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  • 1. Arthur-Farraj, Peter J.
    et al.
    Latouche, Morwena
    Wilton, Daniel K.
    Quintes, Susanne
    Chabrol, Elodie
    Banerjee, Annbily
    Woodhoo, Ashwin
    Jenkins, Billy
    Rahman, Mary
    Turmaine, Mark
    Wicher, Grzegorz K.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Cancer and Vascular Biology.
    Mitter, Richard
    Greensmith, Linda
    Behrens, Axel
    Raivich, Gennadij
    Mirsky, Rhona
    Jessen, Kristjan R.
    c-Jun Reprograms Schwann Cells of Injured Nerves to Generate a Repair Cell Essential for Regeneration2012In: Neuron, ISSN 0896-6273, E-ISSN 1097-4199, Vol. 75, no 4, p. 633-647Article in journal (Refereed)
    Abstract [en]

    The radical response of peripheral nerves to injury (Wallerian degeneration) is the cornerstone of nerve repair. We show that activation of the transcription factor c-Jun in Schwann cells is a global regulator of Wallerian degeneration. c-Jun governs major aspects of the injury response, determines the expression of trophic factors, adhesion molecules, the formation of regeneration tracks and myelin clearance and controls the distinctive regenerative potential of peripheral nerves. A key function of c-Jun is the activation of a repair program in Schwann cells and the creation of a cell specialized to support regeneration. We show that absence of c-Jun results in the formation of a dysfunctional repair cell, striking failure of functional recovery, and neuronal death. We conclude that a single glial transcription factor is essential for restoration of damaged nerves, acting to control the transdifferentiation of myelin and Remak Schwann cells to dedicated repair cells in damaged tissue.

  • 2.
    Barg, Sebastian
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology.
    Olofsson, Charlotta S
    Schriever-Abeln, Jenny
    Wendt, Anna
    Gebre-Medhin, Samuel
    Renström, Erik
    Rorsman, Patrik
    Delay between fusion pore opening and peptide release from large dense-core vesicles in neuroendocrine cells2002In: Neuron, ISSN 0896-6273, E-ISSN 1097-4199, Vol. 33, no 2, p. 287-299Article in journal (Refereed)
    Abstract [en]

    Peptidergic neurotransmission is slow compared to that mediated by classical neurotransmitters. We have studied exocytotic membrane fusion and cargo release by simultaneous capacitance measurements and confocal imaging of single secretory vesicles in neuroendocrine cells. Depletion of the readily releasable pool (RRP) correlated with exocytosis of 10%-20% of the docked vesicles. Some remaining vesicles became releasable after recovery of RRP. Expansion of the fusion pore, seen as an increase in luminal pH, occurred after approximately 0.3 s, and peptide release was delayed by another 1-10 s. We conclude that (1) RRP refilling involves chemical modification of vesicles already in place, (2) the release of large neuropeptides via the fusion pore is negligible and only proceeds after complete fusion, and (3) sluggish peptidergic transmission reflects the time course of vesicle emptying.

  • 3. Delegates, Global Neuroethics Summit
    et al.
    Rommelfanger, Karen S.
    Emory Univ, Ctr Eth, Neuroeth Program, Dept Neurol, 1531 Dickey Dr, Atlanta, GA 30322 USA;Emory Univ, Ctr Eth, Neuroeth Program, Dept Psychiat & Behav Sci, 1531 Dickey Dr, Atlanta, GA 30322 USA.
    Jeong, Sung-Jin
    Korea Brain Res Inst, 61 Choeomdan Ro, Daegu 41068, South Korea.
    Ema, Arisa
    Univ Tokyo, Coll Arts & Sci, Sci & Technol Studies, Tokyo 1138654, Japan.
    Fukushi, Tamami
    Japan Agcy Med Res & Dev, Dept Res Infrastruct, Tokyo, Japan.
    Kasai, Kiyoto
    UTIAS, Dept Neuropsychiat, WPI IRCN, Bunkyo Ku, 7-3-1 Hongo, Tokyo 1138655, Japan;UTIAS, Int Res Ctr Neurointelligence, WPI IRCN, Bunkyo Ku, 7-3-1 Hongo, Tokyo 1138655, Japan.
    Ramos, Khara M.
    NINDS, Off Sci Liaison, Off Director, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA.
    Salles, Arleen
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Centre for Research Ethics and Bioethics.
    Singh, Ilina
    Univ Oxford, Dept Psychiat, Oxford, England;Univ Oxford, Wellcome Ctr Eth & Humanities, Oxford, England.
    Neuroethics Questions to Guide Ethical Research in the International Brain Initiatives2018In: Neuron, ISSN 0896-6273, E-ISSN 1097-4199, Vol. 100, no 1, p. 19-36Article, review/survey (Refereed)
    Abstract [en]

