| 1. |
- Apostolova, Galina, et al.
(författare)
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Neurotransmitter phenotype-specific expression changes in developing sympathetic neurons
- 2007
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Ingår i: Molecular and Cellular Neuroscience. - : Elsevier BV. - 1044-7431 .- 1095-9327. ; 35:3, s. 397-408
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Tidskriftsartikel (refereegranskat)abstract
- During late developmental phases individual sympathetic neurons undergo a switch from noradrenergic to cholinergic neurotransmission. This phenomenon of plasticity depends on target-derived signals in vivo and is triggered by neurotrophic factors in neuronal cultures. To analyze genome-wide expression differences between the two transmitter phenotypes we employed DNA microarrays. RNA expression profiles were obtained from chick paravertebral sympathetic ganglia, treated with neurotrophin 3, glial cell line-derived neurotrophic factor or ciliary neurotrophic factor, all of which stimulate cholinergic differentiation. Results were compared with the effect of nerve growth factor, which functions as a pro-noradrenergic stimulus. The gene set common to all three comparisons defined the noradrenergic and cholinergic synexpression groups. Several functional categories, such as signal transduction, G-protein-coupled signaling, cation transport, neurogenesis and synaptic transmission, were enriched in these groups. Experiments based on the prediction that some of the identified genes play a role in the neurotransmitter switch identified bone morphogenetic protein signaling as an inhibitor of cholinergic differentiation.
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| 2. |
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| 3. |
- Holm, Pontus, et al.
(författare)
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Loss- and gain-of-function analyses reveal targets of Pax6 in the developing mouse telencephalon.
- 2007
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Ingår i: Molecular and Cellular Neuroscience. - : Elsevier BV. - 1044-7431 .- 1095-9327. ; 34:1, s. 99-119
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Forskningsöversikt (refereegranskat)abstract
- Appropriate neurogenesis and patterning of the forebrain requires the transcription factor Pax6, yet it is largely unknown how Pax6 exerts its effects at the molecular level. To characterize Pax6-mediated regulation of gene expression during murine forebrain neurogenesis, we performed microarray analysis with tissue from the dorsal Pax6-dependent telencephalon and the ventral Pax6-negative telencephalon at the onset of neurogenesis (E12) and at mid-neurogenesis (E15) in wild-type and Pax6-deficient mutant littermates. In the Pax6-deficient cortex the expression levels of various transcription factors involved in neurogenesis (like Satb2, Nfia, AP-2 gamma, NeuroD6, Ngn2, Tbr2, Bhlhb5) and the retinoic acid signalling molecule Rlbp1 were reduced. Regulation by Pax6 could be confirmed upon electroporation of a Pax6- and a dominant-negative Pax6-containing vector into embryonic cortex. Taken together, our data reveal novel insights into the molecular pathways regulated by Pax6 during cortical neurogenesis. Most intriguingly, this analysis revealed time- and region-specific differences in Pax6-mediated transcription, explaining the specific function of Pax6 at early and later stages of neurogenesis. (c) 2006 Elsevier Inc. All rights reserved.
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| 4. |
- Ishii, Yoko, et al.
(författare)
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Characterization of neuroprogenitor cells expressing the PDGF beta-receptor within the subventricular zone of postnatal mice.
- 2008
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Ingår i: Molecular and cellular neurosciences. - : Elsevier BV. - 1095-9327 .- 1044-7431. ; 37:3, s. 507-18
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Tidskriftsartikel (refereegranskat)abstract
- We report a considerable number of cells in the ventricular and the subventricular zones (SVZ) of newborn mice to stain positive for the PDGF beta-receptor (PDGFRB). Many of them also stained for nestin and/or GFAP but less frequently for the neuroblast marker doublecortin and for the mitotic marker Ki-67. The SVZ of mice with nestin-Cre conditional deletion of PDGFRB expressed the receptor only on blood vessels and was devoid of any morphological abnormality. PDGFRB(-/-) neurospheres showed a higher rate of apoptosis without any significant decrease in proliferation. They demonstrated reduced capacities of migration and neuronal differentiation in response to not only PDGF-BB but also bFGF. Furthermore, the PDGFR kinase inhibitor STI571 blocked the effects of bFGF in control neurosphere cultures. bFGF increased the activity of the PDGFRB promoter as well as the expression and phosphorylation of PDGFRB. These results suggest the presence of the signaling convergence between PDGF and FGF. PDGFRB is needed for survival, and the effects of bFGF in migration and neural differentiation of the cells may be potentiated by induction of PDGFRB.
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| 5. |
- Korhonen, Laura, et al.
