DOCSLIB.ORG

BMC Neuroscience Biomed Central

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
BMC Neuroscience Biomed Central BMC Neuroscience BioMed Central Research article Open Access Regulation of prokineticin 2 expression by light and the circadian clock Michelle Y Cheng1, Eric L Bittman2, Samer Hattar3 and Qun-Yong Zhou*1 Address: 1Department of Pharmacology, University of California, Irvine, CA, USA, 2Department of Biology, University of Massachusetts, Amherst, MA, USA and 3Departments of Biology and Neuroscience, Johns Hopkins University, Baltimore, MD, USA Email: Michelle Y Cheng - [email protected]; Eric L Bittman - [email protected]; Samer Hattar - [email protected]; Qun- Yong Zhou* - [email protected] * Corresponding author Published: 11 March 2005 Received: 17 November 2004 Accepted: 11 March 2005 BMC Neuroscience 2005, 6:17 doi:10.1186/1471-2202-6-17 This article is available from: http://www.biomedcentral.com/1471-2202/6/17 © 2005 Cheng et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Background: The suprachiasmatic nucleus (SCN) contains the master circadian clock that regulates daily rhythms of many physiological and behavioural processes in mammals. Previously we have shown that prokineticin 2 (PK2) is a clock-controlled gene that may function as a critical SCN output molecule responsible for circadian locomotor rhythms. As light is the principal zeitgeber that entrains the circadian oscillator, and PK2 expression is responsive to nocturnal light pulses, we further investigated the effects of light on the molecular rhythm of PK2 in the SCN. In particular, we examined how PK2 responds to shifts of light/dark cycles and changes in photoperiod. We also investigated which photoreceptors are responsible for the light-induced PK2 expression in the SCN. To determine whether light requires an intact functional circadian pacemaker to regulate PK2, we examined PK2 expression in cryptochrome1,2-deficient (Cry1-/-Cry2-/-) mice that lack functional circadian clock under normal light/dark cycles and constant darkness. Results: Upon abrupt shifts of the light/dark cycle, PK2 expression exhibits transients in response to phase advances but rapidly entrains to phase delays. Photoperiod studies indicate that PK2 responds differentially to changes in light period. Although the phase of PK2 expression expands as the light period increases, decreasing light period does not further condense the phase of PK2 expression. Genetic knockout studies revealed that functional melanopsin and rod-cone photoreceptive systems are required for the light-inducibility of PK2. In Cry1-/-Cry2-/- mice that lack a functional circadian clock, a low amplitude PK2 rhythm is detected under light/dark conditions, but not in constant darkness. This suggests that light can directly regulate PK2 expression in the SCN. Conclusion: These data demonstrate that the molecular rhythm of PK2 in the SCN is regulated by both the circadian clock and light. PK2 is predominantly controlled by the endogenous circadian clock, while light plays a modulatory role. The Cry1-/-Cry2-/- mice studies reveal a light-driven PK2 rhythm, indicating that light can induce PK2 expression independent of the circadian oscillator. The light inducibility of PK2 suggests that in addition to its role in clock-driven rhythms of locomotor behaviour, PK2 may also participate in the photic entrainment of circadian locomotor rhythms. Page 1 of 11 (page number not for citation purposes) BMC Neuroscience 2005, 6:17 http://www.biomedcentral.com/1471-2202/6/17 Background lation of the rhythm of PK2 expression in the SCN. In Light is the principal zeitgeber that entrains circadian particular, we investigated the photoreceptive mecha- rhythms of physiology and behaviour [1,2]. The major nisms responsible for the light-induced PK2 expression in light input pathway to the suprachiasmatic nucleus (SCN) the SCN. Utilizing Cry1-/-Cry2-/- mice, we also deter- is the retinohypothalamic tract [3], which