scholarly journals Glutamatergic Fate of Neural Progenitor Cells of Rats with Inherited Audiogenic Epilepsy

2020 ◽  
Vol 10 (5) ◽  
pp. 311
Author(s):  
Alexandra A. Naumova ◽  
Ekaterina A. Oleynik ◽  
Elena V. Chernigovskaya ◽  
Margarita V. Glazova
Keyword(s):  
Protein Kinase ◽  
Progenitor Cells ◽  
Neural Progenitor Cells ◽  
Glycogen Synthase ◽  
Neural Progenitor ◽  
Cell Number ◽  
Gamma Aminobutyric Acid ◽  
Audiogenic Epilepsy ◽  
Extracellular Signal ◽  
Stimulation Of

Epilepsy is associated with aberrant neurogenesis in the hippocampus and may underlie the development of hereditary epilepsy. In the present study, we analyzed the differentiation fate of neural progenitor cells (NPC), which were isolated from the hippocampus of embryos of Krushinsky-Molodkina (KM) rats genetically prone to audiogenic epilepsy. NPCs from embryos of Wistar rats were used as the control. We found principal differences between Wistar and KM NPC in unstimulated controls: Wistar NPC culture contained both gamma-aminobutyric acid (GABA) and glutamatergic neurons; KM NPC culture was mainly represented by glutamatergic cells. The stimulation of glutamatergic differentiation of Wistar NPC resulted in a significant increase in glutamatergic cell number that was accompanied by the activation of protein kinase A. The stimulation of KM NPC led to a decrease in immature glutamatergic cell number and was associated with the activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) and protein kinase B/ glycogen synthase kinase 3 beta (Akt/GSK3β), which indicates the activation of glutamatergic cell maturation. These results suggest genetically programmed abnormalities in KM rats that determine the glutamatergic fate of NPC and contribute to the development of audiogenic epilepsy.

scholarly journals Insulin action in cultured human myoblasts: contribution of different signalling pathways to regulation of glycogen synthesis

1996 ◽  
Vol 320 (3) ◽  
pp. 871-877 ◽  
Author(s):  
Steven J. HUREL ◽  
Justin J. ROCHFORD ◽  
Andrew C. BORTHWICK ◽  
Anne M. WELLS ◽  
Jackie R. VANDENHEEDE ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Glycogen Synthase ◽  
Insulin Signalling ◽  
Protein Kinase B ◽  
Glycogen Synthesis ◽  
Experimental Systems ◽  
Extracellular Signal ◽  
Insulin Control ◽  
Metabolic Action ◽  
Stimulation Of

A key metabolic action of insulin is the stimulation of non-oxidative glucose utilization in skeletal muscle, by increasing both glucose uptake and glycogen synthesis. The molecular mechanism underlying this process has been investigated using a variety of experimental systems. We report here the use of cultured human myoblasts to study insulin control of glycogen synthesis in humans. In these cells insulin stimulates glycogen synthesis approx. 2.2-fold, associated with a similar activation of glycogen synthase (GS) which occurs within 5–10 min of the addition of insulin. Insulin also causes inactivation of glycogen synthase kinase-3 (GSK-3) and activation of protein kinase B, both processes being sufficiently rapid to account for the effects of insulin on GS. Activation by insulin of the protein kinases p70s6K, p90s6K and extracellular signal-regulated kinase 2 (ERK2) is observed, but is significantly slower than the activation of GS. Selective inhibitors of the p70s6K pathway (rapamycin), the ERK2/p90s6K pathway (PD98059) and phosphatidylinositol 3-kinase (wortmannin) have been used to probe the contribution of these components to insulin signalling in human muscle. Wortmannin blocks activation of both glycogen synthesis and GS and inactivation of GSK-3. PD98059 is without effect on these events, while rapamycin is without effect on inactivation of GSK-3 but partially blocks activation of glycogen synthesis and GS. Taken together, these findings suggest that protein kinase B is responsible for the inactivation of GSK-3, but that an additional rapamycin-sensitive mechanism may contribute to the activation of GS and stimulation of glycogen synthesis.

scholarly journals Short Term Development and Fate of MGE-Like Neural Progenitor Cells in Jaundiced and Non-Jaundiced Rat Brain

2018 ◽  
Vol 27 (4) ◽  
pp. 654-665 ◽  
Author(s):  
Fu-Chen Yang ◽  
Julia Draper ◽  
Peter G. Smith ◽  
Jay L. Vivian ◽  
Steven M. Shapiro ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Neural Progenitor Cells ◽  
Neural Progenitor ◽  
Brain Regions ◽  
Gamma Aminobutyric Acid ◽  
Post Transplantation ◽  
Elevated Bilirubin ◽  
Survival And Development ◽  
Spinal Interneuron ◽  
Bilirubin Toxicity

Neonatal hyperbilirubinemia targets specific brain regions and can lead to kernicterus. One of the most debilitating symptoms of kernicterus is dystonia, which results from bilirubin toxicity to the globus pallidus (GP). Stem cell transplantation into the GP to replace lost neurons and restore basal ganglia circuits function is a potential therapeutic strategy to treat dystonia in kernicterus. In this study we transplanted human medial ganglionic eminence (MGE)-like neural progenitor cells (NPCs) that we differentiated into a primarily gamma-aminobutyric acid (GABA)ergic phenotype, into the GP of non-immunosuppressed jaundiced (jj) and non-jaundiced (Nj) rats. We assessed the survival and development of graft cells at three time-points post-transplantation. While grafted MGE-like NPCs survived and generated abundant fibers in both jj and Nj brains, NPC survival was greater in the jj brain. These results were consistent with our previous finding that excitatory spinal interneuron-like NPCs exhibited a higher survival rate in the jj brain than in the Nj brain. Our findings further support our hypothesis that slightly elevated bilirubin levels in the jj brain served as an antioxidant and immunosuppressant to protect the transplanted cells. We also identified graft fibers growing toward brain regions that receive projections from the GP, as well as host fibers extending toward the graft. These promising findings suggest that MGE-like NPCs may have the capacity to restore the circuits connecting GP and other nuclei.

2-Deoxy-d-glucose protects neural progenitor cells against oxidative stress through the activation of AMP-activated protein kinase

2009 ◽  
Vol 449 (3) ◽  
pp. 201-206 ◽  
Author(s):  
Mikyung Park ◽  
Kwan Sung Song ◽  
Hyun Kyu Kim ◽  
Young Joo Park ◽  
Hyung Sik Kim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protein Kinase ◽  
Progenitor Cells ◽  
Neural Progenitor Cells ◽  
Neural Progenitor ◽  
Amp Activated Protein Kinase
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