Assessing the Morphology of Vesicles in Inhibitory Symmetric Synapses in Safety and Fear Conditions in the Rat Lateral Amygdala
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A Guide to Glutamate Receptors
A guide to glutamate receptors 1 Contents Glutamate receptors . 4 Ionotropic glutamate receptors . 4 - Structure ........................................................................................................... 4 - Function ............................................................................................................ 5 - AMPA receptors ................................................................................................. 6 - NMDA receptors ................................................................................................. 6 - Kainate receptors ............................................................................................... 6 Metabotropic glutamate receptors . 8 - Structure ........................................................................................................... 8 - Function ............................................................................................................ 9 - Group I: mGlu1 and mGlu5. .9 - Group II: mGlu2 and mGlu3 ................................................................................. 10 - Group III: mGlu4, mGlu6, mGlu7 and mGlu8 ............................................................ 10 Protocols and webinars . 11 - Protocols ......................................................................................................... 11 - Webinars ......................................................................................................... 12 References and further reading . 13 Excitatory synapse pathway -
Plp-Positive Progenitor Cells Give Rise to Bergmann Glia in the Cerebellum
Citation: Cell Death and Disease (2013) 4, e546; doi:10.1038/cddis.2013.74 OPEN & 2013 Macmillan Publishers Limited All rights reserved 2041-4889/13 www.nature.com/cddis Olig2/Plp-positive progenitor cells give rise to Bergmann glia in the cerebellum S-H Chung1, F Guo2, P Jiang1, DE Pleasure2,3 and W Deng*,1,3,4 NG2 (nerve/glial antigen2)-expressing cells represent the largest population of postnatal progenitors in the central nervous system and have been classified as oligodendroglial progenitor cells, but the fate and function of these cells remain incompletely characterized. Previous studies have focused on characterizing these progenitors in the postnatal and adult subventricular zone and on analyzing the cellular and physiological properties of these cells in white and gray matter regions in the forebrain. In the present study, we examine the types of neural progeny generated by NG2 progenitors in the cerebellum by employing genetic fate mapping techniques using inducible Cre–Lox systems in vivo with two different mouse lines, the Plp-Cre-ERT2/Rosa26-EYFP and Olig2-Cre-ERT2/Rosa26-EYFP double-transgenic mice. Our data indicate that Olig2/Plp-positive NG2 cells display multipotential properties, primarily give rise to oligodendroglia but, surprisingly, also generate Bergmann glia, which are specialized glial cells in the cerebellum. The NG2 þ cells also give rise to astrocytes, but not neurons. In addition, we show that glutamate signaling is involved in distinct NG2 þ cell-fate/differentiation pathways and plays a role in the normal development of Bergmann glia. We also show an increase of cerebellar oligodendroglial lineage cells in response to hypoxic–ischemic injury, but the ability of NG2 þ cells to give rise to Bergmann glia and astrocytes remains unchanged. -
Control of Synapse Number by Glia Erik M
R EPORTS RGCs (8). Similar results were obtained un- der both conditions. After 2 weeks in culture, Control of Synapse Number we used whole-cell patch-clamp recording to measure the significant enhancement of spon- by Glia taneous synaptic activity by astrocytes (Fig. 1, A and B) (9). In the absence of astroglia, Erik M. Ullian,* Stephanie K. Sapperstein, Karen S. Christopherson, little synaptic activity occurred even when Ben A. Barres RGCs were cultured with their tectal target cells (6). This difference in synaptic activity Although astrocytes constitute nearly half of the cells in our brain, their persisted even after a month in culture, indi- function is a long-standing neurobiological mystery. Here we show by quantal cating that it is not accounted for by a matu- analyses, FM1-43 