arises from a mined whether light can drive PK2 expression in the SCN population of retinal ganglion cells [4]. Recent studies independent of a functional circadian clock. have demonstrated that melanopsin-containing retinal ganglion cells, rods, and cones all convey photic informa- Results tion to the SCN, and mice lacking these photoreceptive PK2 responds differentially to the delay and advance of systems cannot be entrained by light [5-11]. Excellent light/dark cycles progress has been made in the understanding of circadian We first examined the effects of abrupt shifts of light/dark photic entrainment [12-15]. This includes light-induced cycles on PK2 mRNA rhythm in the SCN. Animals were transcriptional activation of core clock genes in the SCN, first entrained for two weeks under 12 hour light: 12 hour such as Per1 and Per2, as well as immediate-early gene c- dark (LD), then subjected to either a 6 hour delay (6hrD) fos. Exposure to light pulses at night induces expression of shift or 6 hour advance (6hrA) shift of light/dark cycles. these genes in the SCN, and this light induction mecha- We measured PK2 mRNA in the SCN of these animals to nism has been suggested as a critical pathway for the reset- examine how quickly the PK2 mRNA rhythm re-entrains ting of circadian clock in response to changes in light/dark to the shifted light/dark cycles. Under LD, PK2 mRNA conditions [16-19]. Intercellular signalling mechanisms peaks during the day and remains low or undetectable between SCN neurons are also important in circadian during the night. During the first cycle of the delayed shift photic entrainment, as mice with mutation in a neuropep- (6hrD), the PK2 mRNA rhythm responds quickly: the ris- tide receptor for VIP (Vasoactive Intestinal Peptide) and ing phase of PK2 expression adjusts rapidly to the delayed PACAP (Pituitary Adenylate Cyclase Activating Peptide) light/dark cycles, while the falling phase still resembles are unable to sustain normal circadian behaviour and that of the unshifted light/dark cycles (Figure 1A). In con- exhibit loss of sensitivity to light [20]. trast, the PK2 mRNA rhythm responds very little to a 6 hour advance shift (6hrA). During the first cycle of the In addition to the effect of light on circadian entrainment, advance shift, the PK2 oscillation pattern remains similar light also has a direct effect on physiology and behaviour, to that of the unshifted LD (Figure 1B). These changes in generally termed as "masking" [21,22]. For instance, light PK2 expression during 6hrD or 6hrA shift indicate that the pulses given at night acutely suppress the locomotor endogenous circadian clock exerts dominant control over behaviour of nocturnal rodents [21,22], and this can the PK2 rhythm, as PK2 expression cannot respond imme- occur without functional clockwork [23-27]. Masking diately and completely to the shifts of light/dark cycles. may account for the maintenance under normal light/ dark conditions of wheel-running rhythms in crypto- As it normally takes about 1–2 days for locomotor chrome-deficient (Cry1-/-Cry2-/-) mice, which are behav- rhythms to stably entrain to phase delays and about 5–6 iourally arrhythmic under constant darkness. The days to entrain to phase advances [30,31], we next exam- contribution of masking to normal locomotor activity ined the timecourse of shifts of the PK2 rhythm to 6 hour rhythms is unclear, as is the participation of the SCN in phase advances and delays. Consistent with the animal's masking effects of light. Vitaterna et al (1999) first locomotor behaviour, the PK2 mRNA rhythm reaches sta- observed a light-driven Per2 rhythm in the SCN in Cry1-/- ble phase within 2 days of 6hrD shift (Figure 1C). In con- Cry2-/- mice, and have suggested that the light-driven trast, only the rise of PK2 reaches stable phase within 2 molecular rhythm in the SCN may be related to the pres- days of 6hrA shift, while the fall of PK2 takes longer (Fig- ervation of their locomotor rhythm [25]. ure 