Foundations of Cellular Life
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Nervous Tissue
Nervous Tissue Prof.Prof. ZhouZhou LiLi Dept.Dept. ofof HistologyHistology andand EmbryologyEmbryology Organization:Organization: neuronsneurons (nerve(nerve cells)cells) neuroglialneuroglial cellscells Function:Function: Ⅰ Neurons 1.1. structurestructure ofof neuronneuron somasoma neuriteneurite a.a. dendritedendrite b.b. axonaxon 1.11.1 somasoma (1)(1) nucleusnucleus LocatedLocated inin thethe centercenter ofof soma,soma, largelarge andand palepale--stainingstaining nucleusnucleus ProminentProminent nucleolusnucleolus (2)(2) cytoplasmcytoplasm (perikaryon)(perikaryon) a.a. NisslNissl bodybody b.b. neurofibrilneurofibril NisslNissl’’ss bodiesbodies LM:LM: basophilicbasophilic massmass oror granulesgranules Nissl’s Body (TEM) EMEM:: RERRER,, freefree RbRb FunctionFunction:: producingproducing thethe proteinprotein ofof neuronneuron structurestructure andand enzymeenzyme producingproducing thethe neurotransmitterneurotransmitter NeurofibrilNeurofibril thethe structurestructure LM:LM: EM:EM: NeurofilamentNeurofilament micmicrotubulerotubule FunctionFunction cytoskeleton,cytoskeleton, toto participateparticipate inin substancesubstance transporttransport LipofuscinLipofuscin (3)(3) CellCell membranemembrane excitableexcitable membranemembrane ,, receivingreceiving stimutation,stimutation, fromingfroming andand conductingconducting nervenerve impulesimpules neurite: 1.2 Dendrite dendritic spine spine apparatus Function: 1.3 Axon axon hillock, axon terminal, axolemma Axoplasm: microfilament, microtubules, neurofilament, mitochondria, -
Absence of S100A4 in the Mouse Lens Induces an Aberrant Retina-Specific Differentiation Program and Cataract
www.nature.com/scientificreports OPEN Absence of S100A4 in the mouse lens induces an aberrant retina‑specifc diferentiation program and cataract Rupalatha Maddala1*, Junyuan Gao2, Richard T. Mathias2, Tylor R. Lewis1, Vadim Y. Arshavsky1,3, Adriana Levine4, Jonathan M. Backer4,5, Anne R. Bresnick4 & Ponugoti V. Rao1,3* S100A4, a member of the S100 family of multifunctional calcium‑binding proteins, participates in several physiological and pathological processes. In this study, we demonstrate that S100A4 expression is robustly induced in diferentiating fber cells of the ocular lens and that S100A4 (−/−) knockout mice develop late‑onset cortical cataracts. Transcriptome profling of lenses from S100A4 (−/−) mice revealed a robust increase in the expression of multiple photoreceptor‑ and Müller glia‑specifc genes, as well as the olfactory sensory neuron‑specifc gene, S100A5. This aberrant transcriptional profle is characterized by corresponding increases in the levels of proteins encoded by the aberrantly upregulated genes. Ingenuity pathway network and curated pathway analyses of diferentially expressed genes in S100A4 (−/−) lenses identifed Crx and Nrl transcription factors as the most signifcant upstream regulators, and revealed that many of the upregulated genes possess promoters containing a high‑density of CpG islands bearing trimethylation marks at histone H3K27 and/or H3K4, respectively. In support of this fnding, we further documented that S100A4 (−/−) knockout lenses have altered levels of trimethylated H3K27 and H3K4. Taken together, -
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. -
Was Not Reached, However, Even After Six to Sevenhours. A
PROTEIN SYNTHESIS IN THE ISOLATED GIANT AXON OF THE SQUID* BY A. GIUDITTA,t W.-D. DETTBARN,t AND MIROSLAv BRZIN§ MARINE BIOLOGICAL LABORATORY, WOODS HOLE, MASSACHUSETTS Communicated by David Nachmansohn, February 2, 1968 The work of Weiss and his associates,1-3 and more recently of a number of other investigators,4- has established the occurrence of a flux of materials from the soma of neurons toward the peripheral regions of the axon. It has been postulated that this mechanism would account for the origin of most of the axonal protein, although the time required to cover the distance which separates some axonal tips from their cell bodies would impose severe delays.4 On the other hand, a number of observations7-9 have indicated the occurrence of local mechanisms of synthesis in peripheral axons, as suggested by the kinetics of appearance of individual proteins after axonal transection. In this paper we report the incorporation of radioactive amino acids into the protein fraction of the axoplasm and of the axonal envelope obtained from giant axons of the squid. These axons are isolated essentially free from small fibers and connective tissue, and pure samples of axoplasm may be obtained by extru- sion of the axon. Incorporation of amino acids into axonal protein has recently been reported using systems from mammals'0 and fish."I Materials and Methods.