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  • 1.
    Bhandage, Amol K.
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Birnir: Molecular Physiology and Neuroscience.
    Cunningham, Janet L.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Ekselius: Psychiatry.
    Jin, Zhe
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Birnir: Molecular Physiology and Neuroscience.
    Shen, Qiujin
    Uppsala University, Science for Life Laboratory, SciLifeLab. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Molecular tools.
    Bongiovanni, Santiago
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Ekselius: Psychiatry.
    Korol, Sergiy
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Birnir: Molecular Physiology and Neuroscience.
    Syk, Mikaela
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Ekselius: Psychiatry.
    Kamali-Moghaddam, Masood
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Molecular tools. Uppsala University, Science for Life Laboratory, SciLifeLab.
    Ekselius, Lisa
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Ekselius: Psychiatry.
    Birnir, Bryndis
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Birnir: Molecular Physiology and Neuroscience.
    Depression, GABA, and Age Correlate with Plasma Levels of Inflammatory Markers2019In: International Journal of Molecular Sciences, ISSN 1422-0067, E-ISSN 1422-0067, Vol. 20, no 24, article id 6172Article in journal (Refereed)
    Abstract [en]

    Immunomodulation is increasingly being recognised as a part of mental diseases. Here, we examined whether levels of immunological protein markers changed with depression, age, or the inhibitory neurotransmitter gamma-aminobutyric acid (GABA). An analysis of plasma samples from patients with a major depressive episode and control blood donors (CBD) revealed the expression of 67 inflammatory markers. Thirteen of these markers displayed augmented levels in patients compared to CBD. Twenty-one markers correlated with the age of the patients, whereas 10 markers correlated with the age of CBD. Interestingly, CST5 and CDCP1 showed the strongest correlation with age in the patients and CBD, respectively. IL-18 was the only marker that correlated with the MADRS-S scores of the patients. Neuronal growth factors (NGFs) were significantly enhanced in plasma from the patients, as was the average plasma GABA concentration. GABA modulated the release of seven cytokines in anti-CD3-stimulated peripheral blood mononuclear cells (PBMCs) from the patients. The study reveals significant changes in the plasma composition of small molecules during depression and identifies potential peripheral biomarkers of the disease.

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  • 2.
    Flood, Louise
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Birnir: Molecular Physiology and Neuroscience.
    Korol, Sergiy
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Birnir: Molecular Physiology and Neuroscience.
    Ekselius, Lisa
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Ekselius: Psychiatry. Uppsala Univ, Uppsala Univ Hosp, Dept Neurosci, Psychiat, Uppsala, Sweden.
    Birnir, Bryndis
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Birnir: Molecular Physiology and Neuroscience.
    Jin, Zhe
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Birnir: Molecular Physiology and Neuroscience. NingXia Med Univ, Dept Neurosurg, Gen Hosp, Ningxia, Peoples R China.
    Interferon-gamma potentiates GABA(A) receptor-mediated inhibitory currents in rat hippocampal CA1 pyramidal neurons2019In: Journal of Neuroimmunology, ISSN 0165-5728, E-ISSN 1872-8421, Vol. 337, article id UNSP 577050Article in journal (Refereed)
    Abstract [en]

    The neural transmission and plasticity can be differentially modulated by various elements of the immune system. Interferon-gamma (IFN-gamma) is a "pro-inflammatory" cytokine mainly produced by T lymphocytes, activates its corresponding receptor and plays important roles under both homeostatic and inflammatory conditions. However, the impact of IFN-gamma on the gamma-aminobutyric acid (GABA)-mediated currents in the hippocampus, a major brain region involved in the cognitive function, has not been investigated. Here we detected abundant expression of both IFN-gamma receptor subunit gene transcripts (Ifngrl and Ifngr2) in the rat hippocampus by quantitative PCR. In addition, we pre-incubated rat hippocampal slices with IFN-gamma (100 ng/ml) and recorded GABA-activated spontaneous and miniature postsynaptic inhibitory currents (sIPSCs and mIPSCs) and tonic currents in hippocampal CAl pyramidal neurons by the whole-cell patch-clamp method. The pre-incubation with IFN-gamma increased the frequency but not the mean amplitude, rise time or decay time of both sIPSCs and mIPSCs in hippocampal CAl pyramidal neurons, suggesting a presynaptic effect of IFN-gamma. Moreover, the GABA-activated tonic currents were enhanced by IFN-gamma. In conclusion, the potentiation of GABAergic currents in hippocampal neurons by IFN-gamma may contribute to the disturbed neuronal excitability and cognitive dysfunction during neuroinflammation.