imaging, immunostaining, and electron microscopy that few rational delay. To examine whether glia reg- synapses form in the absence of glial cells and that the few synapses that do ulate synaptic activity by enhancing postsyn- form are functionally immature. Astrocytes increase the number of mature, aptic responsiveness, we measured the re- functional synapses on central nervous system (CNS) neurons by sevenfold and sponse of RGCs to pulses of L-glutamate are required for synaptic maintenance in vitro. We also show that most syn- applied to the cell somas. Regardless of the apses are generated concurrently with the development of glia in vivo. These presence of glia, RGCs responded with in- data demonstrate a previously unknown function for glia in inducing and ward currents (Fig. 1C) that were blocked by stabilizing CNS synapses, show that CNS synapse number can be profoundly glutamate receptor antagonists (10). -
Area-Specific Synapse Structure in Branched Posterior Nucleus Axons Reveals a New Level of Complexity in Thalamocortical Networks
The Journal of Neuroscience, March 25, 2020 • 40(13):2663–2679 • 2663 Systems/Circuits Area-Specific Synapse Structure in Branched Posterior Nucleus Axons Reveals a New Level of Complexity in Thalamocortical Networks Javier Rodriguez-Moreno,1 Cesar Porrero,1 Astrid Rollenhagen,2 Mario Rubio-Teves,1 Diana Casas-Torremocha,1 X Lidia Alonso-Nanclares,3 Rachida Yakoubi,2 XAndrea Santuy,3 XAngel Merchan-Pe´rez,3,5,6 XJavier DeFelipe,3,4,5 Joachim H.R. Lu¨bke,2,7,8* and XFrancisco Clasca1* 1Department of Anatomy and Neuroscience, School of Medicine, Auto´noma de Madrid University, 28029 Madrid, Spain, 2Institute of Neuroscience and Medicine INM-10, Research Centre Ju¨lich GmbH, 52425 Ju¨lich, Germany, 3Laboratorio Cajal de Circuitos Corticales, Centro de Tecnología Biome´dica, Universidad Polite´cnica de Madrid, Pozuelo de Alarco´n, 28223 Madrid, Spain, 4Instituto Cajal, Consejo Superior de Investigaciones Científicas, Arce 37 28002, Madrid, Spain, 5CIBERNED, Centro de Investigacio´n Biome´dica en Red de Enfermedades Neurodegenerativas, 28031 Madrid, Spain, 6Departamento de Arquitectura y Tecnología de Sistemas Informa´ticos, Universidad Polite´cnica de Madrid. Boadilla del Monte, 28660 Madrid, Spain, 7Department of Psychiatry, Psychotherapy and Psychosomatics, Medical Faculty RWTH University Hospital Aachen, 52074 Aachen, Germany, and 8JARA-Translational Brain Medicine, 52425 Ju¨lich-Aachen, Germany Thalamocortical posterior nucleus (Po) axons innervating the vibrissal somatosensory (S1) and motor (MC) cortices are key links in the brain neuronal network that allows rodents to explore the environment whisking with their motile snout vibrissae. Here, using fine-scale high-end 3D electron microscopy, we demonstrate in adult male C57BL/6 wild-type mice marked differences between MC versus S1 Po synapses in (1) bouton and active zone size, (2) neurotransmitter vesicle pool size, (3) distribution of mitochondria around synapses, and (4) proportion of synapses established on dendritic spines and dendritic shafts. -
The Interplay Between Neurons and Glia in Synapse Development And
Available online at www.sciencedirect.com ScienceDirect The interplay between neurons and glia in synapse development and plasticity Jeff A Stogsdill and Cagla Eroglu In the brain, the formation of complex neuronal networks and regulate distinct aspects of synaptic development and amenable to experience-dependent remodeling is complicated circuit connectivity. by the diversity of neurons and synapse types. The establishment of a functional brain depends not only on The intricate communication between neurons and glia neurons, but also non-neuronal glial cells. Glia are in and their cooperative roles in synapse formation are now continuous bi-directional communication with neurons to direct coming to light due in large part to advances in genetic the formation and refinement of synaptic connectivity. This and imaging tools. This article will examine the progress article reviews important findings, which uncovered cellular made in our understanding of the role of mammalian and molecular aspects of the neuron–glia cross-talk that perisynaptic glia (astrocytes and microglia) in synapse govern the formation and remodeling of synapses and circuits. development, maturation, and plasticity since the previ- In vivo evidence demonstrating the critical interplay between ous Current Opinion article [1]. An integration of past and neurons and glia will be the major focus. Additional attention new findings of glial control of synapse development and will be given to how aberrant communication between neurons plasticity is tabulated in Box 1. and glia may contribute to neural pathologies. Address Glia control the formation of synaptic circuits Department of Cell Biology, Duke University Medical Center, Durham, In the CNS, glial cells are in tight association with NC 27710, USA synapses in all brain regions [2]. -