    Increasingly, national governments across the globe are prioritizing investments in neuroscience. Currently, seven active or in-development national-level brain research initiatives exist, spanning four continents. Engaging with the underlying values and ethical concerns that drive brain research across cultural and continental divides is critical to future research. Culture influences what kinds of science are supported and where science can be conducted through ethical frameworks and evaluations of risk. Neuroscientists and philosophers alike have found themselves together encountering perennial questions; these questions are engaged by the field of neuroethics, related to the nature of understanding the self and identity, the existence and meaning of free will, defining the role of reason in human behavior, and more. With this Perspective article, we aim to prioritize and advance to the foreground a list of neuroethics questions for neuroscientists operating in the context of these international brain initiatives.

  • 4. Dudai, Yadin
    et al.
    Evers, Kathinka
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Centre for Research Ethics and Bioethics.
    To simulate or not to simulate: What are the questions?2014In: Neuron, ISSN 0896-6273, E-ISSN 1097-4199, Vol. 84, no 2, p. 254-261Article, review/survey (Refereed)
    Abstract [en]

    Simulation is a powerful method in science and engineering. However, simulation is an umbrella term, and its meaning and goals differ among disciplines. Rapid advances in neuroscience and computing draw increasing attention to large-scale brain simulations. What is the meaning of simulation, and what should the method expect to achieve? We discuss the concept of simulation from an integrated scientific and philosophical vantage point and pinpoint selected issues that are specific to brain simulation.

  • 5. Dufour, Audrey
    et al.
    Seibt, Julie
    Passante, Lara
    Depaepe, Vanessa
    Ciossek, Thomas
    Frisén, Jonas
    Kullander, Klas
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience.
    Flanagan, John G
    Polleux, Franck
    Vanderhaeghen, Pierre
    Area specificity and topography of thalamocortical projections are controlled by ephrin/Eph genes2003In: Neuron, ISSN 0896-6273, E-ISSN 1097-4199, Vol. 39, no 3, p. 453-65Article in journal (Other academic)
  • 6. Egea, J
    et al.
    Nissen, UV
    Dufour, A
    Sahin, M
    Greer, P
    Kullander, Klas
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Developmental Genetics.
    Mrsic-Flogel, TD
    Greenberg, ME
    Kiehn, O
    Vanderhaeghen, P
    Klein, R
    Regulation of EphA 4 kinase activity is required for a subset of axon guidance decisions suggesting a key role for receptor clustering in Eph function2005In: Neuron, ISSN 0896-6273, E-ISSN 1097-4199, Vol. 47, no 4, p. 515-528Article in journal (Refereed)
    Abstract [en]

    Signaling by receptor tyrosine kinases (RTKs) is mediated by their intrinsic kinase activity. Typically, kinase-activating mutations result in ligand-independent signaling and gain-of-function phenotypes. Like other RTKs, Ephs require kinase activity to signal, but signaling by Ephs in vitro also requires clustering by their membrane bound ephrin ligands. The relative importance of Eph kinase activity and clustering for in vivo functions is unknown. We find that knockin mice expressing a mutant form of EphA4 (EphA4(EE)), whose kinase is constitutively activated in the absence of ephrinB ligands, are deficient in the development of thalamocortical projections and some aspects of central pattern generator rhythmicity. Surprisingly, other functions of EphA4 were regulated normally by EphA4(EE), including midline axon guidance, hindlimb locomotion, in vitro growth cone collapse, and phosphorylation of ephexin1. These results suggest that signaling of Eph RTKs follows a multistep process of induced kinase activity and higher-order clustering different from RTKs responding to soluble ligands.