(författare)
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Hippocalcin protects against caspase-12-induced and age-dependent neuronal degeneration
- 2005
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Ingår i: Molecular and Cellular Neuroscience. - Uppsala Univ, Ctr Biomed, Dept Neurosci, Neurobiol Unit, S-75123 Uppsala, Sweden. Uppsala Univ, Ctr Biomed, Dept Neurosci, Unit Physiol, S-75123 Uppsala, Sweden. Toho Univ, Sch Med, Dept Physiol, Ohta Ku, Tokyo 1438540, Japan. Minerva Med Res Inst, Biomedicum Helsinki, FIN-00290 Helsinki, Finland. : ACADEMIC PRESS INC ELSEVIER SCIENCE. - 1044-7431 .- 1095-9327. ; 28:1, s. 85-95
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Tidskriftsartikel (refereegranskat)abstract
- Hippocalcin is a neuronal calcium binding protein, but its physiological function in brain is unknown. We show here that hippocampal neurons from hippocalcin-deficient mice are more vulnerable to degeneration, particularly using thapsigargin, elevating intracellular calcium. Caspase-12 was activated in neurons lacking hippocalcin, while calpain was unchanged. Neuronal viability was accompanied by endoplasmic reticulum (ER) stress and a change in the relative induction of the ER chaperone, BiP/GRP78. Neuronal apoptosis inhibitor protein (NAIP), known to interact with hippocalcin, was not altered, but hippocampal neurons from gene-deleted mice were more sensitive to excitotoxicity caused by kainic acid. In addition, an age-dependent increase in neurodegeneration occurred in the gene-deleted mice, showing that hippocalcin contributes to neuronal viability during aging. (C) 2004 Elsevier Inc. All rights reserved.
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| 6. |
- Larsson, Jimmy, et al.
(författare)
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Nuclear receptor binding protein 2 is induced during neural progenitor differentiation and affects cell survival
- 2008
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Ingår i: Molecular and Cellular Neuroscience. - : Elsevier BV. - 1044-7431 .- 1095-9327. ; 39:1, s. 32-9
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Tidskriftsartikel (refereegranskat)abstract
- We previously identified nuclear receptor binding protein 2 (NRBP2) in a screen for genes induced by differentiation of neural stem/progenitor cells. Here we show that during embryonic mouse brain development NRBP2 was expressed in the walls of the third and fourth ventricles, and in the hippocampus. In the adult brain, Purkinje cells of the cerebellum and neurons in the CA3 region of the hippocampus were main sites of NRBP2 expression. Analysis of a pediatric medulloblastoma showed that clusters of NRBP2 positive tumor cells co-expressed neurofilament, but not GFAP. Thus, NRBP2 was associated with neuronal differentiation both in normal and malignant brain tissue. We report that NRBP2 is a 55-60 kDa protein with mainly cytoplasmic location. In vitro, NRBP2 protein levels increased as neural stem/progenitor cells differentiated, and its down regulation by siRNA rendered neural progenitor cells more vulnerable to apoptosis. NRBP2 has no previously assigned function and our studies suggest a role for NRBP2 in neural progenitor cell survival.
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| 9. |
- Winther, Åsa M E, 1968-, et al.
(författare)
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Tachykinin-related peptides modulate odor perception and locomotoractivity in Drosophila
- 2006
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Ingår i: Molecular and Cellular Neuroscience. - : Elsevier BV. - 1044-7431 .- 1095-9327. ; 31:3, s. 399-406
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Tidskriftsartikel (refereegranskat)abstract
- The invertebrate tachykinin-related peptides (TKRPs) constitute aconserved family, structurally related to the mammalian tachykinins,including members such as substance P and neurokinins A and B.Although their expression has been documented in the brains of insectsand mammals, their neural functions remain largely unknown,particularly in behavior. Here, we have studied the role of TKRPs inDrosophila. We have analyzed the olfactory perception and thelocomotor activity of individuals in which TKRPs are eliminated inthe nervous system specifically, by using RNAi constructs to silencegene expression. The perception of specific odorants and concentrationsis modified towards a loss of sensitivity, thus resulting in asignificant change of the behavioral response towards indifference. Inlocomotion assays, the TKRP-deficient flies show hyperactivity. Weconclude that these peptides are modulators of olfactory perceptionand locomotion activity in agreement with their abundant expression inthe olfactory lobes and central complex. In these brain centers, TKRPsseem to enhance the regulatory inhibition of the neurons in which theyare expressed.
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| 10. |
- Azadi, Seifollah, et al.
(författare)
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Up-regulation and increased phosphorylation of protein kinase C (PKC) delta, mu and theta in the degenerating rd1 mouse retina.
- 2006
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Ingår i: Molecular and Cellular Neuroscience. - : Elsevier BV. - 1044-7431. ; 31:4, s. 759-773
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Tidskriftsartikel (refereegranskat)abstract
- The rd1 mouse serves as a model for inherited photoreceptor degeneration: retinitis pigmentosa. Microarray techniques were employed to compare the transcriptomes of rd1 and congenic wild-type retinas at postnatal day 11, when degenerative processes have started but most photoreceptors are still present. Of the several genes that were differentially expressed, focus was put on those associated with the protein kinase C (PKC) signaling pathway, in particular PKCδ, μ and θ. Microarray identified these as being up-regulated in the rd1 retina, which was confirmed by QRT-PCR. Western blotting and immunostaining, using antibodies against either total or phosphorylated variants of the PKC isoforms, revealed increased expression and phosphorylation of PKCδ, μ and θ in the rd1 retina at the protein level as well. Our results suggest that these PKC isoforms are involved in rd1 degeneration.
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