| 1. |
- Forsberg-Nilsson, Karin, et al.
(författare)
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Platelet-derived growth factor induces chemotaxis of neuroepithelial stem cells
- 1998
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Ingår i: Journal of Neuroscience Research. - 0360-4012 .- 1097-4547. ; 53:5, s. 521-530
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Tidskriftsartikel (refereegranskat)abstract
- The ability of differentiating cells to migrate within the developing central nervous system (CNS) depends on extrinsic guidance signals, some of which are growth factors. In this study we have investigated the chemotactic response of cultured stem cells from the embryonic rat cortex to platelet-derived growth factor (PDGF). Nestin-positive stem cells from the developing CNS can be maintained and expanded in vitro under serum-free conditions in the presence of basic fibroblast growth factor (bFGF). Northern blot analysis of PDGF receptor expression revealed both α- and β-receptors on bFGF-treated neural stem cells. Both PDGF-AA and PDGF-BB readily induced directed migration of cultured neuroepithelial cells as measured in a microchemotaxis assay. Blocking of the migratory response was achieved by incubation with PDGF isoform-specific antibodies. More than 90% of the migrating cells were nestin-positive and incorporation of BrdU was also seen suggesting the cells to be immature and not yet committed to a specific cell lineage. These findings suggest a role for PDGF in cell migration in the developing cortex.
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| 2. |
- Kullander, Klas, et al.
(författare)
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Specificity of neurotrophin-3 determined by loss-of-function mutagenesis
- 1997
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Ingår i: Journal of Neuroscience Research. - 0360-4012 .- 1097-4547. ; 50:3, s. 496-503
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Tidskriftsartikel (refereegranskat)abstract
- Neurotrophin-3 (NT-3) is a member of the family of neurotrophic factors, which also includes nerve growth factor (NGF) and which have specific activities on different subsets of vertebrate neurons. The aim of this study was to determine which residues in NT-3 direct its specificity to the cognate TrkC receptor. It was possible to replace 80% of the residues in NT-3 with NGF residues without loss of specific activity. Residues D72, Y85, R87, W101, S107, and A111, together with either the residues F12, V18, V20, M37, V42, F54, and K57 or the variable regions IV and V, accounted for the specificity of NT-3. It is concluded that NGF and NT-3 use overlapping as well as separated regions for determination of specificities for their cognate receptors TrkA and TrkC, respectively.
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| 3. |
- Aho, Leena, et al.
(författare)
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Heavy alcohol consumption and neuropathological lesions : a post-mortem human study
- 2009
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Ingår i: Journal of Neuroscience Research. - : Wiley. - 0360-4012 .- 1097-4547. ; 87:12, s. 2786-2792
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Tidskriftsartikel (refereegranskat)abstract
- Epidemiological studies have indicated that excessive alcohol consumption leads to cognitive impairment, but the specific pathological mechanism involved remains unknown. The present study evaluated the association between heavy alcohol intake and the neuropathological hallmark lesions of the three most common neurodegenerative disorders, i.e., Alzheimer's disease (AD), dementia with Lewy bodies (DLB), and vascular cognitive impairment (VCI), in post-mortem human brains. The study cohort was sampled from the subjects who underwent a medicolegal autopsy during a 6-month period in 1999 and it included 54 heavy alcohol consumers and 54 age- and gender-matched control subjects. Immunohistochemical methodology was used to visualize the aggregation of beta-amyloid, hyperphosphorylated tau, and alpha-synuclein and the extent of infarcts. In the present study, no statistically significant influence was observed for alcohol consumption on the extent of neuropathological lesions encountered in the three most common degenerative disorders. Our results indicate that alcohol-related dementia differs from VCI, AD, and DLB; i.e., it has a different etiology and pathogenesis.
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| 4. |
- Alfonso, Julieta, et al.