  • 7. Egea, Joaquim
    et al.
    Nissen, Ulla Vig
    Dufour, Audrey
    Sahin, Mustafa
    Greer, Paul
    Kullander, Klas
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience.
    Mrsic-Flogel, Thomas D
    Greenberg, Michael E
    Kiehn, Ole
    Vanderhaeghen, Pierre
    Klein, Rüdiger
    Regulation of EphA 4 kinase activity is required for a subset of axon guidance decisions suggesting a key role for receptor clustering in Eph function2005In: Neuron, ISSN 0896-6273, E-ISSN 1097-4199, Vol. 47, no 4, p. 515-528Article in journal (Refereed)
    Abstract [en]

    Signaling by receptor tyrosine kinases (RTKs) is mediated by their intrinsic kinase activity. Typically, kinase-activating mutations result in ligand-independent signaling and gain-of-function phenotypes. Like other RTKs, Ephs require kinase activity to signal, but signaling by Ephs in vitro also requires clustering by their membrane bound ephrin ligands. The relative importance of Eph kinase activity and clustering for in vivo functions is unknown. We find that knockin mice expressing a mutant form of EphA4 (EphA4(EE)), whose kinase is constitutively activated in the absence of ephrinB ligands, are deficient in the development of thalamocortical projections and some aspects of central pattern generator rhythmicity. Surprisingly, other functions of EphA4 were regulated normally by EphA4(EE), including midline axon guidance, hindlimb locomotion, in vitro growth cone collapse, and phosphorylation of ephexin1. These results suggest that signaling of Eph RTKs follows a multistep process of induced kinase activity and higher-order clustering different from RTKs responding to soluble ligands.

  • 8. Ernfors, P
    et al.
    Hallböök, F
    Ebendal, T
    Shooter, E M
    Radeke, M J
    Misko, T P
    Persson, H
    Developmental and regional expression of beta-nerve growth factor receptor mRNA in the chick and rat.1988In: Neuron, ISSN 0896-6273, E-ISSN 1097-4199, Vol. 1, no 10, p. 983-96Article in journal (Refereed)
    Abstract [en]

    Hybridization probes from the transmembrane region of the chick NGF receptor (NGF-R) that show high homology with the rat NGF-R were used to demonstrate an abundant 4.5 kb NGF-R mRNA in the chick embryo at E3.5. The level remained high until E12 but decreased to adult levels by E18. The highest levels at E8 were in spinal cord, bursa of Fabricius, gizzard, femoralis muscle, and skin. In situ hybridization to E7 embryos showed high expression of the NGF-R gene in spinal cord, particularly the lateral motor column, and in dorsal root, sympathetic, and nodose ganglia. NGF-R mRNA expression was observed throughout brain development and in all regions of the adult brain, with high levels in cerebellum and septum. Lymphoid tissues of chick and rat also expressed the receptor. The complex and widespread expression of NGF-R mRNA in areas not known to be NGF targets suggests broader functions for NGF.

  • 9. Hallböök, F
    et al.
    Ibáñez, C F
    Persson, H
    Evolutionary studies of the nerve growth factor family reveal a novel member abundantly expressed in Xenopus ovary.1991In: Neuron, ISSN 0896-6273, E-ISSN 1097-4199, Vol. 6, no 5, p. 845-58Article in journal (Refereed)
    Abstract [en]

    Evolutionary conservation of members of the NGF family in vertebrates was studied by DNA sequence analysis of PCR fragments for NGF, BDNF, and NT-3 from human, rat, chicken, viper, Xenopus, salmon, and ray. The results showed that the three factors are highly conserved from fishes to mammals. Phylogenetic trees reflecting the evolution and speciation of the members of the NGF family were constructed. In addition, the gene for a fourth member of the family, neurotrophin-4 (NT-4), was isolated from Xenopus and viper. The NT-4 gene encodes a precursor protein of 236 amino acids, which is processed into a 123 amino acid mature NT-4 protein with 50%-60% amino acid identity to NGF, BDNF, and NT-3. The NT-4 protein was shown to interact with the low affinity NGF receptor and elicited neurite outgrowth from explanted dorsal root ganglia with no and lower activity in sympathetic and nodose ganglia, respectively. Northern blot analysis of different tissues from Xenopus showed NT-4 mRNA only in ovary, where it was present at levels over 100-fold higher than those of NGF mRNA in heart.