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  • 3.
    Korol, Sergiy
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Birnir: Molecular Physiology and Neuroscience.
    Jin, Zhe
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Birnir: Molecular Physiology and Neuroscience.
    Birnir, Bryndis
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Birnir: Molecular Physiology and Neuroscience.
    GABA(A) Receptor-Mediated Currents and Hormone mRNAs in Cells Expressing More Than One Hormone Transcript in Intact Human Pancreatic Islets2020In: International Journal of Molecular Sciences, ISSN 1422-0067, E-ISSN 1422-0067, Vol. 21, no 2, article id 600Article in journal (Refereed)
    Abstract [en]

    In pancreatic islets, the major cell-types are alpha, beta and delta cells. The gamma-aminobutyric acid (GABA) signalling system is expressed in human pancreatic islets. In single hormone transcript-expressing cells, we have previously characterized the functional properties of islet GABA(A) receptors (iGABA(A)Rs). Here, we extended these studies to islet cells expressing mRNAs for more than one hormone and sought for correlation between iGABA(A)R activity level and relative mRNA expression ratio. The single-cell RT-PCR in combination with the patch-clamp current recordings was used to examine functional properties of iGABA(A)Rs in the multiple hormone mRNA-expressing cells. We detected cells expressing double (alpha/beta, alpha/delta, beta/delta cell-types) and triple (alpha/beta/delta cell-type) hormone transcripts. The most common mixed-identity cell-type was the alpha/beta group where the cells could be grouped into beta- and alpha-like subgroups. The beta-like cells had low GCG/INS expression ratio (<0.6) and significantly higher frequency of iGABA(A)R single-channel openings than the alpha-like cells where the GCG/INS expression ratio was high (>1.2). The hormone expression levels and iGABA(A)R single-channel characteristics varied in the alpha/beta/delta cell-type. Clearly, multiple hormone transcripts can be expressed in islet cells whereas iGABA(A)R single-channel functional properties appear to be alpha or beta cell specific.

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  • 4.
    Kvarnung, Malin
    et al.
    Karolinska Univ Hosp, Dept Clin Genet, Stockholm, Sweden;Karolinska Inst, Ctr Mol Med, Dept Mol Med & Surg, Stockholm, Sweden.
    Shahsavani, Mansoureh
    Karolinska Inst, Ctr Mol Med, Dept Mol Med & Surg, Stockholm, Sweden;Karolinska Inst, Biomed, Dept Neurosci, Stockholm, Sweden.
    Taylan, Fulya
    Karolinska Inst, Ctr Mol Med, Dept Mol Med & Surg, Stockholm, Sweden.
    Moslem, Mohsen
    Karolinska Inst, Biomed, Dept Neurosci, Stockholm, Sweden.
    Breeuwsma, Nicole
    Karolinska Inst, Biomed, Dept Neurosci, Stockholm, Sweden.
    Laan, Loora
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Medicinsk genetik och genomik. Uppsala University, Science for Life Laboratory, SciLifeLab.
    Schuster, Jens
    Uppsala University, Science for Life Laboratory, SciLifeLab. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Medicinsk genetik och genomik.
    Jin, Zhe
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Birnir: Molecular Physiology and Neuroscience.
    Nilsson, Daniel
    Karolinska Univ Hosp, Dept Clin Genet, Stockholm, Sweden;Karolinska Inst, Ctr Mol Med, Dept Mol Med & Surg, Stockholm, Sweden.
    Lieden, Agne
    Karolinska Univ Hosp, Dept Clin Genet, Stockholm, Sweden;Karolinska Inst, Ctr Mol Med, Dept Mol Med & Surg, Stockholm, Sweden.
    Anderlid, Britt-Marie
    Karolinska Univ Hosp, Dept Clin Genet, Stockholm, Sweden;Karolinska Inst, Ctr Mol Med, Dept Mol Med & Surg, Stockholm, Sweden.
    Nordenskjold, Magnus
    Karolinska Univ Hosp, Dept Clin Genet, Stockholm, Sweden;Karolinska Inst, Ctr Mol Med, Dept Mol Med & Surg, Stockholm, Sweden.
    Lundberg, Elisabeth Syk
    Karolinska Univ Hosp, Dept Clin Genet, Stockholm, Sweden;Karolinska Inst, Ctr Mol Med, Dept Mol Med & Surg, Stockholm, Sweden.
    Birnir, Bryndis
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Birnir: Molecular Physiology and Neuroscience.
    Dahl, Niklas
    Uppsala University, Science for Life Laboratory, SciLifeLab. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Medicinsk genetik och genomik.
    Nordgren, Ann
    Karolinska Univ Hosp, Dept Clin Genet, Stockholm, Sweden;Karolinska Inst, Ctr Mol Med, Dept Mol Med & Surg, Stockholm, Sweden.
    Lindstrand, Anna
    Karolinska Univ Hosp, Dept Clin Genet, Stockholm, Sweden;Karolinska Inst, Ctr Mol Med, Dept Mol Med & Surg, Stockholm, Sweden.
    Falk, Anna
    Karolinska Inst, Biomed, Dept Neurosci, Stockholm, Sweden.
    Ataxia in Patients With Bi-Allelic NFASC Mutations and Absence of Full-Length NF1862019In: Frontiers in Genetics, ISSN 1664-8021, E-ISSN 1664-8021, Vol. 10, article id 896Article in journal (Refereed)
    Abstract [en]

