Granular cells: A new indicator of neuronal cell death in the spinal ganglia of the rat

1994 ◽  
Vol 52 ◽  
pp. 34-35
Author(s):  
Kevin M. Imel ◽  
J. Franklin Bailey ◽  
Mark DeSantis
Keyword(s):  
Dorsal Root Ganglia ◽  
Axonal Regeneration ◽  
Dorsal Root ◽  
Osmium Tetroxide ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Spinal Ganglia ◽  
Indirect Methods ◽  
Rat Pups ◽  
Dense Bodies

Damage to axons in the neonatal mammal results in the death of the affected neurons rather than survival and axonal regeneration as generally seen in the adult. This phenomenon has been well documented using indirect methods such as counting cells in histological sections of the experimentally damaged versus control tissue. Recent experiments have shown that cells with osmiophilic dense bodies, which have been termed “granules”, become apparent at the light microscopic level in ipsilateral lumbar dorsal root ganglia after destruction of the sciatic nerve on that side in neonatal rats. Within 84 - 96 hours after the lesion, the rat pups were anesthetized, perfused with 4% paraformaldehyde and the ganglia post-fixed in 1% unbuffered osmium tetroxide for at least 72 hours. Such a lengthy exposure to osmium was found to be necessary to visualize the granules.This offers the possibility of using these granules as a direct indicator of neuronal death in the lumbar dorsal root ganglia. The cells containing these granules were usually chromatolytic neuronal somata which had an eccentrically positioned nucleus (when a nucleus or nuclear remnant was still present) and peripheral aggregation of the rough endoplasmic reticulum (i.e. Nissl bodies).

The nerve injury and the dying neurons: diagnosis and prevention

2011 ◽  
Vol 36 (9) ◽  
pp. 730-734 ◽  
Author(s):  
G. Terenghi ◽  
A. Hart ◽  
M. Wiberg
Keyword(s):  
Cell Death ◽  
Peripheral Nerve ◽  
Nerve Injury ◽  
Dorsal Root Ganglia ◽  
Peripheral Nerve Injury ◽  
Dorsal Root ◽  
Nerve Repair ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Pharmacological Intervention

Following distal nerve injury significant sensory neuronal cell death occurs in the dorsal root ganglia, while after a more proximal injury, such as brachial plexus injury, a sizeable proportion of spinal motoneurons also undergo cell death. This phenomenon has been undervalued for a long time, but it has a significant role in the lack of functional recuperation, as neuronal cells cannot divide and be replaced, hence the resulting nerve regeneration is usually suboptimal. It is now accepted that this cell death is due to apoptosis, as indicated by analysis of specific genes involved in the apoptotic signalling cascade. Immediate nerve repair, either by direct suturing or nerve grafting, gives a degree of neuroprotection, but this approach does not fully prevent neuronal cell death and importantly it is not always possible. Our work has shown that pharmacological intervention using either acetyl-L-carnitine (ALCAR) or N-acetyl-cysteine (NAC) give complete neuroprotection in different types of peripheral nerve injury. Both compounds are clinically safe and experimental work has defined the best dose, timing after injury and duration of administration. The efficacy of neuroprotection of ALCAR and NAC can be monitored non-invasively using MRI, as demonstrated experimentally and more recently by clinical studies of the volume of dorsal root ganglia. Translation to patients of this pharmacological intervention requires further work, but the available results indicate that this approach will help to secure a better functional outcome following peripheral nerve injury and repair.

scholarly journals NEURONAL APOPTOSIS AND INTERVENTION STRATEGIES

2014 ◽  
Author(s):  
Giorgio Terenghi
Keyword(s):  
Cell Death ◽  
Peripheral Nerve ◽  
Nerve Injury ◽  
Dorsal Root Ganglia ◽  
Peripheral Nerve Injury ◽  
Dorsal Root ◽  
Nerve Repair ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Pharmacological Intervention