  • 10. Kullander, Klas
    et al.
    Mather, N K
    Diella, F
    Dottori, M
    Boyd, A W
    Klein, R
    Kinase-dependent and kinase-independent functions of EphA4 receptors in major axon tract formation in vivo2001In: Neuron, ISSN 0896-6273, E-ISSN 1097-4199, Vol. 29, no 1, p. 73-84Article in journal (Refereed)
    Abstract [en]

    The EphA4 receptor tyrosine kinase regulates the formation of the corticospinal tract (CST), a pathway controlling voluntary movements, and of the anterior commissure (AC), connecting the neocortical temporal lobes. To study EphA4 kinase signaling in these processes, we generated mice expressing mutant EphA4 receptors either lacking kinase activity or with severely downregulated kinase activity. We demonstrate that EphA4 is required for CST formation as a receptor for which it requires an active kinase domain. In contrast, the formation of the AC is rescued by kinase-dead EphA4, suggesting that in this structure EphA4 acts as a ligand for which its kinase activity is not required. Unexpectedly, the cytoplasmic sterile-alpha motif (SAM) domain is not required for EphA4 functions. Our findings establish both kinase-dependent and kinase-independent functions of EphA4 in the formation of major axon tracts.

  • 11.
    Lagerström, Malin C.
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Developmental Genetics.
    Rogoz, Katarzyna
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Developmental Genetics.
    Abrahamsen, Bjarke
    Persson, Emma
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Developmental Genetics.
    Reinius, Björn
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Developmental Genetics.
    Nordenankar, Karin
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Developmental Genetics.
    Ölund, Caroline
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Developmental Genetics.
    Smith, Casey
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Developmental Genetics.
    Mendez, José Alfredo
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Developmental Genetics.
    Chen, Zhou-Feng
    Wood, John N.
    Wallén-Mackenzie, Åsa
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Developmental Genetics.
    Kullander, Klas
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Developmental Genetics.
    VGLUT2-Dependent Sensory Neurons in the TRPV1 Population Regulate Pain and Itch2010In: Neuron, ISSN 0896-6273, E-ISSN 1097-4199, Vol. 68, no 3, p. 529-542Article in journal (Refereed)
    Abstract [en]

    The natural response to itch sensation is to scratch, which relieves the itch through an unknown mechanism. Interaction between pain and itch has been frequently demonstrated, and the selectivity hypothesis of itch, based on data from electrophysiological and behavioral experiments, postulates the existence of primary pain afferents capable of repressing itch. Here, we demonstrate that deletion of vesicular glutamate transporter (VGLUT) 2 in a subpopulation of neurons partly overlapping with the vanilloid receptor (TRPV1) primary afferents resulted in a dramatic increase in itch behavior accompanied by a reduced responsiveness to thermal pain. The increased itch behavior was reduced by administration of antihistaminergic drugs and by genetic deletion of the gastrin-releasing peptide receptor, demonstrating a dependence on VGLUT2 to maintain normal levels of both histaminergic and nonhistaminergic itch. This study establishes that VGLUT2 is a major player in TRPV1 thermal nociception and also serves to regulate a normal itch response.

  • 12.
    MacAskill, Andrew F.
    et al.
    Department of Neuroscience, Physiology, and Pharmacology, University College London, Gower Street, London WC1E 6BT, UK.
    Rinholm, Johanne E.
    Department of Neuroscience, Physiology, and Pharmacology, University College London, Gower Street, London WC1E 6BT, UK.
    Twelvetrees, Alison E.
    Department of Neuroscience, Physiology, and Pharmacology, University College London, Gower Street, London WC1E 6BT, UK.
    Arancibia-Carcamo, I. Lorena
    Department of Neuroscience, Physiology, and Pharmacology, University College London, Gower Street, London WC1E 6BT, UK.
    Muir, James
    Department of Neuroscience, Physiology, and Pharmacology, University College London, Gower Street, London WC1E 6BT, UK.
    Fransson, Åsa
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm , Ludwig Institute for Cancer Research.
    Aspenström, Pontus
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm , Ludwig Institute for Cancer Research.
    Attwell, David
    Department of Neuroscience, Physiology, and Pharmacology, University College London, Gower Street, London WC1E 6BT, UK.
    Kittler, Josef T.
    Department of Neuroscience, Physiology, and Pharmacology, University College London, Gower Street, London WC1E 6BT, UK.
    Miro1 is a calcium sensor for glutamate receptor-dependent localization of mitochondria at synapses.2009In: Neuron, ISSN 0896-6273, E-ISSN 1097-4199, Vol. 61, no 4, p. 541-555Article in journal (Refereed)
    Abstract [en]