    The etiology of hereditary ataxia syndromes is heterogeneous, and the mechanisms underlying these disorders are often unknown. Here, we utilized exome sequencing in two siblings with progressive ataxia and muscular weakness and identified a novel homozygous splice mutation (c.3020-1G > A) in neurofascin (NFASC). In RNA extracted from fibroblasts, we showed that the mutation resulted in inframe skipping of exon 26, with a deprived expression of the full-length transcript that corresponds to NFASC isoform NF186. To further investigate the disease mechanisms, we reprogrammed fibroblasts from one affected sibling to induced pluripotent stem cells, directed them to neuroepithelial stem cells and finally differentiated to neurons. In early neurogenesis, differentiating cells with selective depletion of the NF186 isoform showed significantly reduced neurite outgrowth as well as fewer emerging neurites. Furthermore, whole-cell patch-clamp recordings of patient-derived neuronal cells revealed a lower threshold for openings, indicating altered Na+ channel kinetics, suggesting a lower threshold for openings as compared to neuronal cells without the NFASC mutation. Taken together, our results suggest that loss of the full-length NFASC isoform NF186 causes perturbed neurogenesis and impaired neuronal biophysical properties resulting in a novel early-onset autosomal recessive ataxia syndrome.

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  • 5.
    Lam, Matti
    et al.
    Karolinska Inst, Dept Neurosci, Stockholm, Sweden.
    Moslem, Mohsen
    Karolinska Inst, Dept Neurosci, Stockholm, Sweden.
    Bryois, Julien
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
    Pronk, Robin J.
    Karolinska Inst, Dept Neurosci, Stockholm, Sweden.
    Uhlin, Elias
    Karolinska Inst, Dept Neurosci, Stockholm, Sweden.
    Ellström, Ivar Dehnisch
    Karolinska Inst, Dept Med Biochem & Biophys, Stockholm, Sweden.
    Laan, Loora
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Medicinsk genetik och genomik. Uppsala University, Science for Life Laboratory, SciLifeLab.
    Olive, Jessica
    Karolinska Inst, Dept Neurosci, Stockholm, Sweden.
    Morse, Rebecca
    Karolinska Inst, Dept Neurosci, Stockholm, Sweden.
    Rönnholm, Harriet
    Karolinska Inst, Dept Neurosci, Stockholm, Sweden.
    Louhivuori, Lauri
    Karolinska Inst, Dept Med Biochem & Biophys, Stockholm, Sweden.
    Korol, Sergiy V.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Birnir: Molecular Physiology and Neuroscience.
    Dahl, Niklas
    Uppsala University, Science for Life Laboratory, SciLifeLab. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Medicinsk genetik och genomik.
    Uhlén, Per
    Karolinska Inst, Dept Med Biochem & Biophys, Stockholm, Sweden.
    Anderlid, Britt-Marie
    Karolinska Inst, Dept Mol Med & Surg, Stockholm, Sweden.
    Kele, Malin
    Karolinska Inst, Dept Neurosci, Stockholm, Sweden.
    Sullivan, Patrick F.
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
    Falk, Anna
    Karolinska Inst, Dept Neurosci, Stockholm, Sweden.
    Single cell analysis of autism patient with bi-allelic NRXN1-alpha deletion reveals skewed fate choice in neural progenitors and impaired neuronal functionality2019In: Experimental Cell Research, ISSN 0014-4827, E-ISSN 1090-2422, Vol. 383, no 1, article id UNSP 111469Article in journal (Refereed)
    Abstract [en]

    We generated human iPS derived neural stem cells and differentiated cells from healthy control individuals and an individual with autism spectrum disorder carrying bi-allelic NRXN1-alpha deletion. We investigated the expression of NRXN1-alpha during neural induction and neural differentiation and observed a pivotal role for NRXN1-alpha during early neural induction and neuronal differentiation. Single cell RNA-seq pinpointed neural stem cells carrying NRXN1-alpha deletion shifting towards radial glia-like cell identity and revealed higher proportion of differentiated astroglia. Furthermore, neuronal cells carrying NRXN1-alpha deletion were identified as immature by single cell RNA-seq analysis, displayed significant depression in calcium signaling activity and presented impaired maturation action potential profile in neurons investigated with electrophysiology. Our observations propose NRXN1-alpha plays an important role for the efficient establishment of neural stem cells, in neuronal differentiation and in maturation of functional excitatory neuronal cells.

