Investigations Into Neuronal Cilia Utilizing Mouse Models
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Activation of the Dopaminergic Pathway from VTA to the Medial
RESEARCH ARTICLE Activation of the dopaminergic pathway from VTA to the medial olfactory tubercle generates odor-preference and reward Zhijian Zhang1,2†, Qing Liu1†, Pengjie Wen1, Jiaozhen Zhang1, Xiaoping Rao1, Ziming Zhou3, Hongruo Zhang3, Xiaobin He1, Juan Li1, Zheng Zhou4, Xiaoran Xu3, Xueyi Zhang3, Rui Luo3, Guanghui Lv2, Haohong Li2, Pei Cao1, Liping Wang4, Fuqiang Xu1,2* 1Center for Brain Science, Key Laboratory of Magnetic Resonance in Biological Systems, Wuhan Institute of Physics and Mathematics, Chinese Academy of Sciences, Wuhan, China; 2Wuhan National Laboratory for Optoelectronics, Wuhan, China; 3College of Life Sciences, Wuhan University, Wuhan, China; 4Shenzhen Key Lab of Neuropsychiatric Modulation and Collaborative Innovation Center for Brain Science, CAS Center for Excellence in Brain Science, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, China Abstract Odor-preferences are usually influenced by life experiences. However, the neural circuit mechanisms remain unclear. The medial olfactory tubercle (mOT) is involved in both reward and olfaction, whereas the ventral tegmental area (VTA) dopaminergic (DAergic) neurons are considered to be engaged in reward and motivation. Here, we found that the VTA (DAergic)-mOT pathway could be activated by different types of naturalistic rewards as well as odors in DAT-cre mice. Optogenetic activation of the VTA-mOT DAergic fibers was able to elicit preferences for space, location and neutral odor, while pharmacological blockade of the dopamine receptors in the *For correspondence: mOT fully prevented the odor-preference formation. Furthermore, inactivation of the mOT- [email protected] projecting VTA DAergic neurons eliminated the previously formed odor-preference and strongly †These authors contributed affected the Go-no go learning efficiency. -
Long-Range Gabaergic Projections Contribute to Cortical Feedback
bioRxiv preprint doi: https://doi.org/10.1101/2020.12.19.423599; this version posted December 20, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC 4.0 International license. Long-range GABAergic projections contribute to cortical feedback control of sensory processing. Camille Mazo1,2, *, Soham Saha1, Antoine Nissant1, Enzo Peroni1, Pierre-Marie Lledo1, # and Gabriel Lepousez1,#,* 1 Laboratory for Perception and Memory, Institut Pasteur, F-75015 Paris, France; Centre National de la Recherche Scientifique (CNRS), Unité Mixte de Recherche (UMR-3571), F-75015 Paris, France. * Corresponding authors to whom correspondence should be addressed: Laboratory for Perception and Memory, Institut Pasteur, 25 rue du Dr. Roux, 75 724 Paris Cedex 15, France. Tel: (33) 1 45 68 95 23 E-mail: [email protected] E-mail: [email protected] # Jointly supervised this work 2 now at Champalimaud Research, Champalimaud Center for the Unknown, Lisbon, Portugal Keywords: Sensory circuits, Top-down, Inhibitory, Centrifugal, Olfactory system, Barrel cortex 1 bioRxiv preprint doi: https://doi.org/10.1101/2020.12.19.423599; this version posted December 20, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC 4.0 International license. Abstract In sensory systems, cortical areas send excitatory projections back to subcortical areas to dynamically adjust sensory processing. -
Estrogen Receptors Α, Β and GPER in the CNS and Trigeminal System - Molecular and Functional Aspects Karin Warfvinge1,2, Diana N
