124 PCREB IMMUNOHISTOCHEMICAL STAINING OF DORSAL ROOT GANGLIA AFTER ACUTE AND REPEATED URINARY PATHOGENIC E. COLI INFECTION INTO RAT BLADDER

2010 ◽  
Vol 9 (2) ◽  
pp. 71
Author(s):  
J.H. Lee ◽  
D.K. Lee ◽  
S.J. Lee ◽  
J.I. Kim
Urology ◽  
2007 ◽  
Vol 70 (3) ◽  
pp. 200
Author(s):  
W. Sung ◽  
H. Rho ◽  
S.J. Lee ◽  
S.G. Chang ◽  
J. Kim

2008 ◽  
Vol 71 (11) ◽  
pp. 2307-2311 ◽  
Author(s):  
SCOTT HAFNER ◽  
MARY T. SUTTON ◽  
JOSEPH HILL ◽  
PATRICK C. McCASKEY ◽  
LYNDA COLLINS KELLEY

A method is described for the identification of dorsal root ganglia (DRG)–associated sensory neurons within advanced meat recovery (AMR) product derived from bovine vertebral columns. This method relies on the unique microanatomy of sensory neurons and immunohistochemical staining, primarily for glial fibrillary acidic protein. Sensory neurons are variably sized unipolar neurons, exhibiting a single-cell process that is rarely seen in histologic sections. These neurons are surrounded by a prominent ring of glial fibrillary acidic protein–positive satellite cells that produce a distinctive and readily identifiable staining pattern in histologic sections. Fragmented DRG were detected to the 0.25% level in samples of ground beef or nonvertebral-origin AMR product spiked with these sensory ganglia. Similarly examined commercially produced nonvertebral-origin AMR product (n = 157) did not contain sensory ganglia, while 3.3% of vertebral-origin AMR product (n = 364) contained fragmented DRG.


2015 ◽  
Vol 193 (4S) ◽  
Author(s):  
Hiroki Ito ◽  
Naoki Aizawa ◽  
Rino Sugiyama ◽  
Jun Kamei ◽  
Yoshiyuki Akiyama ◽  
...  

2015 ◽  
Vol 14 (2) ◽  
pp. e895-e895a
Author(s):  
H. Ito ◽  
N. Aizawa ◽  
R. Sugiyama ◽  
J. Kamei ◽  
Y. Akiyama ◽  
...  

Development ◽  
1991 ◽  
Vol 111 (3) ◽  
pp. 647-655 ◽  
Author(s):  
H.D. Pomeranz ◽  
T.P. Rothman ◽  
M.D. Gershon

Experiments were done to test the hypothesis that the avian gut is colonized by cells derived from both vagal and sacral regions of the neural crest. A fluorescent dye, diI (1,1-dioctadecyl-3,3,3′,3′-tetramethylindocarbocyanine perchlorate), and a replication-deficient retrovirus (LZ10; Galileo et al. 1990) were employed as tracers. Since LZ10 was constructed with lacZ of E. coli as a reporter gene, infected cells were identified by demonstrating beta-galactosidase immunoreactivity. DiI and LZ10 were injected between the neural tube and surface ectoderm (before the migration of crest cells away from the injection sites) at vagal, truncal (diI only), or sacral axial levels. The bowel was examined 4 days later in order to allow crest-derived cells sufficient time to migrate to the gut. Following injections of either tracer into the vagal crest, labelled cells were found in the gizzard and duodenum. When diI or LZ10 was injected into the sacral crest, labelled cells were seen in the post-umbilical bowel and ganglion of Remak. In the hindgut, marked cells were concentrated in the mesenchyme, just internal to the serosa, and were never observed rostral to the umbilicus. No fluorescent cells were ever found in the bowel following truncal injections of diI, although such cells were observed in sympathetic ganglia. Labelled cells were always found in dorsal root ganglia, no matter which tracer or level of the crest was injected. In embryos injected with LZ10, infected cells in the gut and dorsal root ganglia displayed a neural crest marker (NC-1 immunoreactivity). These observations confirm that the gut is colonized by cells from the sacral as well as the vagal region of the neural crest and that the emigres from the sacral crest are confined to the post-umbilical bowel.


Author(s):  
V.J. Montpetit ◽  
S. Dancea ◽  
L. Tryphonas ◽  
D.F. Clapin

Very large doses of pyridoxine (vitamin B6) are neurotoxic in humans, selectively affecting the peripheral sensory nerves. We have undertaken a study of the morphological and biochemical aspects of pyridoxine neurotoxicity in an animal model system. Early morphological changes in dorsal root ganglia (DRG) associated with pyridoxine megadoses include proliferation of neurofilaments, ribosomes, rough endoplasmic reticulum, and Golgi complexes. We present in this report evidence of the formation of unique aggregates of microtubules and membranes in the proximal processes of DRG which are induced by high levels of pyridoxine.