1D). Thus, we further examined whether the PK2 rhythm is stably entrained after 6 days of 6hrA shift. As We previously found that prokineticin 2 (PK2) is a first expected, the PK2 rhythm is completely entrained to 6hrA order clock-controlled gene, whose expression in the SCN shift after 6 days (Figure 1D). Together, the differential is regulated by CLOCK and BMAL1 acting on the E-boxes responses of PK2 rhythm to a 6hrD or 6hrA shift indicate in the gene's promoter [28]. We have also demonstrated that the endogenous circadian clock predominantly con- that PK2 may function as a SCN output molecule that trols PK2 rhythm, as circadian oscillators typically show transmits circadian locomotor rhythm via activation of a rapid phase delays but advance with transients [31,32]. G protein-coupled receptor [28,29]. Interestingly, we also The entrainment patterns of PK2 during phase shifts are observed that PK2 expression is rapidly induced by light consistent with behavioural studies in animals and pulses administered at night [28], a characteristic that is human subjects [30,31]. usually seen with core clockwork genes but not clock-con- trolled genes. Here we further investigated the light regu- Page 2 of 11 (page number not for citation purposes) BMC Neuroscience 2005, 6:17 http://www.biomedcentral.com/1471-2202/6/17 A LD B LD 6hrD 6hrA LD 3000 LD 3000 6hrD LD 2500 2500 LD 6hrA 2000 2000 1500 1500 1000 1000 PK2 mRNA (dpm/mg) 500 PK2 mRNA (dpm/mg) 500 0 0 LD 1 4 7 10 13 16 19 22 1 4 7 10 13 16 19 22 LD 1 4 7 10 13 16 19 22 1 4 7 10 13 16 19 22 6hrD 13 16 19 22 1 4 7 10 13 16 6hrA 13 16 19 22 1 4 7 10 13 16 C LD D LD 6hrD 6hrA LD 3000 LD 3000 LD LD 6hrA 6hrD 6hrA+2LD 2500 6hrD+2LD 2500 6hrA+6LD 2000 2000 1500 1500 1000 1000 PK2 mRNA (dpm/mg) PK2 mRNA (dpm/mg) 500 500 0 0 LD 1 4 7 10 13 16 19 22 1 4 7 10 13 16 19 22 LD 1 4 7 10 13 16 19 22 1 4 7 10 13 16 19 22 6hrD 13 16 19 22 1 4 7 10 13 16 6hrA 13 16 19 22 1 4 7 10 13 16 TemporalFigure 1 profiles of PK2 mRNA in the SCN in response to abrupt shifts of light/dark cycles Temporal profiles of PK2 mRNA in the SCN in response to abrupt shifts of light/dark cycles.
Load more

Recommended publications
  • Photoperiodic Responses on Expression of Clock Genes, Synaptic Plasticity Markers, and Protein Translation Initiators the Impact of Blue-Enriched Light
    Photoperiodic Responses on Expression of Clock Genes, Synaptic Plasticity Markers, and Protein Translation Initiators The Impact Of Blue-Enriched Light Master report Jorrit Waslander, s2401878 Behavioral Cognitive Neuroscience research master, N-track University of Groningen, the Netherlands Internship at: Bergen Stress and Sleep Group, University of Bergen, Norway Date: 13-7-2018 Internal supervisor, University of Groningen: P. (Peter) Meerlo External supervisor, University of Bergen: J. (Janne) Grønli Daily supervisor, University of Bergen: A. (Andrea) R. Marti Photoperiodic Responses in the PFC Table of Contents Summary ................................................................................................................................................. 3 Introduction ............................................................................................................................................. 5 Research Objective .............................................................................................................................. 8 Hypotheses .......................................................................................................................................... 8 Methods ................................................................................................................................................ 10 Experimental procedure .................................................................................................................... 10 Ethics ............................................................................................................................................