Warfvinge et al. The Journal of Headache and Pain (2020) 21:131 The Journal of Headache https://doi.org/10.1186/s10194-020-01197-0 and Pain RESEARCH ARTICLE Open Access Estrogen receptors α, β and GPER in the CNS and trigeminal system - molecular and functional aspects Karin Warfvinge1,2, Diana N. Krause2,3†, Aida Maddahi1†, Jacob C. A. Edvinsson1,4, Lars Edvinsson1,2,5* and Kristian A. Haanes1 Abstract Background: Migraine occurs 2–3 times more often in females than in males and is in many females associated with the onset of menstruation. The steroid hormone, 17β-estradiol (estrogen, E2), exerts its effects by binding and activating several estrogen receptors (ERs). Calcitonin gene-related peptide (CGRP) has a strong position in migraine pathophysiology, and interaction with CGRP has resulted in several successful drugs for acute and prophylactic treatment of migraine, effective in all age groups and in both sexes. Methods: Immunohistochemistry was used for detection and localization of proteins, release of CGRP and PACAP investigated by ELISA and myography/perfusion arteriography was performed on rat and human arterial segments. Results: ERα was found throughout the whole brain, and in several migraine related structures. ERβ was mainly found in the hippocampus and the cerebellum. In trigeminal ganglion (TG), ERα was found in the nuclei of neurons; these neurons expressed CGRP or the CGRP receptor in the cytoplasm. G-protein ER (GPER) was observed in the cell membrane and cytoplasm in most TG neurons. We compared TG from males and females, and females expressed more ER receptors. For neuropeptide release, the only observable difference was a baseline CGRP release being higher in the pro-estrous state as compared to estrous state. -
Does the Kappa Opioid Receptor System Contribute to Pain Aversion?
UC Irvine UC Irvine Previously Published Works Title Does the kappa opioid receptor system contribute to pain aversion? Permalink https://escholarship.org/uc/item/8gx6n97q Authors Cahill, Catherine M Taylor, Anna MW Cook, Christopher et al. Publication Date 2014 DOI 10.3389/fphar.2014.00253 Peer reviewed eScholarship.org Powered by the California Digital Library University of California REVIEW ARTICLE published: 17 November 2014 doi: 10.3389/fphar.2014.00253 Does the kappa opioid receptor system contribute to pain aversion? Catherine M. Cahill 1,2,3 *, Anna M. W. Taylor1,4 , Christopher Cook1,2 , Edmund Ong1,3 , Jose A. Morón5 and Christopher J. Evans 4 1 Department of Anesthesiology and Perioperative Care, University of California Irvine, Irvine, CA, USA 2 Department of Pharmacology, University of California Irvine, Irvine, CA, USA 3 Department of Biomedical and Molecular Sciences, Queen’s University, Kingston, ON, Canada 4 Semel Institute for Neuroscience and Human Behavior, University of California Los Angeles, Los Angeles, CA, USA 5 Department of Anesthesiology, Columbia University Medical Center, New York, NY, USA Edited by: The kappa opioid receptor (KOR) and the endogenous peptide-ligand dynorphin have Dominique Massotte, Institut des received significant attention due the involvement in mediating a variety of behavioral Neurosciences Cellulaires et Intégratives, France and neurophysiological responses, including opposing the rewarding properties of drugs of abuse including opioids. Accumulating evidence indicates this system is involved in Reviewed by: Lynn G. Kirby, University of regulating states of motivation and emotion. Acute activation of the KOR produces an Pennsylvania, USA increase in motivational behavior to escape a threat, however, KOR activation associated Clifford John Woolf, Boston Children’s with chronic stress leads to the expression of symptoms indicative of mood disorders. -
A Cortical Pathway Modulates Sensory Input Into the Olfactory Striatum 3 4 5 Kate A