2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 55.2-56
Author(s):  
R. Raoof ◽  
C. Martin ◽  
H. De Visser ◽  
J. Prado ◽  
S. Versteeg ◽  
...  

Background:Pain is a major debilitating symptom of knee osteoarthritis (OA). However, the extent of joint damage in OA does not correlate well with the severity of pain. The mechanisms that govern OA pain are poorly understood. Immune cells infiltrating nervous tissue may contribute to pain maintenance.Objectives:Here we investigated the role of macrophages in the initiation and maintenance of OA pain.Methods:Knee joint damage was induced by an unilateral injection of mono-iodoacetate (MIA) or after application of a groove at the femoral condyles of rats fed on high fat diet. Pain-like behaviors were followed over time using von Frey test and dynamic weight bearing. Joint damage was assessed by histology. Dorsal root ganglia (DRG) infiltrating immune cells were assessed over time using flow cytometry. To deplete monocytes and macrophages, Lysmcrex Csfr1-Stop-DTR were injected intrathecal or systemically with diptheria toxin (DT).Results:Intraarticular monoiodoacetate injection induced OA and signs of persistent pain, such as mechanical hyperalgesia and deficits in weight bearing. The persisting pain-like behaviors were associated with accumulation of F4/80+macrophages with an M1-like phenotype in the lumbar DRG appearing from 1 week after MIA injection, and that persisted till at least 4 weeks after MIA injection. Macrophages infiltrated DRG were also observed in the rat groove model of OA, 12 weeks after application of a groove at the femoral condyles. Systemic or local depletion of DRG macrophages during established MIA-induced OA completely ablated signs of pain, without affecting MIA-induced knee pathology. Intriguingly when monocytes/macrophages were depleted prior to induction of osteoarthritis, pain-like behaviors still developed, however these pain-like behaviors did not persist over time.In vitro,sensory neurons innervating the affected OA joint programmed macrophages into a M1 phenotype. Local repolarization of M1-like DRG macrophages towards M2 by intrathecal injection of M2 macrophages or anti-inflammatory cytokines resolved persistent OA-induced pain.Conclusion:Overall we show that macrophages infiltrate the DRG after knee damage and acquire a M1-like phenotype and maintain pain independent of the lesions in the knee joint. DRG-infiltrating macrophages are not required for induction of OA pain. Reprogramming M1-like DRG-infiltrating macrophages may represent a potential strategy to treat OA pain.Acknowledgments:This project has received funding from the European Union’s Horizon 2020 research and innovation programme under the Marie Sklodowska-Curie grant agreements No 814244 and No 642720. Dutch Arthritis SocietyDisclosure of Interests:Ramin Raoof: None declared, Christian Martin: None declared, Huub de Visser: None declared, Judith Prado: None declared, Sabine Versteeg: None declared, Anne Heinemans: None declared, Simon Mastbergen: None declared, Floris Lafeber Shareholder of: Co-founder and shareholder of ArthroSave BV, Niels Eijkelkamp: None declared


Author(s):  
Irene Riquelme ◽  
Miguel Angel Reina ◽  
André P. Boezaart ◽  
Francisco Reina ◽  
Virginia García-García ◽  
...  

2021 ◽  
Vol 22 (11) ◽  
pp. 5499
Author(s):  
Veronica Corsetti ◽  
Carla Perrone-Capano ◽  
Michael Sebastian Salazar Intriago ◽  
Elisabetta Botticelli ◽  
Giancarlo Poiana ◽  
...  

Dorsal root ganglia (DRG) neurons synthesize acetylcholine (ACh), in addition to their peptidergic nature. They also release ACh and are cholinoceptive, as they express cholinergic receptors. During gangliogenesis, ACh plays an important role in neuronal differentiation, modulating neuritic outgrowth and neurospecific gene expression. Starting from these data, we studied the expression of choline acetyltransferase (ChAT) and vesicular ACh transporter (VAChT) expression in rat DRG neurons. ChAT and VAChT genes are arranged in a “cholinergic locus”, and several splice variants have been described. Using selective primers, we characterized splice variants of these cholinergic markers, demonstrating that rat DRGs express R1, R2, M, and N variants for ChAT and V1, V2, R1, and R2 splice variants for VAChT. Moreover, by RT-PCR analysis, we observed a progressive decrease in ChAT and VAChT transcripts from the late embryonic developmental stage (E18) to postnatal P2 and P15 and in the adult DRG. Interestingly, Western blot analyses and activity assays demonstrated that ChAT levels significantly increased during DRG ontogenesis. The modulated expression of different ChAT and VAChT splice variants during development suggests a possible differential regulation of cholinergic marker expression in sensory neurons and confirms multiple roles for ACh in DRG neurons, both in the embryo stage and postnatally.


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