Viral Transduction of DRG Neurons

2020 ◽  
pp. 55-62
Author(s):  
Yo Sasaki
Keyword(s):  
Drg Neurons ◽  
Viral Transduction

Paired helical filaments (PHF) in rats: An experimental animal model for Alzheimer's disease

1987 ◽  
Vol 45 ◽  
pp. 842-843
Author(s):  
V.J.A. Montpetit ◽  
S. Dancea ◽  
S.W. French ◽  
D.F. Clapin
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Animal Model ◽  
Paired Helical Filaments ◽  
Ethanol Intoxication ◽  
Drg Neurons ◽  
Critical Difference ◽  
Suitable Animal Model ◽  
The Central Nervous System ◽  
Chronic Ethanol Intoxication

A continuing problem in Alzheimer research is the lack of a suitable animal model for the disease. The absence of neurofibrillary tangles of paired helical filaments is the most critical difference in the processes by which the central nervous system ages in most species other than man. However, restricting consideration to single phenomena, one may identify animal models for specific aspects of Alzheimer's disease. Abnormal fibers resembling PHF have been observed in dorsal root ganglia (DRG) neurons of rats in a study of chronic ethanol intoxication and spontaneously in aged rats. We present in this report evidence that PHF-like filaments occur in ethanol-treated rats of young age. In control animals lesions similar in some respects to our observations of cytoskeletal pathology in pyridoxine induced neurotoxicity were observed.Male Wistar BR rats (Charles River Labs) weighing 350 to 400 g, were implanted with a single gastrostomy cannula and infused with a liquid diet containing 30% of total calories as fat plus ethanol or isocaloric dextrose.

LXRs Protect DRG Neurons from High-Fat Diet–Induced ER Stress and Allodynia

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 553-P
Author(s):  
VIRGINIE AUBERT
Keyword(s):  
Er Stress ◽  
High Fat Diet ◽  
High Fat ◽  
Drg Neurons

2168-P: A Novel Method for Efficient and Homogeneous Viral Transduction of Pancreatic Islets

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 2168-P
Author(s):  
BURCAK YESILDAG ◽  
JOAN MIR-COLL ◽  
APARNA NEELAKANDHAN ◽  
FELIX FORSCHLER ◽  
ADELINN BIERNATH ◽  
...  
Keyword(s):  
Pancreatic Islets ◽  
Novel Method ◽  
Viral Transduction

scholarly journals hNGF Peptides Elicit the NGF-TrkA Signalling Pathway in Cholinergic Neurons and Retain Full Neurotrophic Activity in the DRG Assay

Biomolecules ◽  
2020 ◽  
Vol 10 (2) ◽  
pp. 216 ◽  
Author(s):  
Viviana Triaca ◽  
Elena Fico ◽  
Valentina Sposato ◽  
Silvia Caioli ◽  
Maria Teresa Ciotti ◽  
...  
Keyword(s):  
Dorsal Root ◽  
Cholinergic Neurons ◽  
Early Gene ◽  
Low Molecular Weight ◽  
Primary Neurons ◽  
Brain Delivery ◽  
Drg Neurons ◽  
Neurotrophic Activity ◽  
Mapk Signalling

In the last decade, Nerve Growth Factor (NGF)-based clinical approaches have lacked specific and efficient Tyrosine Kinase A (TrkA) agonists for brain delivery. Nowadays, the characterization of novel small peptidomimetic is taking centre stage in preclinical studies, in order to overcome the main size-related limitation in brain delivery of NGF holoprotein for Central Nervous System (CNS) pathologies. Here we investigated the NGF mimetic properties of the human NGF 1–14 sequence (hNGF1–14) and its derivatives, by resorting to primary cholinergic and dorsal root ganglia (DRG) neurons. Briefly, we observed that: 1) hNGF1–14 peptides engage the NGF pathway through TrkA phosphorylation at tyrosine 490 (Y490), and activation of ShcC/PI3K and Plc-γ/MAPK signalling, promoting AKT-dependent survival and CREB-driven neuronal activity, as seen by levels of the immediate early gene c-Fos, of the cholinergic marker Choline Acetyltransferase (ChAT), and of Brain Derived Neurotrophic Factor (BDNF); 2) their NGF mimetic activity is lost upon selective TrkA inhibition by means of GW441756; 3) hNGF1–14 peptides are able to sustain DRG survival and differentiation in absence of NGF. Furthermore, the acetylated derivative Ac-hNGF1–14 demonstrated an optimal NGF mimetic activity in both neuronal paradigms and an electrophysiological profile similar to NGF in cholinergic neurons. Cumulatively, the findings here reported pinpoint the hNGF1–14 peptide, and in particular its acetylated derivative, as novel, specific and low molecular weight TrkA specific agonists in both CNS and PNS primary neurons.

Does prostaglandin upregulate the tetrodotoxin-resistant Na+ current in DRG neurons?