bioRxiv preprint doi: https://doi.org/10.1101/235291; this version posted December 16, 2017. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. 1 2 A cortical pathway modulates sensory input into the olfactory striatum 3 4 5 Kate A. White1,2,3, Yun-Feng Zhang4, Zhijian Zhang5, Janardhan P. Bhattarai4, Andrew 6 H. Moberly4, Estelle in ‘t Zandt1,2, Huijie Mi6, Xianglian Jia7, Marc V. Fuccillo4, Fuqiang 7 Xu5, Minghong Ma4, Daniel W. Wesson1,2,3* 8 9 1Department of Pharmacology & Therapeutics 10 2Center for Smell and Taste 11 University of Florida 12 1200 Newell Dr.; Gainesville, FL, 32610. U.S.A. 13 3Department of Neurosciences 14 Case Western Reserve University 15 2109 Adelbert Rd.; Cleveland, OH, 44106. U.S.A. 16 4Department of Neuroscience 17 University of Pennsylvania Perelman School of Medicine 18 211 CRB, 415 Curie Blvd; Philadelphia, PA, 19104. U.S.A 19 5Center for Brain Science 20 Wuhan Institute of Physics and Mathematics 21 Chinese Academy of Sciences 22 Wuhan 430071, China 23 6College of Life Sciences 24 Wuhan University 25 Wuhan 430072, China 26 7Shenzhen Institutes of Advanced Technology 27 Chinese Academy of Sciences 28 Shenzhen 518055, China 29 30 *corresponding author; [email protected] 31 RUNNING HEAD: Olfactory striatum input 32 33 Author Contributions: Conceptualization: K.A.W. and D.W.W.; Methodology: K.A.W., Z.Z., F.X., 34 M.M., and D.W.W.; Investigation: K.A.W., Y-F.Z., Z.Z., J.P.B., A.H.M., E.I.Z., H.M., and X.J.; 35 Resources: M.V.F.; Writing – Original Draft: K.A.W., Z.Z., M.M., and D.W.W.; Writing – Review & 36 Editing: all authors; Visualization: K.A.W., Z.Z., Y-F.Z., J.P.B., D.W.W.; Supervision: F.X., M.M., 37 and D.W.W.; Funding Acquisition: K.A.W., F.X., M.M., and D.W.W. -
(12) United States Patent (10) Patent No.: US 6,969,702 B2 Bertilsson Et Al
USOO6969702B2 (12) United States Patent (10) Patent No.: US 6,969,702 B2 Bertilsson et al. (45) Date of Patent: Nov. 29, 2005 (54) COMPOUNDS AND METHODS FOR OTHER PUBLICATIONS INCREASING NEUROGENESIS Jackowski, "Neural injury repair: hope for the future as (75) Inventors: Göran Bertilsson, Västerhaninge (SE); barriers to effective CNS regeneration become clearer,' Rikard Erlandsson, Sundyberg (SE); British Journal of Neurosurgery, (1995), 9, p. 303-317.* Jonas Frisen, Stockholm (SE); Anders Asanuma et al. (1996). Mol. Brain Res. 41: 210-215. Haegerstrand, Danderyd (SE); Jessica Cameron and McKay (1998). Current Opinion in Neurobiol. Heidrich, Arsta (SE); Nina Hellström, 8: 677-680. Södertälje (SE); Johan Haggblad, Cassidy and Frisen (2001). Nature 412: 690-691. Västgötagränd (SE); Katarina Jansson, Dinter et al. (1997). J. Mol. Med. 75: 95-102. Johanneshov (SE); Jarkko Kortesmaa, D'Sa and Duman (2002). Bipolar Disorders 4: 183–194. Stockholm (SE); Per Lindquist, Duman et al. (2001). J. Pharmacol. and Ex. Therapeutics Bromma (SE); Hanna Lundh, Solna 299: 4O1-4O7. (SE); Jacqueline McGuire, Stockholm Duman et al. (2001). Neuropsychopharmacol. 25: 836-844. (SE); Alex Mercer, Bromma (SE); Duprat et al. (2000). Mol. Pharmacol. 57: 906–912. Karl Nyberg, Uppsala (SE); Amina Hallbergson et al. (2003). J. Clinical Investigation 112: Ossoinak, Stockholm (SE); Cesare 1128-1133. Patrone, Hägersten (SE); Harriet Hartikka et al. (1992). J. Neuroscience Res. 32: 190–201. Iona et al. (1998). Mol. Pharmacol. 53: 23-32. Rönnholm, Trångsund (SE); Lilian Kim et al. (2000). Society for Neuroscience 26: 2316, Wikström, Spånga (SE); Olof Abstract No. 868.2. Zachrisson, Spånga (SE) Malberg et al. (2000). J. -
Imaging Elevated Brain Arachidonic Acid Signaling in Unanesthetized Serotonin Transporter (5-HTT)-Deficient Mice