    [Show full text]
  • Anatomical and Behavioral Investigation of C1ql3 in the Mouse Suprachiasmatic Nucleus David C
    University of Connecticut OpenCommons@UConn UCHC Articles - Research University of Connecticut Health Center Research 6-2017 Anatomical and Behavioral Investigation of C1ql3 in the Mouse Suprachiasmatic Nucleus David C. Martinelli University of Connecticut School of Medicine and Dentistry Follow this and additional works at: https://opencommons.uconn.edu/uchcres_articles Part of the Life Sciences Commons, and the Medicine and Health Sciences Commons Recommended Citation Martinelli, David C., "Anatomical and Behavioral Investigation of C1ql3 in the Mouse Suprachiasmatic Nucleus" (2017). UCHC Articles - Research. 311. https://opencommons.uconn.edu/uchcres_articles/311 HHS Public Access Author manuscript Author ManuscriptAuthor Manuscript Author J Biol Rhythms Manuscript Author . Author Manuscript Author manuscript; available in PMC 2017 November 01. Published in final edited form as: J Biol Rhythms. 2017 June ; 32(3): 222–236. doi:10.1177/0748730417704766. Anatomical and Behavioral Investigation of C1ql3 in the Mouse Suprachiasmatic Nucleus Kylie S. Chew*,†, Diego C. Fernandez*,1, Samer Hattar*,‡,1, Thomas C. Südhof§,‖, and David C. Martinelli§,¶,2 *Department of Biology, The Johns Hopkins University, Baltimore, Maryland †Department of Biology, Stanford University School of Medicine, Stanford, California ‡The Solomon Snyder- Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland §Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, California ‖Howard Hughes
    [Show full text]
  • The Photoreceptors and Neural Circuits Driving the Pupillary Light Reflex
    THE PHOTORECEPTORS AND NEURAL CIRCUITS DRIVING THE PUPILLARY LIGHT REFLEX by Alan C. Rupp A dissertation submitted to Johns Hopkins University in conformity with the requirements for the degree of Doctor of Philosophy Baltimore, Maryland January 28, 2016 This work is protected by a Creative Commons license: Attribution-NonCommercial CC BY-NC Abstract The visual system utilizes environmental light information to guide animal behavior. Regulation of the light entering the eye by the pupillary light reflex (PLR) is critical for normal vision, though its precise mechanisms are unclear. The PLR can be driven by two mechanisms: (1) an intrinsic photosensitivity of the iris muscle itself, and (2) a neural circuit originating with light detection in the retina and a multisynaptic neural circuit that activates the iris muscle. Even within the retina, multiple photoreceptive mechanisms— rods, cone, or melanopsin phototransduction—can contribute to the PLR, with uncertain relative importance. In this thesis, I provide evidence that the retina almost exclusively drives the mouse PLR using bilaterally asymmetric brain circuitry, with minimal role for the iris intrinsic photosensitivity. Intrinsically photosensitive retinal ganglion cells (ipRGCs) relay all rod, cone, and melanopsin light detection from the retina to brain for the PLR. I show that ipRGCs predominantly relay synaptic input originating from rod photoreceptors, with minimal input from cones or their endogenous melanopsin phototransduction. Finally, I provide evidence that rod signals reach ipRGCs using a non- conventional retinal circuit, potentially through direct synaptic connections between rod bipolar cells and ipRGCs. The results presented in this thesis identify the initial steps of the PLR and provide insight into the precise mechanisms of visual function.