2007 ◽  
Vol 18 (1) ◽  
pp. 8-14
Author(s):  
Jun-ichi Kakimura ◽  
Taixing Zheng ◽  
Tomoya Matsutomi ◽  
Chizumi Nakamoto ◽  
Nobukuni Ogata
Keyword(s):  
Na Current ◽  
Drg Neurons

scholarly journals Exendin-4 Promotes Schwann Cell Survival/Migration and Myelination In Vitro

2021 ◽  
Vol 22 (6) ◽  
pp. 2971
Author(s):  
Shizuka Takaku ◽  
Masami Tsukamoto ◽  
Naoko Niimi ◽  
Hideji Yako ◽  
Kazunori Sango
Keyword(s):  
Phosphatidyl Inositol ◽  
Specific Protein ◽  
Myelin Protein ◽  
Drg Neurons ◽  
Antibody Treatment ◽  
Pi3k Inhibitor Ly294002 ◽  
Adult Rat ◽  
Drg Neuron ◽  
Peripheral Nerve Lesions

Besides its insulinotropic actions on pancreatic β cells, neuroprotective activities of glucagon-like peptide-1 (GLP-1) have attracted attention. The efficacy of a GLP-1 receptor (GLP-1R) agonist exendin-4 (Ex-4) for functional repair after sciatic nerve injury and amelioration of diabetic peripheral neuropathy (DPN) has been reported; however, the underlying mechanisms remain unclear. In this study, the bioactivities of Ex-4 on immortalized adult rat Schwann cells IFRS1 and adult rat dorsal root ganglion (DRG) neuron–IFRS1 co-culture system were investigated. Localization of GLP-1R in both DRG neurons and IFRS1 cells were confirmed using knockout-validated monoclonal Mab7F38 antibody. Treatment with 100 nM Ex-4 significantly enhanced survival/proliferation and migration of IFRS1 cells, as well as stimulated the movement of IFRS1 cells toward neurites emerging from DRG neuron cell bodies in the co-culture with the upregulation of myelin protein 22 and myelin protein zero. Because Ex-4 induced phosphorylation of serine/threonine-specific protein kinase AKT in these cells and its effects on DRG neurons and IFRS1 cells were attenuated by phosphatidyl inositol-3′-phosphate-kinase (PI3K) inhibitor LY294002, Ex-4 might act on both cells to activate PI3K/AKT signaling pathway, thereby promoting myelination in the co-culture. These findings imply the potential efficacy of Ex-4 toward DPN and other peripheral nerve lesions.

scholarly journals C-terminal domain small phosphatase 1 (CTDSP1) regulates growth factor expression and axonal regeneration in peripheral nerve tissue

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Noreen M. Gervasi ◽  
Alexander Dimtchev ◽  
Desraj M. Clark ◽  
Marvin Dingle ◽  
Alexander V. Pisarchik ◽  
...  
Keyword(s):  
Chronic Pain ◽  
Peripheral Nerve ◽  
Neurotrophic Factor ◽  
Axon Growth ◽  
Nerve Tissue ◽  
Mesenchymal Progenitor Cells ◽  
Drg Neurons ◽  
Peripheral Neurons ◽  
Terminal Domain ◽  
Factor Expression

AbstractPeripheral Nerve Injury (PNI) represents a major clinical and economic burden. Despite the ability of peripheral neurons to regenerate their axons after an injury, patients are often left with motor and/or sensory disability and may develop chronic pain. Successful regeneration and target organ reinnervation require comprehensive transcriptional changes in both injured neurons and support cells located at the site of injury. The expression of most of the genes required for axon growth and guidance and for synapsis formation is repressed by a single master transcriptional regulator, the Repressor Element 1 Silencing Transcription factor (REST). Sustained increase of REST levels after injury inhibits axon regeneration and leads to chronic pain. As targeting of transcription factors is challenging, we tested whether modulation of REST activity could be achieved through knockdown of carboxy-terminal domain small phosphatase 1 (CTDSP1), the enzyme that stabilizes REST by preventing its targeting to the proteasome. To test whether knockdown of CTDSP1 promotes neurotrophic factor expression in both support cells located at the site of injury and in peripheral neurons, we transfected mesenchymal progenitor cells (MPCs), a type of support cells that are present at high concentrations at the site of injury, and dorsal root ganglion (DRG) neurons with REST or CTDSP1 specific siRNA. We quantified neurotrophic factor expression by RT-qPCR and Western blot, and brain-derived neurotrophic factor (BDNF) release in the cell culture medium by ELISA, and we measured neurite outgrowth of DRG neurons in culture. Our results show that CTDSP1 knockdown promotes neurotrophic factor expression in both DRG neurons and the support cells MPCs, and promotes DRG neuron regeneration. Therapeutics targeting CTDSP1 activity may, therefore, represent a novel epigenetic strategy to promote peripheral nerve regeneration after PNI by promoting the regenerative program repressed by injury-induced increased levels of REST in both neurons and support cells.

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