrantly spliced isoforms in the neuronal cell body of the GM may not be transported to the axon. This might affect the WM as a consequence of Wallerian degeneration secondary to cell body damage. Our findings may have implications for analysis of the pathological mechanisms and exploring potential therapeutic targets.

scholarly journals Dual Role of Herpes Simplex Virus 1 pUS9 in Virus Anterograde Axonal Transport and Final Assembly in Growth Cones in Distal Axons

2015 ◽  
Vol 90 (5) ◽  
pp. 2653-2663 ◽  
Author(s):  
Monica Miranda-Saksena ◽  
Ross A. Boadle ◽  
Russell J. Diefenbach ◽  
Anthony L. Cunningham
Keyword(s):  
Axonal Transport ◽  
Cell Body ◽  
Virus Assembly ◽  
Neuronal Cell ◽  
Growth Cones ◽  
Neuronal Cell Body ◽  
Anterograde Axonal Transport ◽  
Simplex Virus ◽  
Hsv 1

ABSTRACTThe herpes simplex virus type 1 (HSV-1) envelope protein pUS9 plays an important role in virus anterograde axonal transport and spread from neuronal axons. In this study, we used both confocal microscopy and transmission electron microscopy (TEM) to examine the role of pUS9 in the anterograde transport and assembly of HSV-1 in the distal axon of human and rat dorsal root ganglion (DRG) neurons using US9 deletion (US9−), repair (US9R), and wild-type (strain F, 17, and KOS) viruses. Using confocal microscopy and single and trichamber culture systems, we observed a reduction but not complete block in the anterograde axonal transport of capsids to distal axons as well as a marked (∼90%) reduction in virus spread from axons to Vero cells with the US9 deletion viruses. Axonal transport of glycoproteins (gC, gD, and gE) was unaffected. Using TEM, there was a marked reduction or absence of enveloped capsids, in varicosities and growth cones, in KOS strain and US9 deletion viruses, respectively. Capsids (40 to 75%) in varicosities and growth cones infected with strain 17, F, and US9 repair viruses were fully enveloped compared to less than 5% of capsids found in distal axons infected with the KOS strain virus (which also lacks pUS9) and still lower (<2%) with the US9 deletion viruses. Hence, there was a secondary defect in virus assembly in distal axons in the absence of pUS9 despite the presence of key envelope proteins. Overall, our study supports a dual role for pUS9, first in anterograde axonal transport and second in virus assembly in growth cones in distal axons.IMPORTANCEHSV-1 has evolved mechanisms for its efficient transport along sensory axons and subsequent spread from axons to epithelial cells after reactivation. In this study, we show that deletion of the envelope protein pUS9 leads to defects in virus transport along axons (partial defect) and in virus assembly and egress from growth cones (marked defect). Virus assembly and exit in the neuronal cell body are not impaired in the absence of pUS9. Thus, our findings indicate that pUS9 contributes to the overall HSV-1 anterograde axonal transport, including a major role in virus assembly at the axon terminus, which is not essential in the neuronal cell body. Overall, our data suggest that the process of virus assembly at the growth cones differs from that in the neuronal cell body and that HSV-1 has evolved different mechanisms for virus assembly and exit from different cellular compartments.

scholarly journals The transport properties of axonal microtubules establish their polarity orientation.

1993 ◽  
Vol 120 (6) ◽  
pp. 1427-1437 ◽  
Author(s):  
P W Baas ◽  
F J Ahmad
Keyword(s):  
Transport Properties ◽  
Cell Body ◽  
Sympathetic Neurons ◽  
Neuronal Cell ◽  
Axon Growth ◽  
Progressive Increase ◽  
Neuronal Cell Body ◽  
Drug Concentrations ◽  
Efficient Mechanisms ◽  
Uniform Polarity