    Energy use, mainly to reverse ion movements in neurons, is a fundamental constraint on brain information processing. Trafficking of mitochondria to locations in neurons where there are large ion fluxes is essential for powering neural function. Mitochondrial trafficking is regulated by Ca2+ entry through ionotropic glutamate receptors, but the underlying mechanism is unknown. We show that the protein Miro1 links mitochondria to KIF5 motor proteins, allowing mitochondria to move along microtubules. This linkage is inhibited by micromolar levels of Ca2+ binding to Miro1. With the EF hand domains of Miro1 mutated to prevent Ca2+ binding, Miro1 could still facilitate mitochondrial motility, but mitochondrial stopping induced by glutamate or neuronal activity was blocked. Activating neuronal NMDA receptors with exogenous or synaptically released glutamate led to Miro1 positioning mitochondria at the postsynaptic side of synapses. Thus, Miro1 is a key determinant of how energy supply is matched to energy usage in neurons.

  • 13. Mazei-Robison, Michelle S.
    et al.
    Koo, Ja Wook
    Friedman, Allyson K.
    Lansink, Carien S.
    Robison, Alfred J.
    Vinish, Monika
    Krishnan, Vaishnav
    Kim, Seyun
    Siuta, Michael A.
    Galli, Aurelio
    Niswender, Kevin D.
    Appasani, Raghu
    Horvath, Monika C.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Forensic Medicine.
    Neve, Rachel L.
    Worley, Paul F.
    Snyder, Solomon H.
    Hurd, Yasmin L.
    Cheer, Joseph F.
    Han, Ming-Hu
    Russo, Scott J.
    Nestler, Eric J.
    Role for mTOR Signaling and Neuronal Activity in Morphine-Induced Adaptations in Ventral Tegmental Area Dopamine Neurons2011In: Neuron, ISSN 0896-6273, E-ISSN 1097-4199, Vol. 72, no 6, p. 977-990Article in journal (Refereed)
    Abstract [en]

    While the abuse of opiate drugs continues to rise, the neuroadaptations that occur with long-term drug exposure remain poorly understood. We describe here a series of chronic morphine-induced adaptations in ventral tegmental area (VTA) dopamine neurons, which are mediated via downregulation of AKT-mTORC2 (mammalian target of rapamycin complex-2). Chronic opiates decrease the size of VTA dopamine neurons in rodents, an effect seen in humans as well, and concomitantly increase the excitability of the cells but decrease dopamine output to target regions. Chronic morphine decreases mTORC2 activity, and overexpression of Rictor, a component of mTORC2, prevents morphine-induced changes in cell morphology and activity. Further, local knockout of Rictor in VTA decreases DA soma size and reduces rewarding responses to morphine, consistent with the hypothesis that these adaptations represent a mechanism of reward tolerance. Together, these findings demonstrate a novel role for AKT-mTORC2 signaling in mediating neuroadaptations to opiate drugs of abuse.

  • 14.
    Salles, Arleen
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Centre for Research Ethics and Bioethics.
    Bjaalie, Jan
    Evers, Kathinka
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Centre for Research Ethics and Bioethics.
    Farisco, Michele
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Centre for Research Ethics and Bioethics.
    Fothergill, Tyr
    Guerrero, Manuel
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Centre for Research Ethics and Bioethics.
    Maslen, Hannah
    Muller, Jeffrey
    Prescott, Tony
    Stahl, Bernd
    Walter, Henrik
    Zilles, Karl
    Amunts, Katrin
    The Human Brain Project: Responsible Brain Research for the Benefit of Society2019In: Neuron, ISSN 0896-6273, E-ISSN 1097-4199, Vol. 101, no 3, p. 380-384Article, review/survey (Refereed)
  • 15.
    Shariatgorji, Mohammadreza
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Pharmacy, Department of Pharmaceutical Biosciences.
    Nilsson, Anna
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Pharmacy, Department of Pharmaceutical Biosciences.
    Goodwin, Richard J A
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Pharmacy, Department of Pharmaceutical Biosciences.
    Källback, Patrik
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Pharmacy, Department of Pharmaceutical Biosciences.
    Schintu, Nicoletta
    Zhang, Xiaoqun
    Crossman, Alan R
    Bezard, Erwan
    Svenningsson, Per
    Andrén, Per E
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Pharmacy, Department of Pharmaceutical Biosciences.
    Direct targeted quantitative molecular imaging of neurotransmitters in brain tissue sections2014In: Neuron, ISSN 0896-6273, E-ISSN 1097-4199, Vol. 84, no 4, p. 697-707Article in journal (Refereed)
    Abstract [en]

    Current neuroimaging techniques have very limited abilities to directly identify and quantify neurotransmitters from brain sections. We have developed a molecular-specific approach for the simultaneous imaging and quantitation of multiple neurotransmitters, precursors, and metabolites, such as tyrosine, tryptamine, tyramine, phenethylamine, dopamine, 3-methoxytyramine, serotonin, GABA, glutamate, acetylcholine, and L-alpha-glycerylphosphorylcholine, in histological tissue sections at high spatial resolutions. The method is employed to directly measure changes in the absolute and relative levels ofneurotransmitters in specific brain structures in animal disease models and in response to drug treatments, demonstrating the power of mass spectrometry imaging in neuroscience.