Neuropsychopharmacology (2009) 34, 1695–1709 & 2009 Nature Publishing Group All rights reserved 0893-133X/09 $32.00 www.neuropsychopharmacology.org Imaging Elevated Brain Arachidonic Acid Signaling in Unanesthetized Serotonin Transporter (5-HTT)-Deficient Mice Mireille Basselin*,1, Meredith A Fox2, Lisa Chang1, Jane M Bell1, Dede Greenstein3, Mei Chen1, 2 1 Dennis L Murphy and Stanley I Rapoport 1Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, MD, USA; 2Laboratory of Clinical Science, National Institutes of Health, Bethesda, MD, USA; 3Child Psychiatry Branch, National Institute of Mental Health, National Institutes of Health, Bethesda, MD, USA Certain polymorphisms reduce serotonin (5-HT) reuptake transporter (5-HTT) function and increase susceptibility to psychiatric +/À disorders. Heterozygous (5-HTT )-deficient mice, models for humans with these polymorphisms, have elevated brain 5-HT concentrations and behavioral abnormalities. As postsynaptic 5-HT2A/2C receptors are coupled to cytosolic phospholipase A2 (cPLA2), which releases arachidonic acid (AA) from membrane phospholipid, 5-HTT-deficient mice may have altered brain AA signaling and metabolism. To test this hypothesis, signaling was imaged as an AA incorporation coefficient k* in unanesthetized homozygous knockout À/À +/À +/+ (5-HTT ), 5-HTT and wild-type (5-HTT ), mice following saline (baseline) or 1.5 mg/kg s.c. DOI, a partial 5-HT2A/2C receptor agonist. Enzyme activities, metabolite concentrations, and head-twitch responses to DOI were also measured. Baseline k* was widely +/À À/À +/+ +/+ elevated by 20–70% in brains of 5-HTT and 5-HTT compared to 5-HTT mice. DOI increased k* in 5-HTT mice, but decreased k* in 5-HTT-deficient mice. -
Extending Our Understanding of Cardiovascular Risk From
EDITORIALS www.jasn.org multiprotein cilia-destined cargo within the cell. Then through 13. Tyler KM, Fridberg A, Toriello KM, Olson CL, Cieslak JA, Hazlett TL, association of an adaptor molecule containing a cilia-targeting Engman DM: Flagellar membrane localization via association with lipid rafts. J Cell Sci 122: 859–866, 2009 motif, perhaps such as cystin, multiple proteins deliver to the 14. Rohatgi R, Milenkovic L, Scott MP: Patched1 regulates hedgehog cilium. Further complexity in this model arises from the fact signaling at the primary cilium. Science 317: 372–376, 2007 that not all proteins constitutively localize to cilia but require an external stimulus that promotes cilia entry. A good example of this is Hedgehog signaling. It was recently shown upon bind- See related article, “Cystin Localizes to Primary Cilia via Membrane Microdo- ing of Hedgehog to its receptor Patched, the protein Smooth- mains and a Targeting Motif,” on pages 2570–2580. ened is targeted to the cilium14; therefore, multiple targeting motifs and adaptors likely regulate ciliary entry of proteins either in a constitutive manner or in response to a specific cue. Understanding these targeting signals will be key as we con- It’s about Time: Extending our tinue to unravel the mysteries of the cilia. Understanding of Cardiovascular Risk from DISCLOSURES Chronic Kidney Disease This work was supported in part by National Institutes of Health (NIH DK069605) and Polycystic Kidney Disease Foundation (162G08a) grants. Ann Young and Amit X. Garg Division of Nephrology and Department of Epidemiology and Bio- statistics, University of Western Ontario, London, Ontario, Canada REFERENCES J Am Soc Nephrol 20: 2486–2487, 2009. -
Polycystin-2 Takes Different Routes to the Somatic and Ciliary Plasma Membrane