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    FULLTEXT01
  • 6.
    Schuster, Jens
    et al.
    Uppsala University, Science for Life Laboratory, SciLifeLab. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Medicinsk genetik och genomik.
    Laan, Loora
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Medicinsk genetik och genomik. Uppsala University, Science for Life Laboratory, SciLifeLab.
    Klar, Joakim
    Uppsala University, Science for Life Laboratory, SciLifeLab. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Medicinsk genetik och genomik.
    Jin, Zhe
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Birnir: Molecular Physiology and Neuroscience.
    Huss, Mikael
    Stockholm Univ, Dept Biochem & Biophys, Sci Life Lab, Wallenberg Long Term Bioinformat Support, Stockholm, Sweden.
    Korol, Sergiy
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Birnir: Molecular Physiology and Neuroscience.
    Noraddin, Feria Hikmet
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical and experimental pathology. Uppsala University, Science for Life Laboratory, SciLifeLab.
    Sobol, Maria
    Uppsala University, Science for Life Laboratory, SciLifeLab. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Medicinsk genetik och genomik.
    Birnir, Bryndis
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Birnir: Molecular Physiology and Neuroscience.
    Dahl, Niklas
    Uppsala University, Science for Life Laboratory, SciLifeLab. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Medicinsk genetik och genomik.
    Transcriptomes of Dravet syndrome iPSC derived GABAergic cells reveal dysregulated pathways for chromatin remodeling and neurodevelopment2019In: Neurobiology of Disease, ISSN 0969-9961, E-ISSN 1095-953X, Vol. 132, article id 104583Article in journal (Refereed)
    Abstract [en]

    Dravet syndrome (DS) is an early onset refractory epilepsy typically caused by de novo heterozygous variants in SCN1A encoding the a-subunit of the neuronal sodium channel Na(v)1.1. The syndrome is characterized by age related progression of seizures, cognitive decline and movement disorders. We hypothesized that the distinct neurodevelopmental features in DS are caused by the disruption of molecular pathways in Na(v)1.1 haploinsufficient cells resulting in perturbed neural differentiation and maturation. Here, we established DS-patient and control induced pluripotent stem cell derived neural progenitor cells (iPSC NPC) and GABAergic interneuronal (iPSC GABA) cells. The DS-patient iPSC GABA cells showed a shift in sodium current activation and a perturbed response to induced oxidative stress. Transcriptome analysis revealed specific dysregulations of genes for chromatin structure, mitotic progression, neural plasticity and excitability in DS-patient iPSC NPCs and DS-patient iPSC GABA cells versus controls. The transcription factors FOXM1 and E2F1, positive regulators of the disrupted pathways for histone modification and cell cycle regulation, were markedly up-regulated in DS-iPSC GABA lines. Our study highlights transcriptional changes and disrupted pathways of chromatin remodeling in Na(v)1.1 haploinsufficient GABAergic cells, providing a molecular framework that overlaps with that of neurodevelopmental disorders and other epilepsies.

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  • 7.
    Seidler, Ursula
    et al.
    Hannover Med Sch, Dept Gastroenterol Hepatol & Endocrinol, Hannover, Germany.
    Nylander, Olof
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Sjöblom/Nylander: Gastrointestinal Physiology.
    Sjöblom, Markus
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Sjöblom/Nylander: Gastrointestinal Physiology.
    Birnir, Bryndis
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Birnir: Molecular Physiology and Neuroscience.
    Herzig, Karl-Heinz
    Univ Oulu, Res Unit Biomed, MRC, Univ Hosp, Oulu, Finland;Univ Oulu, Bioctr Oulu, MRC, Univ Hosp, Oulu, Finland;Poznan Univ Med Sci, Dept Gastroenterol & Metab, Poznan, Poland.
    Gunnar Flemström's legacy in intestinal bicarbonate secretion: A homage to Gunnar Flemström and his work in intestinal bicarbonate secretion2019In: Acta Physiologica, ISSN 1748-1708, E-ISSN 1748-1716, Vol. 227, no 4, article id e13321Article in journal (Other academic)
1 - 7 of 7
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