keyword
MENU ▼
Read by QxMD icon Read
search

spinal mouse

keyword
https://www.readbyqxmd.com/read/28526579/differential-involvement-of-vesicular-and-glial-glutamate-transporters-around-spinal-%C3%AE-motoneurons-in-the-pathogenesis-of-sod1-g93a-mouse-model-of-amyotrophic-lateral-sclerosis
#1
Tomohiro Ohgomori, Ryo Yamasaki, Hideyuki Takeuchi, Kenji Kadomatsu, Jun-Ichi Kira, Shozo Jinno
From a view point of the glutamate excitotoxicity theory, several studies have suggested that abnormal glutamate homeostasis via dysfunction of glial glutamate transporter-1 (GLT-1) may underlie neurodegeneration in amyotrophic lateral sclerosis (ALS). However, the detailed role of GLT-1 in the pathogenies of ALS remains controversial. To assess this issue, here we elucidated structural alterations associated with dysregulation of glutamate homeostasis using SOD1(G93A) mice, a genetic model of familial ALS...
May 16, 2017: Neuroscience
https://www.readbyqxmd.com/read/28522962/alterations-in-cd200-cd200r1-system-during-eae-already-manifest-at-presymptomatic-stages
#2
Tony Valente, Joan Serratosa, Unai Perpiñá, Josep Saura, Carme Solà
In the brain of patients with multiple sclerosis, activated microglia/macrophages appear in active lesions and in normal appearing white matter. However, whether they play a beneficial or a detrimental role in the development of the pathology remains a controversial issue. The production of pro-inflammatory molecules by chronically activated microglial cells is suggested to contribute to the progression of neurodegenerative processes in neurological disease. In the healthy brain, neurons control glial activation through several inhibitory mechanisms, such as the CD200-CD200R1 interaction...
2017: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/28522736/myelin-associated-glycoprotein-mag-inhibits-schwann-cell-migration-and-induces-their-death
#3
Nagarathnamma Chaudhry, Corinne Bachelin, Violetta Zujovic, Melissa Hilaire, Katherine T Baldwin, Rose M Follis, Roman Giger, Bruce D Carter, Anne Baron-Van Evercooren, Marie T Filbin
Remyelination of central nervous system (CNS) axons by Schwann cells (SC) is not efficient, in part due to their poor migration into the adult CNS. Although it is known that migrating SC avoid white matter tracts, the molecular mechanisms underlying this exclusion has never been elucidated. We now demonstrate that myelin-associated glycoprotein (MAG), a well-known inhibitor of neurite outgrowth, inhibits rat SC migration and induces their death via γ secretase-dependent regulated intramembrane proteolysis (RIP) of the p75 neurotrophin receptor (also known as p75 cleavage)...
May 17, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28516219/decreased-sensory-nerve-excitation-and-bone-pain-associated-with-mouse-lewis-lung-cancer-in-trpv1-deficient-mice
#4
Hiroki Wakabayashi, Satoshi Wakisaka, Toru Hiraga, Kenji Hata, Riko Nishimura, Makoto Tominaga, Toshiyuki Yoneda
Bone pain is one of the most common and life-limiting complications of cancer metastasis to bone. Although the mechanism of bone pain still remains poorly understood, bone pain is evoked as a consequence of sensitization and excitation of sensory nerves (SNs) innervating bone by noxious stimuli produced in the microenvironment of bone metastases. We showed that bone is innervated by calcitonin gene-related protein (CGRP)(+) SNs extending from dorsal root ganglia (DRG), the cell body of SNs, in mice. Mice intratibially injected with Lewis lung cancer (LLC) cells showed progressive bone pain evaluated by mechanical allodynia and flinching with increased CGRP(+) SNs in bone and augmented SN excitation in DRG as indicated by elevated numbers of pERK- and pCREB-immunoreactive neurons...
May 17, 2017: Journal of Bone and Mineral Metabolism
https://www.readbyqxmd.com/read/28515487/functional-interaction-between-fus-and-smn-underlies-sma-like-splicing-changes-in-wild-type-hfus-mice