    [Show full text]
  • UC San Diego Electronic Theses and Dissertations
    UC San Diego UC San Diego Electronic Theses and Dissertations Title Ultrastructure of Melanopsin-Expressing Retinal Ganglion Cell Circuitry in the Retina and Brain Regions that Mediate Light-Driven Behavior Permalink https://escholarship.org/uc/item/8kd9v9xp Author Liu, Yu Hsin Publication Date 2017 Peer reviewed|Thesis/dissertation eScholarship.org Powered by the California Digital Library University of California UNIVERSITY OF CALIFORNIA, SAN DIEGO Ultrastructure of Melanopsin-Expressing Retinal Ganglion Cell Circuitry in the Retina and Brain Regions that Mediate Light-Driven Behavior A dissertation submitted in partial satisfaction of the Requirements for the degree Doctor of Philosophy in Neurosciences by Yu Hsin Liu Committee in charge: Professor Satchidananda Panda, Chair Professor Mark Ellisman, Co-Chair Professor Nicola Allen Professor Brenda Bloodgood Professor Ed Callaway Professor David Welsh 2017 Copyright Yu Hsin Liu, 2017 All rights reserved. This Dissertation of Yu Hsin Liu is approved, and it is acceptable in quality and form for publication on microfilm and electronically: _________________________________________ _________________________________________ _________________________________________ _________________________________________ _________________________________________ Co-Chair _________________________________________ Chair University of California, San Diego 2017 iii TABLE OF CONTENTS Signature Page ..................................................................................................... iii Table
    [Show full text]
  • Distinct Iprgc Subpopulations Mediate Light's Acute and Circadian
    RESEARCH ARTICLE Distinct ipRGC subpopulations mediate light’s acute and circadian effects on body temperature and sleep Alan C Rupp1, Michelle Ren2, Cara M Altimus1, Diego C Fernandez1†, Melissa Richardson1, Fred Turek2, Samer Hattar1,3†, Tiffany M Schmidt2* 1Department of Biology, Johns Hopkins University, Baltimore, United States; 2Department of Neurobiology, Northwestern University, Evanston, United States; 3Department of Neuroscience, Johns Hopkins University, Baltimore, United States Abstract The light environment greatly impacts human alertness, mood, and cognition by both acute regulation of physiology and indirect alignment of circadian rhythms. These processes require the melanopsin-expressing intrinsically photosensitive retinal ganglion cells (ipRGCs), but the relevant downstream brain areas involved remain elusive. ipRGCs project widely in the brain, including to the central circadian pacemaker, the suprachiasmatic nucleus (SCN). Here we show that body temperature and sleep responses to acute light exposure are absent after genetic ablation of all ipRGCs except a subpopulation that projects to the SCN. Furthermore, by chemogenetic activation of the ipRGCs that avoid the SCN, we show that these cells are sufficient for acute changes in body temperature. Our results challenge the idea that the SCN is a major relay for the acute effects of light on non-image forming behaviors and identify the sensory cells that initiate light’s profound effects on body temperature and sleep. *For correspondence: DOI: https://doi.org/10.7554/eLife.44358.001 [email protected] Present address: †National Institute of Mental Health, Introduction Bethesda, United States Many essential functions are influenced by light both indirectly through alignment of circadian Competing interests: The rhythms (photoentrainment) and acutely by a direct mechanism (sometimes referred to as ‘masking’) authors declare that no (Mrosovsky et al., 1999; Altimus et al., 2008; Lupi et al., 2008; Tsai et al., 2009; LeGates et al., competing interests exist.
    [Show full text]
  • Regulation of Prokineticin 2 Expression by Light and the Circadian Clock MY Cheng
    University of Massachusetts Amherst ScholarWorks@UMass Amherst Biology Department Faculty Publication Series Biology 2005 Regulation of prokineticin 2 expression by light and the circadian clock MY Cheng EL Bittman S Hattar QY Zhou Follow this and additional works at: https://scholarworks.umass.edu/biology_faculty_pubs Part of the Biology Commons Recommended Citation Cheng, MY; Bittman, EL; Hattar, S; and Zhou, QY, "Regulation of prokineticin 2 expression by light and the circadian clock" (2005). BMC Neuroscience. 45. https://10.1186/1471-2202-6-17 This Article is brought to you for free and open access by the Biology at ScholarWorks@UMass Amherst. It has been accepted for inclusion in Biology Department Faculty Publication Series by an authorized administrator of ScholarWorks@UMass Amherst. For more information, please contact [email protected]. BMC Neuroscience BioMed Central Research article Open Access Regulation of prokineticin 2 expression by light and the circadian clock Michelle Y Cheng1, Eric L Bittman2, Samer Hattar3 and Qun-Yong Zhou*1 Address: 1Department of Pharmacology, University of California, Irvine, CA, USA, 2Department of Biology, University of Massachusetts, Amherst, MA, USA and 3Departments of Biology and Neuroscience, Johns Hopkins University, Baltimore, MD, USA Email: Michelle Y Cheng - [email protected]; Eric L Bittman - [email protected]; Samer Hattar - [email protected]; Qun- Yong Zhou* - [email protected] * Corresponding author Published: 11 March 2005 Received: 17 November 2004 Accepted: 11 March 2005 BMC Neuroscience 2005, 6:17 doi:10.1186/1471-2202-6-17 This article is available from: http://www.biomedcentral.com/1471-2202/6/17 © 2005 Cheng et al; licensee BioMed Central Ltd.