PRESYNAPTIC Α2δ SUBUNITS ARE KEY ORGANIZERS of GLUTAMATERGIC SYNAPSES Clemens L
bioRxiv preprint doi: https://doi.org/10.1101/826016; this version posted October 31, 2019. 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. PRESYNAPTIC α2δ SUBUNITS ARE KEY ORGANIZERS OF GLUTAMATERGIC SYNAPSES Clemens L. Schöpf1, Stefanie Geisler1, Ruslan I. Stanika1, Marta Campiglio1, Walter A. Kaufmann3, Benedikt Nimmervoll1, Bettina Schlick1, Ryuichi Shigemoto3, and Gerald J. Obermair1,2* From Division of Physiology, Medical University Innsbruck, A-6020 Innsbruck1, Division Physiology, Karl Landsteiner University of Health Sciences, A-3500 Krems2, and Institute of Science and Technology Austria, A-3400 Klosterneuburg3, Austria. Running head: Presynaptic α2δ subunits organize synapses Address correspondence to: *Gerald J. Obermair, Univ.-Prof. Dr., Phone: +43-2732-72090490, E-mail: [email protected], [email protected] In nerve cells the genes encoding for α2δ the auxiliary β and α2δ subunits. α2δ subunits, the subunits of voltage-gated calcium channels targets of the widely prescribed anti-epileptic and (VGCCs) have been linked to synaptic functions anti-allodynic drugs gabapentin and pregabalin, are and neurological disease. Here we show that α2δ membrane-anchored extracellular glycoproteins, subunits are essential for the formation and which modulate VGCC trafficking and calcium organization of glutamatergic synapses. Using a currents (Arikkath and Campbell, 2003; Dolphin, cellular α2δ subunit triple loss-of-function model, 2013; Geisler et al., 2015; Obermair et al., 2008; we demonstrate a failure in presynaptic Zamponi et al., 2015). -
Neural Control and Neuromodulationof Lower Urinary
Neural Control and Neuromodulation of Lower Urinary Tract Function William C. de Groat University of Pittsburgh Topics • Anatomy and functions of the lower urinary tract • Peripheral innervation (efferent and afferent nerves) • Central neural control of the lower urinary tract • Lower urinary tract dysfunction • Treatment of dysfunction (neuromodulation) • Research opportunities Anatomy and Functions of the Lower Urinary Tract Functions Two Types of Voiding 1. Urine storage - Reservoir: Bladder INVOLUNTARY (Reflex) (infant & fetus) Defect in 2. Urine release Maturation Maturation - Outlet: Urethra INVOLUNTARY THERAPY VOLUNTARY (Reflex) (adult) (adult) Bladder Parkinson’s, MS, stroke, brain tumors, spinal cord injury, Urethra aging, cystitis Lower Urinary Tract Innervation Two Types of Visceral Afferent Neurons: Bladder & Bowel Aδ-fibers responsible for normal bladder sensations C-fibers contribute to urgency, frequency and incontinence Afferent Sensitivity may be Influenced by Substances Released from the Urothelium Aδ fiber C fiber X CNS Urothelium The Bladder U rothelium Glycosaminoglycan Layer Uroplakin Plaques and Discoidal Vesicles r=_zo_"_"l_a_o_cc-lu---.dens } Umbrella Cell Stratum Intermediate Cell Stratum } Basal Cell Stratum Afferent Nerve fiber Urothelial-Afferent Interactions ( I ( I ( I ( ' ( I ( I ( I Urothelium ( I ( 0 I I I AChR ATP, NO, NKA, ACh, NGF ~erves ' Efferent ' nerves nerves Interaction of Sensory Pathways of Multiple Pelvic Organs Convergent Dichotomizing Branch Bladder point Colon Somatic and Visceral Afferent -
Electrical Synapses and Their Functional Interactions with Chemical Synapses