(författare)
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Analysis of gene expression in the rat hippocampus using Real Time PCR reveals high inter-individual variation in mRNA expression levels
- 2002
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Ingår i: Journal of Neuroscience Research. - : Wiley. - 0360-4012 .- 1097-4547. ; 67:2, s. 225-34
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Tidskriftsartikel (refereegranskat)abstract
- In mammals, gene transcription is a step subjected to tight regulation mechanisms. In fact, changes in mRNA levels in the central nervous system (CNS) can account for numerous phenotypic differences in brain function. We performed a high-resolution analysis of mRNA expression levels for 37 genes selected from a normal rat hippocampus cDNA library. mRNA amounts were quantified using a Real Time PCR SYBR Green assay. We found that, in general, individuals from an inbred rat population (n = 20) have shown 2-3 times differences in the basal level of expression of the genes analyzed. Up to several fold differences among individuals were observed for certain genes. These inter-individual differences were obtained after correction for the different amounts of mRNA in each sample. Power calculations were performed to determine the number of individuals required to detect reliable differences in expression levels between a control and an experimental group. These data indicated that, depending on the variability of the candidate gene selected, it was necessary to analyze from five to 135 individuals in each group to detect differences of 50% in the levels of mRNA expression between two groups investigated. The comparison of mRNA abundance from different genes revealed a wide range of expression levels for the 37 genes, showing a 26,000-fold difference between the highest and lowest expressed gene.
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| 5. |
- Althini, Sanna, et al.
(författare)
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Normal Nigrostriatal Innervation but Dopamine Dysfunction in Mice Carrying Hypomorphic Tyrosine Hydroxylase Alleles
- 2003
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Ingår i: Journal of Neuroscience Research. - : Wiley. - 0360-4012 .- 1097-4547. ; 72:4, s. 444-453
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Tidskriftsartikel (refereegranskat)abstract
- We investigated the use of the mouse tyrosine hydroxylase (TH) gene to drive knock-in constructs in catecholaminergic neurons. Two targeting constructs representing truncated forms of either of the BMP receptors ALK-2 or BMPR-II preceded by an internal ribosome entry site (IRES) were introduced into the 3' untranslated region of TH. An frt-flanked neomycin-resistance (neo(r)) cassette was placed in the 3' end of the targeting constructs. Mice homozygous for the knock-in alleles showed various degrees of hypokinetic behavior, depending mainly on whether the neo(r) cassette was removed. In situ hybridization and immunohistochemistry showed that TH mRNA and protein were variously down-regulated in these mouse strains. Reduced levels of dopamine and noradrenalin were found in several brain areas. However, number and morphology of neurons in substantia nigra and their projections to striatum appeared normal in the neo(r)-positive TH hypomorphic mice as examined by markers for L-aromatic amino acid decarboxylase and the dopamine transporter. Elimination of the neo(r) cassette from the knock-in alleles partially restored TH and dopamine levels. The present neo(r)-positive TH hypomorphic mice show that nigrostriatal innervation develops independently of TH and should find use as a model for conditions of reduced catecholamine synthesis, as seen in, for example, L-dihydroxyphenylalanine-responsive dystonia/infantile parkinsonism.
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| 6. |
- Anderberg, Rozita H, 1976, et al.