    [Show full text]
  • KEENAN-DISSERTATION-2017.Pdf (8.719Mb)
    THE PHOTORECEPTORS AND NEUROTRANSMITTERS DRIVING SUBCONCOIUS RESPONSES TO LIGHT by William Thomas Keenan A dissertation submitted to Johns Hopkins University in conformity with the requirements for the degree of Doctor of Philosophy Baltimore, Maryland October, 2017 © William T. Keenan 2017 All Rights Reserved Abstract Our sensory systems allow us to detect and successfully navigate the environment. The visual system translates environmental light into our conscious perception of sight, as well as subconscious physiological responses such as circadian photoentrainment, the pupillary light reflex, and mood modulation among others. The first step in these processes is photon detection by photoreceptors in the neural retina of the eye. In mammals, 3 general classes of photoreceptors exist: rods, cones, and intrinsically photosensitive retinal ganglion cells (ipRGCs). ipRGCs, in addition to being photoreceptors, are the critical relay for light information from rods and cones to brain areas responsible for the subconscious responses to light. In order for this light information to get to the brain, ipRGCs are known to employ 2 distinct neurotransmitters: glutamate and PACAP. However, the contribution of each photoreceptor and neurotransmitter to subconscious behaviors remains unclear. In this thesis, I demonstrate the role each photoreceptor plays in responding to the multitude of potential environmental light conditions. I show, similar to the photoreceptors, the neurotransmitters relay distinct and necessary aspects of the information detected by the photoreceptors. In addition, I identify novel neurotransmitters within subsets of ipRGCs which may be responsible for relaying their own unique aspect of the light environment to the brain. Thesis advisor: Samer Hattar, Ph.D. Secondary reader: Haiqing Zhao, Ph.D.
    [Show full text]
  • Table of Contents (PDF)
    The Journal of Neuroscience September 24, 2014 • Volume 34 Number 39 • www.jneurosci.org i This Week in The Journal Journal Club 12947 A Role for the Human Substantia Nigra in Reinforcement Learning Archy O. de Berker and Robb B. Rutledge 12950 Neurocognitive Mechanisms for Vocal Emotions: Sounds, Meaning, Action Nadine Lavan and Ce´sar F. Lima Brief Communications ᭹ 13033 The Role of p75NTR in Cholinergic Basal Forebrain Structure and Function Cover legend: Thalamic axonal arbors from Zoran Boskovic, Fabienne Alfonsi, Bree A. Rumballe, Sachini Fonseka, corticothalamic neurons of the primary Francois Windels, and Elizabeth J. Coulson somatosensory (S1) cortex. Colorized fluorescent 13077 An Anti-Neuroinflammatory That Targets Dysregulated Glia Enhances the Efficacy of image from an in vitro slice containing CNS-Directed Gene Therapy in Murine Infantile Neuronal Ceroid Lipofuscinosis EYFP-expressing corticothalamic fibers originating Shannon L. Macauley, Andrew M.S. Wong, Charles Shyng, David P. Augner, from a small injection of virus transducing Josh T. Dearborn, Yewande Pearse, Marie S. Roberts, Stephen C. Fowler, channelrhodopsin2-EYFP into deep S1 cortex. For Jonathan D. Cooper, D. Martin Watterson, and Mark S. Sands more details, see the article by Lee et al. (pages 13170–13182). 13163 Retrospectively and Prospectively Modulated Hippocampal Place Responses Are Differentially Distributed along a Common Path in a Continuous T-Maze Julien Catanese, Alessandro Viggiano, Erika Cerasti, Michae¨l B. Zugaro, and Sidney I. Wiener Articles CELLULAR/MOLECULAR
    [Show full text]
  • 2-Aminoethoxydiphenylborane Is an Acute Inhibitor of Directly Photosensitive Retinal Ganglion Cell Activity in Vitro and in Vivo