REVIEWS Electrical synapses and their functional interactions with chemical synapses Alberto E. Pereda Abstract | Brain function relies on the ability of neurons to communicate with each other. Interneuronal communication primarily takes place at synapses, where information from one neuron is rapidly conveyed to a second neuron. There are two main modalities of synaptic transmission: chemical and electrical. Far from functioning independently and serving unrelated functions, mounting evidence indicates that these two modalities of synaptic transmission closely interact, both during development and in the adult brain. Rather than conceiving synaptic transmission as either chemical or electrical, this article emphasizes the notion that synaptic transmission is both chemical and electrical, and that interactions between these two forms of interneuronal communication might be required for normal brain development and function. Communication between neurons is required for Electrical and chemical synapses are now known to brain function, and the quality of such communica- coexist in most organisms and brain structures, but details tion enables hardwired neural networks to act in a of the properties and distribution of these two modalities of dynamic fashion. Functional interactions between transmission are still emerging. Most research efforts neurons occur at anatomically identifiable cellular have focused on exploring the mechanisms of chemi- regions called synapses. Although the nature of synaptic cal transmission, and considerably less is known transmission has been an area of enormous controversy about those underlying electrical transmission. It was (BOX 1), two main modalities of synaptic transmission — thought that electrical synapses were more abundant namely, chemical and electrical — are now recognized. At in invertebrates and cold-blooded vertebrates than chemical synapses, information is transferred through in mammals. -
Developmental Changes in Calcium Channel Types Mediating Central Synaptic Transmission
The Journal of Neuroscience, January 1, 2000, 20(1):59–65 Developmental Changes in Calcium Channel Types Mediating Central Synaptic Transmission Shinichi Iwasaki,1 Akiko Momiyama,2 Osvaldo D. Uchitel,3 and Tomoyuki Takahashi1 1Department of Neurophysiology, University of Tokyo Faculty of Medicine, Tokyo 113-0033, Japan, 2Laboratory of Cerebral Structure, National Institute for Physiological Sciences, Myodaiji, Okazaki 444-8585, Japan, and 3Departamento de Ciencias Biologicas, Laboratorio de Fisiologia y Biologia, Molecular, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Buenos Aires 1428, Argentina Multiple types of high-voltage-activated Ca 21 channels trigger fact, Ca 21 currents directly recorded from the auditory calyceal neurotransmitter release at the mammalian central synapse. presynaptic terminal were identified as N-, P/Q-, and R-types at Among them, the v-conotoxin GVIA-sensitive N-type channels postnatal day 7 (P7) to P10 but became predominantly P/Q- and the v-Aga-IVA-sensitive P/Q-type channels mediate fast type at P13. In contrast to thalamic and cerebellar IPSCs and synaptic transmission. However, at most central synapses, it is brainstem auditory EPSCs, N-type Ca 21 channels persistently not known whether the contributions of different Ca 21 channel contribute to cerebral cortical EPSCs and spinal IPSCs types to synaptic transmission remain stable throughout post- throughout postnatal months. Thus, in adult animals, synaptic natal development. We have addressed this question by testing transmission is predominantly mediated by P/Q-type channels type-specific Ca 21 channel blockers at developing central syn- at a subset of synapses and mediated synergistically by multi- apses. -
GABA Enhances Transmission at an Excitatory Glutamatergic Synapse
The Journal of Neuroscience, August 15, 2001, 21(16):5935–5943 GABA Enhances Transmission at an Excitatory Glutamatergic Synapse Scott Gutovitz, John T. Birmingham, Jason A. Luther, David J. Simon, and Eve Marder Volen Center and Biology Department, Brandeis University, Waltham, Massachusetts 02454-9110 GABA mediates both presynaptic and postsynaptic inhibition at -(Aminomethyl)-4-chlorobenzenepropanoic acid (baclofen) many synapses. In contrast, we show that GABA enhances was an effective agonist for the GABA-evoked enhancement transmission at excitatory synapses between the lateral gastric but did not increase the postjunctional conductance. Muscimol and medial gastric motor neurons and the gastric mill 6a and 9 activated a rapid postsynaptic conductance but did not en- (gm6a, gm9) muscles and between the lateral pyloric motor hance the amplitude of the nerve-evoked EJPs. GABA had no neuron and pyloric 1 (p1) muscles in the stomach of the lobster effect on iontophoretic responses to glutamate and decreased Homarus americanus. Two-electrode current-clamp or voltage- the coefficient of variation of nerve-evoked EJPs. In the pres- clamp techniques were used to record from muscle fibers. The ence or absence of tetrodotoxin, GABA increased the fre- innervating nerves were stimulated to evoke excitatory junc- quency but not the amplitude of miniature endplate potentials. tional potentials (EJPs) or excitatory junctional currents. Bath These data suggest that GABA acts presynaptically via a application of GABA first decreased the amplitude of evoked GABAB-like receptor to increase the release of EJPs in gm6a and gm9 muscles, but not the p1 muscle, by neurotransmitter. activating a postjunctional conductance increase that was blocked by picrotoxin. -