#5
Alessia Mirra, Simona Rossi, Silvia Scaricamazza, Michela Di Salvio, Illari Salvatori, Cristiana Valle, Paola Rusmini, Angelo Poletti, Gianluca Cestra, Maria Teresa Carrì, Maur O Cozzolino
Several of the identified genetic factors in Amyotrophic Lateral Sclerosis (ALS) point to dysfunction in RNA processing as a major pathogenic mechanism. However, whether a precise RNA pathway is particularly affected remains unknown. Evidence suggests that FUS, that is mutated in familial ALS, and SMN, the causative factor in Spinal Muscular Atrophy (SMA), cooperate to the same molecular pathway, i.e. regulation of alternative splicing, and that disturbances in SMN-regulated functions, either caused by depletion of SMN protein (as in the case of SMA) or by pathogenic interactions between FUS and SMN (as in the case of ALS) might be a common theme in both diseases...
May 17, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28514232/ppar%C3%AE-agonists-attenuate-trigeminal-neuropathic-pain
#6
Danielle N Lyons, Liping Zhang, Robert J Danaher, Craig S Miller, Karin N Westlund
The aim of this study is to investigate the role of peroxisome proliferator-activated receptor-gamma isoform (PPARγ), in trigeminal neuropathic pain utilizing a novel mouse trigeminal inflammatory compression (TIC) injury model. The study determined that the PPARγ nuclear receptor plays a significant role in trigeminal nociception transmission, evidenced by: (1) Intense PPARγ immunoreactivity is expressed 3 weeks after TIC nerve injury in the spinal trigeminal caudalis, the termination site of trigeminal nociceptive nerve fibers...
May 16, 2017: Clinical Journal of Pain
https://www.readbyqxmd.com/read/28511915/altered-ionic-currents-and-amelioration-by-igf-1-and-pacap-in-motoneuron-derived-cells-modelling-sbma
#7
Aura M Jiménez Garduño, Leon J Juárez-Hernández, María J Polanco, Laura Tosatto, Daniela Michelatti, Daniele Arosio, Manuela Basso, Maria Pennuto, Carlo Musio
Spinal and bulbar muscular atrophy (SBMA), also known as Kennedy's disease, is a motor neuron disease caused by the expansion of a polymorphic CAG tandem repeat encoding a polyglutamine (polyQ) tract in the androgen receptor (AR) gene. SBMA is triggered by the binding of mutant AR to its natural ligands, testosterone and dihydrotestosterone (DHT). To investigate the neuronal alterations of motor neuron cell models of SBMA, we applied patch-clamp methods to verify how polyQ expansions in the AR alter cell ionic currents...
May 10, 2017: Biophysical Chemistry
https://www.readbyqxmd.com/read/28507510/enhanced-axonal-extension-of-subcortical-projection-neurons-isolated-from-murine-embryonic-cortex-using-neuropilin-1
#8
Noritaka Sano, Takafumi Shimogawa, Hideya Sakaguchi, Yoshihiko Ioroi, Yoshifumi Miyawaki, Asuka Morizane, Susumu Miyamoto, Jun Takahashi
The cerebral cortical tissue of murine embryo and pluripotent stem cell (PSC)-derived neurons can survive in the brain and extend axons to the spinal cord. For efficient cell integration to the corticospinal tract (CST) after transplantation, the induction or selection of cortical motor neurons is important. However, precise information about the appropriate cell population remains unclear. To address this issue, we isolated cells expressing Neuropilin-1 (NRP1), a major axon guidance molecule receptor during the early developmental stage, from E14...
2017: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/28505922/re-transplanted-human-stem-cell-derived-interneuron-precursors-mitigate%C3%A2-mouse-bladder-dysfunction-and-central-neuropathic-pain-after%C3%A2-spinal-cord-injury
#9
https://www.readbyqxmd.com/read/28504671/reduced-sensory-synaptic-excitation-impairs-motor-neuron-function-via-kv2-1-in-spinal-muscular-atrophy
#10
Emily V Fletcher, Christian M Simon, John G Pagiazitis, Joshua I Chalif, Aleksandra Vukojicic, Estelle Drobac, Xiaojian Wang, George Z Mentis