    The Journal of Neuroscience, April 11, 2007 • 27(15):3981–3086 • 3981 Brief Communications 2-Aminoethoxydiphenylborane Is an Acute Inhibitor of Directly Photosensitive Retinal Ganglion Cell Activity In Vitro and In Vivo Sumathi Sekaran,1 Gurprit S. Lall,2 Katherine L. Ralphs,3 Adrian J. Wolstenholme,3 Robert J. Lucas,2 Russell G. Foster,1 and Mark W. Hankins1 1Circadian and Visual Neuroscience Group, University of Oxford, Wellcome Trust Centre for Human Genetics, Oxford OX3 7BN, United Kingdom, 2Faculty of Life Sciences, University of Manchester, Manchester M13 9PT, United Kingdom, and 3Department of Biology and Biochemistry, University of Bath, Bath BA2 7AY, United Kingdom The mammalian retina contains directly photosensitive retinal ganglion cells (RGCs), which use the photopigment melanopsin. The generation of mice lacking melanopsin has been invaluable in elucidating the function of these cells. These animals display deficiencies in circadian photoentrainment, the pupil light reflex, and the circadian regulation of the cone pathway. Interpreting the results from such gene knock-out models is always complicated by neuronal plasticity and the potential for restructuring of neuronal networks. Until now, the study of photosensitive RGCs has lacked an acute inhibitor. 2-Aminoethoxydiphenylborane (2-APB) is an antagonist at IP3 receptors and an inhibitor of canonical transient receptor potential ion channels (TRPCs). Here, we show that 2-APB is an extremely potent in vitro inhibitor of the photosensitive RGCs and that its effect is independent of store-dependent Ca 2ϩ release. The identification of canonical TRPC6 and TRPC7 ion channels in melanopsin-expressing ganglion cells suggests that 2-APB may act directly on a TRPC ion channel.
    [Show full text]
  • (Tolloid/BMP-1) Is Regulated in Aplysia Neurons by Treatments That Induce Long-Term Sensitization
    The Journal of Neuroscience, January 15, 1997, 17(2):755–764 A Developmental Gene (Tolloid/BMP-1) Is Regulated in Aplysia Neurons by Treatments that Induce Long-Term Sensitization Qing-R Liu,1 Samer Hattar,1 Shogo Endo,1 Kathleen MacPhee,1 Han Zhang,2 Leonard J. Cleary,2 John H. Byrne,2 and Arnold Eskin1 1Department of Biochemical and Biophysical Sciences, University of Houston, Houston, Texas 77204, and 2Department of Neurobiology and Anatomy, University of Texas Medical School, Houston, Texas 77225 Long-term sensitization training, or procedures that mimic the increased by serotonin and behavioral training was 41–45% training, produces long-term facilitation of sensory-motor neu- identical to a developmentally regulated gene family which ron synapses in Aplysia. The long-term effects of these proce- includes Drosophila tolloid and human bone morphogenetic dures require mRNA and protein synthesis (Montarolo et al., protein-1 (BMP-1). Both tolloid and BMP-1 encode metallopro- 1986; Castellucci et al., 1989). Using the techniques of differ- teases that might activate TGF-b (transforming growth factor ential display reverse transcription PCR (DDRT-PCR) and ribo- b)-like molecules or process procollagens. Aplysia tolloid/BMP- nuclease protection assays (RPA), we identified a cDNA whose 1-like protein (apTBL-1) might regulate the morphology and mRNA level was increased significantly in sensory neurons by efficacy of synaptic connections between sensory and motor treatments of isolated pleural-pedal ganglia with serotonin for neurons, which are associated with long-term sensitization. 1.5 hr or by long-term behavioral training of Aplysia. The effects of serotonin and behavioral training on this mRNA were mim- Key words: Aplysia; tolloid; metalloprotease; sensitization; icked by treatments that elevate cAMP.