Following distal nerve injury significant sensory neuronal cell death occurs in the dorsal root ganglia, while after a more proximal injury, such as brachial plexus injury, a sizeable proportion of spinal motoneurons also undergo cell death. This phenomenon has been undervalued for a long time, but it has a significant role in the lack of functional recuperation, as neuronal cells cannot divide and be replaced, hence the resulting nerve regeneration is usually suboptimal. It is now accepted that this cell death is due to apoptosis, as indicated by analysis of specific genes involved in the apoptotic signalling cascade. Immediate nerve repair, either by direct suturing or nerve grafting, gives a degree of neuroprotection, but this approach does not fully prevent neuronal cell death and importantly it is not always possible. Our work has shown that pharmacological intervention using either acetyl-L-carnitine (ALCAR) or N-acetyl-cysteine (NAC) give complete neuroprotection in different types of peripheral nerve injury. Both compounds are clinically safe and experimental work has defined the best dose, timing after injury and duration of administration. The efficacy of neuroprotection of ALCAR and NAC can be monitored non-invasively using MRI, as demonstrated experimentally and more recently by clinical studies of the volume of dorsal root ganglia. Translation to patients of this pharmacological intervention requires further work, but the available results indicate that this approach will help to secure a better functional outcome following peripheral nerve injury and repair.

scholarly journals Hippocampal distribution of IL-1β and IL-1RI following lithium-pilocarpine-induced status epilepticus in the developing rat

2016 ◽  
Vol 88 (suppl 1) ◽  
pp. 653-663 ◽  
Author(s):  
Dulce-Mariely Álvarez-Croda ◽  
Juan Santiago-García ◽  
Jesús S. Medel-Matus ◽  
Joel Martínez-Quiroz ◽  
Angel A. Puig-Lagunes ◽  
...  
Keyword(s):  
Cell Death ◽  
Status Epilepticus ◽  
Mrna Expression ◽  
Dorsal Hippocampus ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Control Group ◽  
Rat Pups ◽  
Fluoro Jade B ◽  
Developing Rat

The contribution of Interleukin-1β (IL-1β) to neuronal injury induced by status epilepticus (SE) in the immature brain remains unclear. The goal of this study was to determine the hippocampal expression of IL-1β and its type 1 receptor (IL-1RI) following SE induced by the lithium-pilocarpine model in fourteen-days-old rat pups; control animals were given an equal volume of saline instead of the convulsant. IL-1β and IL-1RI mRNA hippocampal levels were assessed by qRT-PCR 6 and 24 h after SE or control conditions. IL-1β and IL-1RI expression was detected in the dorsal hippocampus by immunohistochemical procedures; Fluoro-Jade B staining was carried out in parallel sections in order to detect neuronal cell death. IL-1β mRNA expression was increased 6 h following SE, but not at 24 h; however IL-1RI mRNA expression was unaffected when comparing with the control group. IL-1β and IL-1RI immunoreactivity was not detected in control animals. IL-1β and IL-1RI were expressed in the CA1 pyramidal layer, the dentate gyrus granular layer and the hilus 6 h after SE, whereas injured cells were detected 24 h following seizures. Early expression of IL-1β and IL-1RI in the hippocampus could be associated with SE-induced neuronal cell death mechanisms in the developing rat.

Non-neuronal cell cultures from dorsal root ganglia of the adult cat: production of schwann-like cell lines

1981 ◽  
Vol 229 (1) ◽  
pp. 163-181 ◽  
Author(s):  
Jean R. Wrathall ◽  
Donald D. Rigamonti ◽  
Mark R. Braford ◽  
Carl C. Kao
Keyword(s):  
Cell Lines ◽  
Cell Cultures ◽  
Dorsal Root Ganglia ◽  
Dorsal Root ◽  
Neuronal Cell ◽  
Neuronal Cell Cultures ◽  
Adult Cat

Bismuth-induced neuronal cell death in rat dorsal root ganglion: a stereological study

2002 ◽  
Vol 105 (4) ◽  
pp. 351-357 ◽  
Author(s):  
Meredin Stoltenberg ◽  
Jørgen D. Schiønning ◽  
Mark J. West ◽  
Gorm Danscher
Keyword(s):  
Cell Death ◽  
Dorsal Root Ganglion ◽  
Dorsal Root ◽  
Neuronal Cell Death ◽  
Neuronal Cell

Effects of postnatal treadmill exercise on apoptotic neuronal cell death and cell proliferation of maternal-separated rat pups

2012 ◽  
Vol 34 (1) ◽  
pp. 45-56 ◽  
Author(s):  
Seung-Soo Baek ◽  
Tae-Won Jun ◽  
Ki-Jeong Kim ◽  
Mal-Soon Shin ◽  
Sun-Young Kang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Treadmill Exercise ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Rat Pups

scholarly journals miR-129-5p and miR-130a-3p Regulate VEGFR-2 Expression in Sensory and Motor Neurons during Development