(författare)
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Treatment with RNase alleviates brain injury but not neuroinflammation in neonatal hypoxia/ischemia
- 2024
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Ingår i: JOURNAL OF NEUROSCIENCE RESEARCH. - 0360-4012 .- 1097-4547. ; 102:4
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Tidskriftsartikel (refereegranskat)abstract
- There is a need for new treatments to reduce brain injuries derived from neonatal hypoxia/ischemia. The only viable option used in the clinic today in infants born at term is therapeutic hypothermia, which has a limited efficacy. Treatments with exogenous RNase have shown great promise in a range of different adult animal models including stroke, ischemia/reperfusion injury, or experimental heart transplantation, often by conferring vascular protective and anti-inflammatory effects. However, any neuroprotective function of RNase treatment in the neonate remains unknown. Using a well-established model of neonatal hypoxic/ischemic brain injury, we evaluated the influence of RNase treatment on RNase activity, gray and white matter tissue loss, blood-brain barrier function, as well as levels and expression of inflammatory cytokines in the brain up to 6 h after the injury using multiplex immunoassay and RT-PCR. Intraperitoneal treatment with RNase increased RNase activity in both plasma and cerebropinal fluids. The RNase treatment resulted in a reduction of brain tissue loss but did not affect the blood-brain barrier function and had only a minor modulatory effect on the inflammatory response. It is concluded that RNase treatment may be promising as a neuroprotective regimen, whereas the mechanistic effects of this treatment appear to be different in the neonate compared to the adult and need further investigation.
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| 7. |
- Andersson, Henrik, et al.
(författare)
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Orexin A Phosphorylates the gamma-Aminobutyric Acid Type A Receptor beta(2) Subunit on a Serine Residue and Changes the Surface Expression of the Receptor in SH-SY5Y Cells Exposed to Propofol
- 2015
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Ingår i: Journal of Neuroscience Research. - : WILEY-BLACKWELL. - 0360-4012 .- 1097-4547. ; 93:11, s. 1748-1755
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Tidskriftsartikel (refereegranskat)abstract
- Propofol activates the gamma-aminobutyric acid type A receptor (GABA(A)R) and causes a reversible neurite retraction, leaving a thin, thread-like structure behind; it also reverses the transport of vesicles in rat cortical neurons. The awakening peptide orexin A (OA) inhibits this retraction via phospholipase D (PLD) and protein kinase CE (PKCE). The human SH-SY5Y cells express both GABA(A)Rs and orexin 1 and 2 receptors. These cells are used to examine the interaction between OA and the GABAAR. The effects of OA are studied with flow cytometry and immunoblotting. This study shows that OA stimulates phosphorylation on the serine residues of the GABA(A)R beta(2) subunit and that the phosphorylation is caused by the activation of PLD and PKCE. OA administration followed by propofol reduces the cell surface expression of the GABA(A)R, whereas propofol stimulation before OA increases the surface expression. The GABA(A)R beta(2) subunit is important for receptor recirculation, and the effect of OA on propofol-stimulated cells may be due to a disturbed recirculation of the GABA(A)R. (C) 2015 Wiley Periodicals, Inc.
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| 8. |
- Andersson, Mikael, et al.
(författare)
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Subchronic haloperidol increases CB(1) receptor binding and G protein coupling in discrete regions of the basal ganglia.
- 2005
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Ingår i: Journal of Neuroscience Research. - : Wiley. - 0360-4012 .- 1097-4547. ; 82:2, s. 264-72
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Tidskriftsartikel (refereegranskat)abstract
- The present study was designed to test whether chronic neuroleptic treatment, which is known to alter both expression and density of dopamine D(2) receptors in striatal regions, has effects upon function and binding level of the cannabinoid CB(1) receptor in the basal ganglia by using receptor autoradiography. As predicted, subchronic haloperidol treatment resulted in increased binding of (3)H-raclopride and quinpirole-induced guanosine 5'-O-(gamma-[(35)S]thio)triphosphate ([(35)S]GTPgammaS) in the striatum when compared to that measured in control animals. This increased D(2) receptor binding and function after 3 days washout was normalized after a 2-week washout period. Effect of haloperidol treatment was studied for CB(1) receptor binding and CP55,940-stimulated [(35)S]GTPgammaS in the striatum, globus pallidus, and substantia nigra. (3)[H]CP55,940 binding levels were found in rank order from highest to lowest in substantia nigra > globus pallidus > striatum. Furthermore, subchronic haloperidol treatment resulted in elevated binding levels of (3)[H]CP55,940 in the striatum and the substantia nigra and CB(1) receptor-stimulated [(35)S]GTPgammaS bindings in the substantia nigra after 3 days washout. These increased binding levels were normalized at 1-4 weeks after termination of haloperidol treatment. Haloperidol treatment had no significant effect on CB(1) receptor or [(35)S]GTPgammaS binding levels in globus pallidus. The results help to elucidate the underlying biochemical mechanism of CB(1) receptor supersensitivity after haloperidol treatment.