JCB: Article Polycystin-2 takes different routes to the somatic and ciliary plasma membrane Helen Hoffmeister,1 Karin Babinger,1 Sonja Gürster,1 Anna Cedzich,1,2 Christine Meese,1 Karin Schadendorf,3 Larissa Osten,1 Uwe de Vries,1 Anne Rascle,1 and Ralph Witzgall1 1Institute for Molecular and Cellular Anatomy, University of Regensburg, 93053 Regensburg, Germany 2Medical Research Center, Klinikum Mannheim, University of Heidelberg, 68167 Mannheim, Germany 3Center for Electron Microscopy, University of Regensburg, 93053 Regensburg, Germany olycystin-2 (also called TRPP2), an integral mem- a COPII-dependent fashion at the endoplasmic reticulum, brane protein mutated in patients with cystic kidney that polycystin-2 reaches the cis side of the Golgi appara- P disease, is located in the primary cilium where it is tus in either case, but that the trafficking to the somatic thought to transmit mechanical stimuli into the cell interior. plasma membrane goes through the Golgi apparatus After studying a series of polycystin-2 deletion mutants we whereas transport vesicles to the cilium leave the Golgi identified two amino acids in loop 4 that were essential for apparatus at the cis compartment. Such an interpretation the trafficking of polycystin-2 to the somatic (nonciliary) is supported by the finding that mycophenolic acid treat- plasma membrane. However, polycystin-2 mutant proteins ment resulted in the colocalization of polycystin-2 with in which these two residues were replaced by alanine GM130, a marker of the cis-Golgi apparatus. Remark- were still sorted into the cilium, thus indicating that the ably, we also observed that wild-type Smoothened, an trafficking routes to the somatic and ciliary plasma mem- integral membrane protein involved in hedgehog signaling brane compartments are distinct. -
The Transition Zone: an Essential Functional Compartment of Cilia Szymanska and Johnson
The transition zone: an essential functional compartment of cilia Szymanska and Johnson Szymanska and Johnson Cilia 2012, 1:10 http://www.ciliajournal.com/content/1/1/10 Szymanska and Johnson Cilia 2012, 1:10 http://www.ciliajournal.com/content/1/1/10 REVIEW Open Access The transition zone: an essential functional compartment of cilia Katarzyna Szymanska and Colin A Johnson* Abstract Recent studies of the primary cilium have begun to provide further insights into ciliary ultrastructure, with an emerging picture of complex compartmentalization and molecular components that combine in functional modules. Many proteins that are mutated in ciliopathies are localized to the transition zone, a compartment of the proximal region of the cilium. The loss of these components can disrupt ciliary functions such as the control of protein entry and exit from the cilium, the possible trafficking of essential ciliary components, and the regulation of signaling cascades and control of the cell cycle. The discovery of functional modules within the primary cilium may help in understanding the variable phenotypes and pleiotropy in ciliopathies. Keywords: Cilia, Transition zone, IFT, Ciliopathies Review crucial role in left-right patterning. They are located at Cilia are microtubule-based, hair-like organelles that the embryonic node, and although they have a “9+0” occur on the apical surface of most mammalian cells in microtubule pattern they mediate a leftward flow at the G0/G1 of the cell cycle [1], with the exception of bone node in a “whirlpool”-likemannerduetotheretention marrow-derived cells [2]. Defects in cilia structure or of dynein arms between microtubules. The leftward function are the cause of a suite of congenital conditions flow is thought to transport morphogens that are essen- known as ciliopathies, which now include polycystic kid- tial for the first step of symmetry breaking in the devel- ney disease, nephronophthisis, Senior-Løken syndrome, opmental of the mammalian body plan [2]. -
Precise Detection of Direct Glomerular Input Duration by the Olfactory Bulb