Behavioral deficits in neurodegenerative diseases are often attributed to the selective dysfunction of vulnerable neurons via cell-autonomous mechanisms. Although vulnerable neurons are embedded in neuronal circuits, the contributions of their synaptic partners to disease process are largely unknown. Here we show that, in a mouse model of spinal muscular atrophy (SMA), a reduction in proprioceptive synaptic drive leads to motor neuron dysfunction and motor behavior impairments. In SMA mice or after the blockade of proprioceptive synaptic transmission, we observed a decrease in the motor neuron firing that could be explained by the reduction in the expression of the potassium channel Kv2...
May 15, 2017: Nature Neuroscience
https://www.readbyqxmd.com/read/28503634/an-acute-mouse-spinal-cord-slice-preparation-for-studying-glial-activation-ex-vivo
#11
Juan Mauricio Garré, Guang Yang, Feliksas F Bukauskas, Michael V L Bennett
Pathological conditions such as amyotrophic lateral sclerosis, spinal cord injury and chronic pain are characterized by activation of astrocytes and microglia in spinal cord and have been modeled in rodents. In vivo imaging at cellular level in these animal models is limited due to the spinal cord's highly myelinated funiculi. The preparation of acute slices may offer an alternative and valuable strategy to collect structural and functional information in vitro from dorsal, lateral and ventral regions of spinal cord...
January 20, 2017: Bio-protocol
https://www.readbyqxmd.com/read/28501905/investigation-of-pain-mechanisms-by-calcium-imaging-approaches
#12
REVIEW
Michael Anderson, Qin Zheng, Xinzhong Dong
Due to the complex circuitry and plethora of cell types involved in somatosensation, it is becoming increasingly important to be able to observe cellular activity at the population level. In addition, since cells rely on an intricate variety of extracellular factors, it is important to strive to maintain the physiological environment. Many electrophysiological techniques require the implementation of artificially-produced physiological environments and it can be difficult to assess the activity of many cells simultaneously...
May 13, 2017: Neuroscience Bulletin
https://www.readbyqxmd.com/read/28500250/characterization-of-nmb-grp-and-their-receptors-brs3-nmbr-and-grpr-in-chickens
#13
Chunheng Mo, Long Huang, Lin Cui, Can Lv, Dongliang Lin, Liang Song, Guoqiang Zhu, Juan Li, Yajun Wang
The two structurally and functionally related peptides, gastrin-releasing peptide (GRP) and neuromedin B (NMB) play critical roles in many physiological/pathological processes in mammals. However, the information regarding the expression and functionality of avian NMB, GRP, and their receptors is limited. Here, we characterized cNMB, cGRP and their receptors (cNMBR, cGRPR, cBRS3) in chickens. Our results showed that: 1) cNMBR and cGRPR expressed in CHO cells could be potently activated by cNMB and cGRP respectively, as monitored by cell-based luciferase reporter assays, indicating that cNMBR and cGRPR are cNMB- and cGRP-specific receptors; Strikingly, BRS3 of chickens (/spotted gars), which is orthologous to mouse bombesin receptor subtype-3 (BRS3), could be potently activated by GRP and NMB, demonstrating that both peptides are the endogenous ligands for chicken(/spotted gar) BRS3; 2) Quantitative real-time PCR revealed that cGRPR is widely expressed in chicken tissues with abundant expression in the ovary, pancreas, proventriculus, spinal cord and brain, whereas cNMB, cNMBR and cBRS3 are mainly expressed in the brain and testes; 3) Interestingly, qPCR, Western blot, and immuno-staining revealed that cGRP is predominantly expressed in the anterior pituitary and mainly localized to LH-cells, suggesting that cGRP is likely a novel pituitary hormone in chickens...