    [Show full text]
  • SRBR 2006 Program Book
    Tenth Meeting Society for Research on Biological Rhythms Program and Abstracts SRBR May 21–25, 2006 Sandestin Golf and Beach Resort Sandestin, FL SOCIETY FOR RESEARCH ON BIOLOGICAL RHYTHMS i Executive Committee Advisory Board G.T.J. van der Horst Erasmus University William J. Schwartz, President Timothy J. Bartness University of Massachusetts Medical Georgia State University Russell N. Van Gelder School Washington University Vincent M. Cassone Martha Gillette, President-Elect Texas A & M Univeristy David R. Weaver University of Illinois University of Massachusetts Medical Philippe Delagrange Center Paul Hardin, Secretary Institut de Recherches Servier Texas A&M University Program Committee France Marie Dumont University of Montreal Vincent Cassone, Treasurer Carla Green, Program Chair Texas A&M University Russell Foster University of Virginia Imperial College of Science Josephine Arendt, Member-at-Large Greg Cahill University of Surrey Jadwiga M. Giebultowicz University of Houston Oregon State University Benjamin Rusak, Member-at-Large Michael Hastings Dalhousie University Martha Gillette MRC University of Illinois Ueli Schibler, Member-at-Large Takao Kondo University of Geneva Carla Green Nagoya University University of Virginia Journal of Biological Theresa Lee Rhythms Erik Herzog University of Michigan Washington University Johanna Meijer Editor-in-Chief Helena Illnerova Leiden University Czech Academy of Sciences Martin Zatz Ignacio Provencio National Institute of Mental Health Carl Johnson University of Virginia Vanderbilt University Associate Editors Louis Ptacek Elizabeth Klerman University of California, San Francisco Josephine Arendt Brigham & Women’s Hospital University of Surrey Paul Taghert Charalambos P. Kyriacou Washington University Paul Hardin University of Leicester Texas A&M University Joseph Takahashi Jennifer Loros Northwestern University Michael Hastings Dartmouth Medical Center MRC, Cambridge Travel Award Committee Ralph E.
    [Show full text]
  • 2021 NIH Virtual Postbac Poster
    NIH VIRTUAL POSTBAC POSTER DAY APRIL 27–29, 2021 #NIHPPD21 NATIONAL INSTITUTES OF HEALTH NIH VIRTUAL POSTBACCALAUREATE POSTER DAY: APRIL 27–29, 2021 4/27 TUESDAY SESSION POSTERS: 1-315 4/28 WEDNESDAY SESSION POSTERS: 316-627 4/29 THURSDAY SESSION POSTERS: 628-950 DATE INSTITUTE OR CENTER POSTER NUMBERS 4/27 NCI - National Cancer Institute ......................................................... 1 - 137 4/27 NCI-DCEG - National Cancer Institute - Division of Cancer Epidemiology and Genetics ......... 138 - 150 4/27 NHGRI - National Human Genome Research Institute .................................... 151 - 189 4/27 NIDDK - National Institute of Diabetes and Digestive and Kidney Diseases ................... 190 - 242 4/27 NIMHD - National Institute on Minority Health and Health Disparities ....................... 243 - 252 4/27 NINDS - National Institute of Neurological Disorders and Stroke ........................... 253 - 305 4/27 NINR - National Institute of Nursing Research .......................................... 306 - 315 4/28 CC - Clinical Center ................................................................ 316 - 346 4/28 NCCIH - National Center for Complementary and Integrative Health ........................ 347 - 359 4/28 NIAAA - National Institute on Alcohol Abuse and Alcoholism .............................. 360 - 396 4/28 NICHD - Eunice Kennedy Shriver National Institute of Child Health and Human Development .... 397 - 461 4/28 NIDA - National Institute on Drug Abuse ............................................... 462 -
    [Show full text]