2020 ◽  
Vol 21 (11) ◽  
pp. 3839 ◽  
Author(s):  
Kevin Glaesel ◽  
Caroline May ◽  
Katrin Marcus ◽  
Veronika Matschke ◽  
Carsten Theiss ◽  
...  
Keyword(s):  
Dorsal Root Ganglia ◽  
Motor Neurons ◽  
Dorsal Root ◽  
Neurological Diseases ◽  
Neuronal Cell ◽  
Vegf Receptor ◽  
Vascular Endothelial ◽  
Expression Control ◽  
Endothelial Growth Factor

The wide-ranging influence of vascular endothelial growth factor (VEGF) within the central (CNS) and peripheral nervous system (PNS), for example through effects on axonal growth or neuronal cell survival, is mainly mediated by VEGF receptor 2 (VEGFR-2). However, the regulation of VEGFR-2 expression during development is not yet well understood. As microRNAs are considered to be key players during neuronal maturation and regenerative processes, we identified the two microRNAs (miRNAs)—miR-129-5p and miR-130a-3p—that may have an impact on VEGFR-2 expression in young and mature sensory and lower motor neurons. The expression level of VEGFR-2 was analyzed by using in situ hybridization, RT-qPCR, Western blot, and immunohistochemistry in developing rats. microRNAs were validated within the spinal cord and dorsal root ganglia. To unveil the molecular impact of our candidate microRNAs, dissociated cell cultures of sensory and lower motor neurons were transfected with mimics and inhibitors. We depicted age-dependent VEGFR-2 expression in sensory and lower motor neurons. In detail, in lower motor neurons, VEGFR-2 expression was significantly reduced during maturation, in conjunction with an increased level of miR-129-5p. In sensory dorsal root ganglia, VEGFR-2 expression increased during maturation and was accompanied by an overexpression of miR-130a-3p. In a second step, the functional significance of these microRNAs with respect to VEGFR-2 expression was proven. Whereas miR-129-5p seems to decrease VEGFR-2 expression in a direct manner in the CNS, miR-130a-3p might indirectly control VEGFR-2 expression in the PNS. A detailed understanding of genetic VEGFR-2 expression control might promote new strategies for the treatment of severe neurological diseases like ischemia or peripheral nerve injury.

scholarly journals Improved immunoelectron microscopic method for localizing cytoskeletal proteins in Lowicryl K4M embedded tissues.

1986 ◽  
Vol 34 (11) ◽  
pp. 1477-1485 ◽  
Author(s):  
K E Loesser ◽  
K J Doane ◽  
F J Wilson ◽  
F J Roisen ◽  
S Malamed
Keyword(s):  
Immunoelectron Microscopy ◽  
Dorsal Root Ganglia ◽  
Dorsal Root ◽  
Protein A ◽  
Neuronal Cell ◽  
Cytoskeletal Proteins ◽  
Modified Technique ◽  
Adrenocortical Cells ◽  
Thin Sections ◽  
Lowicryl K4m

We have modified the Lowicryl K4M low-temperature dehydration and embedding procedure for immunoelectron microscopy to provide improved ultrastructural detail and facilitate the localization of actin and tubulin in isolated rat adrenocortical cells, chick spinal cord with attached dorsal root ganglia (SC-DRG), and cultured dorsal root ganglia (DRG). Cells and tissues were fixed for immunocytochemistry either in a mixture of 2% paraformaldehyde and 0.25% glutaraldehyde (0.1 M PIPES buffer, pH 7.3) or in a mixture of 0.3% glutaraldehyde and 1.0% ethyldimethylaminopropylcarbodiimide (0.1 M phosphate buffered saline, pH 7.3). Dehydration was in ethanol at progressively lower temperatures to -35 degrees C. Infiltration at -35 degrees C was followed by ultraviolet polymerization at -20 degrees C. Comparable samples were fixed in glutaraldehyde and osmium tetroxide and embedded in Epon 812 or Epon-Araldite. Post-embedding immunostaining of thin sections utilized commercially available monoclonal antibodies to tubulin and actin followed by the protein A-gold technique (Roth et al., Endocrinology 108:247, 1981). Actin immunoreactivity was observed at the periphery of mitochondria and between mitochondria and lipid droplets in rat adrenocortical cells and at the periphery of neuronal cell processes of SC-DRG. Tubulin immunoreactivity was associated with microtubules throughout neurites of cultured DRG. Our modified technique allows preservation of ultrastructural details as well as localization of antigens by immunoelectron microscopy.

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