May 12, 2017: Journal of Molecular Endocrinology
https://www.readbyqxmd.com/read/28495589/reduced-fak-stat3-signaling-contributes-to-er-stress-induced-mitochondrial-dysfunction-and-death-in-endothelial-cells
#14
Kalpita Banerjee, Matt P Keasey, Vladislav Razskazovskiy, Nishant P Visavadiya, Cuihong Jia, Theo Hagg
Excessive endoplasmic reticulum (ER) stress leads to cell loss in many diseases, e.g., contributing to endothelial cell loss after spinal cord injury. Here, we determined whether ER stress-induced mitochondrial dysfunction could be explained by interruption of the focal adhesion kinase (FAK)-mitochondrial STAT3 pathway we recently discovered. ER stress was induced in brain-derived mouse bEnd5 endothelial cells by thapsigargin or tunicamycin and caused apoptotic cell death over a 72h period. In concert, ER stress caused mitochondrial dysfunction as shown by reduced bioenergetic function, loss of mitochondrial membrane potential and increased mitophagy...
May 8, 2017: Cellular Signalling
https://www.readbyqxmd.com/read/28490517/atoh1-promotes-leptomeningeal-dissemination-and-metastasis-of-sonic-hedgehog-subgroup-medulloblastomas
#15
Katie B Grausam, Samuel Dr Dooyema, Laure Bihannic, Hasitha Premathilake, A Sorana Morrissy, Antoine Forget, Amanda M Schaefer, Justin H Gundelach, Slobodan Macura, Diane M Maher, Xin Wang, Alex H Heglin, Xijin Ge, Erliang Zeng, Stephanie Puget, Indra Chandrasekar, Kameswaran Surendran, Richard J Bram, Ulrich Schüller, Michael D Taylor, Olivier Ayrault, Haotian Zhao
Medulloblastoma (MB) arising from the cerebellum is the most common pediatric brain malignancy, with leptomeningeal metastases often present at diagnosis and recurrence associated with poor clinical outcome. In this study, we employed mouse MB models to explore the relationship of tumor pathophysiology and dysregulated expression of the Notch pathway transcription factor ATOH1, which is present in aggressive MB subtypes driven by aberrant Sonic Hedgehog/Patched (SHH/PTCH) signaling. In experiments with conditional Atoh1 mouse mutants crossed to Ptch1(+/-) mice which develop SHH-driven MB[63], animals with Atoh1 transgene expression developed highly penetrant MB at a young age with extensive leptomeningeal disease and metastasis to the spinal cord and brain, resembling xenografts of human SHH MB...
May 10, 2017: Cancer Research
https://www.readbyqxmd.com/read/28490013/sulfatase-2-modulates-fate-change-from-motor-neurons-to-oligodendrocyte-precursor-cells-through-coordinated-regulation-of-shh-signaling-with-sulfatase-1
#16
Wen Jiang, Yugo Ishino, Hirokazu Hashimoto, Kazuko Keino-Masu, Masayuki Masu, Kenji Uchimura, Kenji Kadomatsu, Takeshi Yoshimura, Kazuhiro Ikenaka
Sulfatases (Sulfs) are a group of endosulfatases consisting of Sulf1 and Sulf2, which specifically remove sulfate from heparan sulfate proteoglycans. Although several studies have shown that Sulf1 acts as a regulator of sonic hedgehog (Shh) signaling during embryonic ventral spinal cord development, the detailed expression pattern and function of Sulf2 in the spinal cord remains to be determined. In this study, we found that Sulf2 also modulates the cell fate change from motor neurons (MNs) to oligodendrocyte precursor cells (OPCs) by regulating Shh signaling in the mouse ventral spinal cord in coordination with Sulf1...
May 11, 2017: Developmental Neuroscience
https://www.readbyqxmd.com/read/28488683/progressive-hereditary-spastic-paraplegia-caused-by-a-homozygous-ky-mutation
#17
Yuval Yogev, Yonatan Perez, Iris Noyman, Anwar Abu Madegem, Hagit Flusser, Zamir Shorer, Eugene Cohen, Leonid Kachko, Analia Michaelovsky, Ruth Birk, Arie Koifman, Max Drabkin, Ohad Wormser, Daniel Halperin, Rotem Kadir, Ohad S Birk