16058 • The Journal of Neuroscience, November 26, 2014 • 34(48):16058–16064 Systems/Circuits Precise Detection of Direct Glomerular Input Duration by the Olfactory Bulb Anan Li,1,2 David H. Gire,3 Thomas Bozza,4 and Diego Restrepo1 1Department of Cell and Developmental Biology, Neuroscience Program and Rocky Mountain Taste and Smell Center, University of Colorado Anschutz Medical Campus, Aurora, Colorado 80045, 2Wuhan Institute of Physics and Mathematics, The Chinese Academy of Sciences/State Key Laboratory of Magnetic Resonance and Atomic and Molecular Physics, Wuhan, China 430071, 3Department of Molecular and Cellular Biology, and Center for Brain Science, Harvard University, Cambridge, Massachusetts 02138, and 4Department of Neurobiology, Northwestern University, Evanston, Illinois 60208 Sensory neuron input to the olfactory bulb (OB) was activated precisely for different durations with blue light in mice expressing channelrhodopsin-2 in olfactory sensory neurons. Behaviorally the mice discriminated differences of 10 ms in duration of direct glomer- ular activation. In addition, a subset of mitral/tufted cells in the OB of awake mice responded tonically therefore conveying information on stimulus duration. Our study provides evidence that duration of the input to glomeruli not synchronized to sniffing is detected. This potent cue may be used to obtain information on puffs in odor plumes. Key words: olfactory; puffs Introduction sniffing (Wachowiak, 2011) and because of complex interactions Duration is an important parameter of sensory stimuli exten- between odorants and the epithelium (Schoenfeld and Cleland, sively studied in both the visual and auditory systems (B.G. Cle- 2005; Scott et al., 2014). Here we precisely controlled sensory land et al., 1971; Ikeda and Wright, 1974; Ehrlich et al., 1997; input to the olfactory bulb (OB) with blue light using a strain of Klink and Klump, 2004). -
Cannabinoid Control of Olfactory Processes: the Where Matters
G C A T T A C G G C A T genes Review Cannabinoid Control of Olfactory Processes: The Where Matters Geoffrey Terral 1,2,3, Giovanni Marsicano 1,2 , Pedro Grandes 4,5 and Edgar Soria-Gómez 4,5,6,* 1 INSERM, U1215 NeuroCentre Magendie, 146 rue Léo Saignat, CEDEX, 33077 Bordeaux, France; geoff[email protected] (G.T.); [email protected] (G.M.) 2 University of Bordeaux, 146 rue Léo Saignat, 33000 Bordeaux, France 3 Interdisciplinary Institute for Neuroscience, CNRS, UMR 5297, 33000 Bordeaux, France 4 Department of Neurosciences, University of the Basque Country UPV/EHU, Barrio Sarriena s n, 48940 Leioa, n Spain; [email protected] 5 Achucarro Basque Center for Neuroscience, Science Park of the UPV/EHU, 48940 Leioa, Spain 6 IKERBASQUE, Basque Foundation for Science, Maria Diaz de Haro 3, 48013 Bilbao, Spain * Correspondence: [email protected] or [email protected] Received: 25 February 2020; Accepted: 13 April 2020; Published: 16 April 2020 Abstract: Olfaction has a direct influence on behavior and cognitive processes. There are different neuromodulatory systems in olfactory circuits that control the sensory information flowing through the rest of the brain. The presence of the cannabinoid type-1 (CB1) receptor, (the main cannabinoid receptor in the brain), has been shown for more than 20 years in different brain olfactory areas. However, only over the last decade have we started to know the specific cellular mechanisms that link cannabinoid signaling to olfactory processing and the control of behavior. In this review, we aim to summarize and discuss our current knowledge about the presence of CB1 receptors, and the function of the endocannabinoid system in the regulation of different olfactory brain circuits and related behaviors.