It is well established that axonal microtubules (MTs) are uniformly oriented with their plus ends distal to the neuronal cell body (Heidemann, S. R., J. M. Landers, and M. A. Hamborg. 1981. J. Cell Biol. 91:661-665). However, the mechanisms by which these MTs achieve their uniform polarity orientation are unknown. Current models for axon growth differ with regard to the contributions of MT assembly and transport to the organization and elaboration of the axonal MT array. Do the transport properties or assembly properties of axonal MTs determine their polarity orientation? To distinguish between these possibilities, we wished to study the initiation and outgrowth of axons under conditions that would arrest MT assembly while maintaining substantial levels of preexisting polymer in the cell body that could still be transported into the axon. We found that we could accomplish this by culturing rat sympathetic neurons in the presence of nanomolar levels of vinblastine. In concentrations of the drug up to and including 100 nM, the neurons actively extend axons. The vinblastine-axons are shorter than control axons, but clearly contain MTs. To quantify the effects of the drug on MT mass, we compared the levels of polymer throughout the cell bodies and axons of neurons cultured overnight in the presence of 0, 16, and 50 nM vinblastine with the levels of MT polymer in freshly plated neurons before axon outgrowth. Without drug, the total levels of polymer increase by roughly twofold. At 16 nM vinblastine, the levels of polymer are roughly equal to the levels in freshly plated neurons, while at 50 nM, the levels of polymer are reduced by about half this amount. Thus, 16 nM vinblastine acts as a "kinetic stabilizer" of MTs, while 50 nM results in some net MT disassembly. At both drug concentrations, there is a progressive increase in the levels of MT polymer in the axons as they grow, and a corresponding depletion of polymer from the cell body. These results indicate that highly efficient mechanisms exist in the neuron to transport preassembled MTs from the cell body into the axon. These mechanisms are active even at the expense of the cell body, and even under conditions that promote some MT disassembly in the neuron. MT polarity analyses indicate that the MTs within the vinblastine-axons, like those in control axons, are uniformly plus-end-distal.(ABSTRACT TRUNCATED AT 400 WORDS)

Angiotensin II Increases Vesicular Trafficking in Live Noradrenergic Brain Neurons

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 693-693
Author(s):  
Mohan K Raizada ◽  
Xianyu Wang Wang ◽  
Hong Yang
Keyword(s):  
Angiotensin Ii ◽  
Cell Body ◽  
Neuronal Cell ◽  
Vesicular Trafficking ◽  
Neuronal Cell Body ◽  
Receptor Subtype ◽  
Ang Ii ◽  
Green Fluorescence ◽  
Cmv Promoter ◽  
Prolonged Incubation

P1 Angiotensin II (Ang II) interacts with the AT 1 receptor subtype and stimulates turnover of norepinephrine (NE) by regulating its synthesis, release, and uptake. The cellular mechanism by which Ang II regulates this neurotransmission is not well understood. The aim of this study was to test the hypothesis that Ang II increases vesicular trafficking to increase synaptic release of NE. cDNA encoding full length rat dopamine beta-hydroxylase (DβH) fused to Green Fluorescence Protein (GFP) was cloned in pCl-Neo vector under the control of CMV promoter and used to tag synaptic vesicles. Transfection of cells with this plasmid resulted in the expression of green fluorescence and GFP-DβH fusion protein which was functional as judged by an increase in DβH activity. Transfected neurons expressed bright green fluorescence representing GFP-DβH that was predominantly localized in the cell soma. Few neurites also displayed the fluorescence. Real time confocal microscopic examination of live neurons indicated that Ang II caused a time-dependent increase in both the intensity and the number of neurites depicting green fluorescence. An increase in GFP-DβH in the neurites became apparent within one minute and persisted for 15-20 minutes. A 2.5 fold increase in the GFP-DβH positive neurites was observed by 100 nM Aug II in 15 min [control, 2±0.5 (n=20) versus Ang II treatment, 5±0.4 (n=25)]. Ang II-induced GFP-DβH redistribution was punctate, co-localized with synaptophysin and was blocked by losartan, and not by PD123319. Release of Ang II induced NE paralleled its effect on GFP-DβH distribution. PMA treatment caused translocation of GFP-DβH in a fashion comparable with Ang II. In addition, inactivation of protein kinase C by a prolonged incubation of neurons with PMA, completely blocked the translocation of GFP-DβH from the cell body to neurites. These observations demonstrate that Ang II stimulates trafficking of NE vesicles by a PKC-dependent mechanism. Thus, an increased trafficking of NE containing vesicles from the neuronal cell body to the neurites may be key to Ang II stimulated release of NE from a noradrenergic neuron.

Sign in / Sign up

Export Citation Format

Share Document