  • 16.
    Siwani, Samer
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Developmental Genetics.
    Franca, Arthur S. C.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Developmental Genetics. Univ Fed Rio Grande do Norte, Brain Inst, BR-59056450 Natal, RN, Brazil;Donders Inst Brain Behav & Cognit, NL-6525 EN Nijmegen, Gelderland, Netherlands.
    Mikulovic, Sanja
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Developmental Genetics.
    Reis, Amilcar
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Developmental Genetics.
    Hilscher, Markus M
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Developmental Genetics. Univ Fed Rio Grande do Norte, Brain Inst, BR-59056450 Natal, RN, Brazil.
    Edwards, Steven J.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Developmental Genetics.
    Leão, Richardson N
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Developmental Genetics. Univ Fed Rio Grande do Norte, Brain Inst, BR-59056450 Natal, RN, Brazil.
    Tort, Adriano B. L.
    Univ Fed Rio Grande do Norte, Brain Inst, BR-59056450 Natal, RN, Brazil.
    Kullander, Klas
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Developmental Genetics.
    OLM alpha 2 Cells Bidirectionally Modulate Learning2018In: Neuron, ISSN 0896-6273, E-ISSN 1097-4199, Vol. 99, no 2, p. 404-412Article in journal (Refereed)
    Abstract [en]

    Inhibitory interneurons participate in mnemonic processes. However, defined roles for identified interneuron populations are scarce. A subpopulation of oriens lacunosum-moleculare (OLM) interneurons genetically defined by the expression of the nicotinic receptor alpha 2 subunit has been shown to gate information carried by either the temporoammonic pathway or Schaffer collaterals in vitro. Here we set out to determine whether selective modulation of OLM alpha 2 cells in the intermediate CA1 affects learning and memory in vivo. Our data show that intermediate OLM alpha 2 cells can either enhance (upon their inhibition) or impair (upon their activation) object memory encoding in freely moving mice, thus exerting bidirectional control. Moreover, we find that OLM alpha 2 cell activation inhibits fear-related memories and that OLM alpha 2 cells respond differently to nicotine in the dorsoventral axis. These results suggest that intermediate OLM alpha 2 cells are an important component in the CA1 microcircuit regulating learning and memory processes.

  • 17. Wegmeyer, Heike
    et al.
    Egea, Joaquim
    Rabe, Nadine
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Developmental Genetics.
    Gezelius, Henrik
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Developmental Genetics.
    Filosa, Alessandro
    Enjin, Anders
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Developmental Genetics.
    Varoqueaux, Frederique
    Deininger, Katrin
    Schnütgen, Frank
    Brose, Nils
    Klein, Rüdiger
    Kullander, Klas
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Developmental Genetics.
    Betz, Andrea
    EphA4-Dependent Axon Guidance Is Mediated by the RacGAP α2-Chimaerin2007In: Neuron, ISSN 0896-6273, E-ISSN 1097-4199, Vol. 55, no 5, p. 756-767Article in journal (Refereed)
    Abstract [en]

    Neuronal network formation in the developing nervous system is dependent on the accurate navigation of nerve cell axons and dendrites, which is controlled by attractive and repulsive guidance cues. Ephrins and their cognate Eph receptors mediate many repulsive axonal guidance decisions by intercellular interactions resulting in growth cone collapse and axon retraction of the Eph-presenting neuron. We show that the Rac-specific GTPase-activating protein α2-chimaerin binds activated EphA4 and mediates EphA4-triggered axonal growth cone collapse. α-Chimaerin mutant mice display a phenotype similar to that of EphA4 mutant mice, including aberrant midline axon guidance and defective spinal cord central pattern generator activity. Our results reveal an α-chimaerin-dependent signaling pathway downstream of EphA4, which is essential for axon guidance decisions and neuronal circuit formation in vivo.

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