Twelve individuals of consanguineous Bedouin kindred presented with autosomal recessive progressive spastic paraplegia evident as of age 0-24 months, with spasticity of lower limbs, hyperreflexia, toe walking and equinus deformity. Kyphoscolisois was evident in older patients. Most had atrophy of the lateral aspects of the tongue and few had intellectual disability. Nerve conduction velocity, electromyography and head and spinal cord magnetic resonance imaging were normal in tested subjects. Muscle biopsy showed occasional central nuclei and fiber size variability with small angular fibers...
May 10, 2017: European Journal of Human Genetics: EJHG
https://www.readbyqxmd.com/read/28487080/astrocytic-expression-of-the-rna-regulator-hur-accentuates-spinal-cord-injury-in-the-acute-phase
#18
Thaddaeus Kwan, Candace L Floyd, Jason Patel, Amanda Mohaimany-Aponte, Peter H King
We recently showed that the RNA regulator, HuR, is translocated to the cytoplasm in astrocytes in the acute phase of spinal cord injury (SCI), consistent with its activation. HuR positively modulates expression of many pro-inflammatory factors, including IL-1β, TNF-α, and MMP-12, which are present at high levels in the early phase of SCI and exacerbate tissue damage. Knockdown of HuR in astrocytes blunts expression of these factors in an in vitro stretch injury model of CNS trauma. In this report, we further investigate the impact of HuR in early SCI using a mouse model in which human HuR is transgenically expressed in astrocytes...
May 6, 2017: Neuroscience Letters
https://www.readbyqxmd.com/read/28485722/how-the-discovery-of-iss-n1-led-to-the-first-medical-therapy-for-spinal-muscular-atrophy
#19
REVIEW
N N Singh, M D Howell, E J Androphy, R N Singh
Spinal muscular atrophy (SMA), a prominent genetic disease of infant mortality, is caused by low levels of survival motor neuron (SMN) protein owing to deletions or mutations of the SMN1 gene. SMN2, a nearly identical copy of SMN1 present in humans, cannot compensate for the loss of SMN1 due to predominant skipping of exon 7 during pre-mRNA splicing. With the recent FDA approval of nusinersen (Spinraza™), the potential for correction of SMN2 exon 7 splicing as a SMA therapy has been affirmed. Nusinersen is an antisense oligonucleotide that targets intronic splicing silencer N1 (ISS-N1) discovered in 2004 at the University of Massachusetts Medical School...
May 9, 2017: Gene Therapy
https://www.readbyqxmd.com/read/28484370/clustered-protocadherins-are-required-for-building-functional-neural-circuits
#20
Sonoko Hasegawa, Hiroaki Kobayashi, Makiko Kumagai, Hiroshi Nishimaru, Etsuko Tarusawa, Hiro Kanda, Makoto Sanbo, Yumiko Yoshimura, Masumi Hirabayashi, Takahiro Hirabayashi, Takeshi Yagi
Neuronal identity is generated by the cell-surface expression of clustered protocadherin (Pcdh) isoforms. In mice, 58 isoforms from three gene clusters, Pcdhα, Pcdhβ, and Pcdhγ, are differentially expressed in neurons. Since cis-heteromeric Pcdh oligomers on the cell surface interact homophilically with that in other neurons in trans, it has been thought that the Pcdh isoform repertoire determines the binding specificity of synapses. We previously described the cooperative functions of isoforms from all three Pcdh gene clusters in neuronal survival and synapse formation in the spinal cord...
2017: Frontiers in Molecular Neuroscience
keyword
keyword
70983
1
2
Fetch more papers »
Fetching more papers... Fetching...
Read by QxMD. Sign in or create an account to discover new knowledge that matter to you.
Remove bar
Read by QxMD icon Read
×

Search Tips

Use Boolean operators: AND/OR

diabetic AND foot
diabetes OR diabetic

Exclude a word using the 'minus' sign

Virchow -triad

Use Parentheses

water AND (cup OR glass)

Add an asterisk (*) at end of a word to include word stems

Neuro* will search for Neurology, Neuroscientist, Neurological, and so on

Use quotes to search for an exact phrase

"primary prevention of cancer"
(heart or cardiac or cardio*) AND arrest -"American Heart Association"