Presynaptic Establishment of the Synaptic Cleft Extracellular Matrix Is Required for Post-Synaptic Differentiation
Downloaded from genesdev.cshlp.org on September 27, 2021 - Published by Cold Spring Harbor Laboratory Press Presynaptic establishment of the synaptic cleft extracellular matrix is required for post-synaptic differentiation Jeffrey Rohrbough, Emma Rushton, Elvin Woodruff III, Tim Fergestad, Krishanthan Vigneswaran, and Kendal Broadie1 Department of Biological Sciences, Kennedy Center for Research on Human Development, Vanderbilt University, Nashville, Tennessee 37235, USA Formation and regulation of excitatory glutamatergic synapses is essential for shaping neural circuits throughout development. In a Drosophila genetic screen for synaptogenesis mutants, we identified mind the gap (mtg), which encodes a secreted, extracellular N-glycosaminoglycan-binding protein. MTG is expressed neuronally and detected in the synaptic cleft, and is required to form the specialized transsynaptic matrix that links the presynaptic active zone with the post-synaptic glutamate receptor (GluR) domain. Null mtg embryonic mutant synapses exhibit greatly reduced GluR function, and a corresponding loss of localized GluR domains. All known post-synaptic signaling/scaffold proteins functioning upstream of GluR localization are also grossly reduced or mislocalized in mtg mutants, including the dPix–dPak–Dock cascade and the Dlg/PSD-95 scaffold. Ubiquitous or neuronally targeted mtg RNA interference (RNAi) similarly reduce post-synaptic assembly, whereas post-synaptically targeted RNAi has no effect, indicating that presynaptic MTG induces and maintains the post-synaptic pathways driving GluR domain formation. These findings suggest that MTG is secreted from the presynaptic terminal to shape the extracellular synaptic cleft domain, and that the cleft domain functions to mediate transsynaptic signals required for post-synaptic development. [Keywords: Glutamatergic synaptogenesis; post-synaptic density; glutamate receptor; secretion; Drosophila; neuromuscular junction] Supplemental material is available at http://www.genesdev.org. -
Slitrk2 Controls Excitatory Synapse Development Via PDZ-Mediated
www.nature.com/scientificreports OPEN Slitrk2 controls excitatory synapse development via PDZ-mediated protein interactions Kyung Ah Han 1,2, Jinhu Kim1,2, Hyeonho Kim1,2, Dongwook Kim1, Dongseok Lim1, Jaewon Ko 1 & Ji Won Um 1* Members of the Slitrk (Slit- and Trk-like protein) family of synaptic cell-adhesion molecules control excitatory and inhibitory synapse development through isoform-dependent extracellular interactions with leukocyte common antigen-related receptor protein tyrosine phosphatases (LAR-RPTPs). However, how Slitrks participate in activation of intracellular signaling pathways in postsynaptic neurons remains largely unknown. Here we report that, among the six members of the Slitrk family, only Slitrk2 directly interacts with the PDZ domain-containing excitatory scafolds, PSD-95 and Shank3. The interaction of Slitrk2 with PDZ proteins is mediated by the cytoplasmic COOH-terminal PDZ domain-binding motif (Ile-Ser-Glu-Leu), which is not found in other Slitrks. Mapping analyses further revealed that a single PDZ domain of Shank3 is responsible for binding to Slitrk2. Slitrk2 forms in vivo complexes with membrane-associated guanylate kinase (MAGUK) family proteins in addition to PSD-95 and Shank3. Intriguingly, in addition to its role in synaptic targeting in cultured hippocampal neurons, the PDZ domain-binding motif of Slitrk2 is required for Slitrk2 promotion of excitatory synapse formation, transmission, and spine development in the CA1 hippocampal region. Collectively, our data suggest a new molecular mechanism for conferring isoform-specifc regulatory actions of the Slitrk family in orchestrating intracellular signal transduction pathways in postsynaptic neurons. Synapses are asymmetric intercellular junctions that permit transmission of signals from presynaptic to postsyn- aptic neurons.