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| 9. |
- Andin, Josefine, 1979-, et al.
(författare)
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Arithmetic in the adult deaf signing brain
- 2020
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Ingår i: Journal of Neuroscience Research. - : John Wiley & Sons. - 0360-4012 .- 1097-4547. ; 98:4, s. 643-654
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Tidskriftsartikel (refereegranskat)abstract
- We have previously shown that deaf signers recruit partially different brain regions during simple arithmetic compared to a group of hearing non-signers, despite similar performance. Specifically, hearing individuals show more widespread activation in brain areas that have been related to the verbal system of numerical processing, i.e., the left angular and inferior frontal gyrus, whereas deaf individuals engaged brain areas that have been related to the quantity system of numerical processing, i.e., the right horizontal intraparietal sulcus. This indicates that compared to hearing non-signers, deaf signers can successfully make use of processes located in partially different brain areas during simple arithmetic. In this study, which is a conceptual replication and extension of the above-presented study, the main aim is to understand similarities and differences in neural correlates supporting arithmetic in deaf compared to hearing individuals. The primary objective is to investigate the role of the right horizontal intraparietal gyrus, the left inferior frontal gyrus, the hippocampus, and the left angular gyrus during simple and difficult arithmetic and how these regions are connected to each other. A second objective is to explore what other brain regions support arithmetic in deaf signers. Up to 34 adult deaf signers and the same amount of hearing non-signers will be enrolled in an functional magnetic resonance imaging study that will include simple and difficult subtraction and multiplication. Brain imaging data will be analyzed using whole-brain analysis, region of interest analysis and connectivity analysis. This is the first study to investigate neural underpinnings of arithmetic of different difficulties in deaf individuals.
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| 10. |
- Andin, Josefine, 1979-, et al.
(författare)
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Arithmetic in the signing brain : Differences and similarities in arithmetic processing between deaf signers and hearing non-signers
- 2023
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Ingår i: Journal of Neuroscience Research. - : John Wiley & Sons. - 0360-4012 .- 1097-4547. ; 101:1, s. 172-195
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Tidskriftsartikel (refereegranskat)abstract
- Deaf signers and hearing non-signers have previously been shown to recruit partially different brain regions during simple arithmetic. In light of the triple code model, the differences were interpreted as relating to stronger recruitment of the verbal system of numerical processing, that is, left angular and inferior frontal gyrus, in hearing non-signers, and of the quantity system of numerical processing, that is, right horizontal intraparietal sulcus, for deaf signers. The main aim of the present study was to better understand similarities and differences in the neural correlates supporting arithmetic in deaf compared to hearing individuals. Twenty-nine adult deaf signers and 29 hearing non-signers were enrolled in an functional magnetic resonance imaging study of simple and difficult subtraction and multiplication. Brain imaging data were analyzed using whole-brain analysis, region of interest analysis, and functional connectivity analysis. Although the groups were matched on age, gender, and nonverbal intelligence, the deaf group performed generally poorer than the hearing group in arithmetic. Nevertheless, we found generally similar networks to be involved for both groups, the only exception being the involvement of the left inferior frontal gyrus. This region was activated significantly stronger for the hearing compared to the deaf group but showed stronger functional connectivity with the left superior temporal gyrus in the deaf, compared to the hearing, group. These results lend no support to increased recruitment of the quantity system in deaf signers. Perhaps the reason for performance differences is to be found in other brain regions not included in the original triple code model.
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