-Giant axons of Loligo pealii were dissected and freed from small fibers: they were tied at both ends. Incubations were carried out at 18-20° in sea water previously filtered through Millipore which contained 5 mM Tris pH 7.8 and 10 Muc/ml of a mixture of 15 C'4-labeled amino acids (New England Nuclear Co., Boston, Mass.). -
Neuronal Growth and Death: Minireview Order and Disorder in the Axoplasm
Cell, Vol. 84, 663±666, March 8, 1996, Copyright 1996 by Cell Press Neuronal Growth and Death: Minireview Order and Disorder in the Axoplasm Don W. Cleveland no neurofilaments in axons as a consequence of prema- Ludwig Institute for Cancer Research ture translation termination in NF-L (Ohara et al., 1993). and Departments of Medicine and Neuroscience This results in no detectable NF-L protein, total absence University of California, San Diego of neurofilaments, and resultant axons that almost com- 9500 Gilman Drive pletely fail to grow radially. La Jolla, California 92093 A central limit to neurofilment-dependent radial growth is the velocity and quantity of components deliv- ered to axons by axonal transport. Transport is a neces- Neurons, whose long thin axonal processes represent sity for neurons, as protein synthesis is restricted to the conduits for electrical signaling, are the most asym- cell bodies and dendrites. Membrane-bound particles metric cells in nature. Asymmetry arises in two steps, in axons are trafficked rapidly in both directions using each mediated by different cytoskeletal elements. Initial ATP-dependent microtubule motors. The remaining neurite elongation utilizes actin/myosin for growth cone components, including all known cytoskeletal proteins, locomotion and microtubules as tracks along which pro- teins and membranes are delivered from the cell body toward the developing axon terminus. After a stable synapse has formed, a second phase, termed radial growth, is initiated during which neurofilaments, the in- termediate filaments of most large neurons, accumulate to become the most abundant cytoskeletal elements (Figure 1B) and the axonal diameters increase by up to an order of magnitude (leading to up to a 100-fold in- crease in volume!). -
Evidence for the Glia-Neuron Protein Transfer
CORE Metadata, citation and similar papers at core.ac.uk Provided by PubMed Central EVIDENCE FOR THE GLIA-NEURON PROTEIN TRANSFER HYPOTHESIS FROM INTRACELLULAR PERFUSION STUDIES OF SQUID GIANT AXONS H. GAINER, I. TASAKI, and R. J. LASEK From the Behavioral Biology Branch, National Institute of Child Health and Human Development, the Laboratory of Neurobiology, National Institute of Mental Health, the National Institutes of Health, Bethesda, Maryland 20014, the Department of Anatomy, School of Medicine, Case Western Reserve University, Cleveland, Ohio 44106, and the Marine Biological Laboratory, Woods Hole, Massachusetts 02543 ABSTRACT Incubation of intracellularly perfused squid giant axons in [3H]leucine demon- strated that newly synthesized proteins appeared in the perfusate after a 45-min lag period. The transfer of labeled proteins was shown to occur steadily over 8 h of incubation, in the presence of an intact axonal plasma membrane as evidenced by the ability of the perfused axon to conduct propagated action potentials over this time-period. Intracellularly perfused RNase did not affect this transfer, whereas extracellularly applied puromycin, which blocked de novo protein synthesis in the glial sheath, prevented the appearance of labeled proteins in the perfusate. The uptake of exogenous 14C-labeled bovine serum albumin (BSA) into the axon had entirely different kinetics than the endogenous glial labeled protein transfer process. The data provide support for the glia-neuron protein transfer hypothe- sis (Lasek, R. J., H. Gainer, and J. L. Barker. 1976. J. Cell Biol. 74:501-523; and Lasek, R. J., H. Gainer, and R. J. Przybylski. 1974. Proc. Natl. Acad. Sci, U. -
Nomina Histologica Veterinaria, First Edition
NOMINA HISTOLOGICA VETERINARIA Submitted by the International Committee on Veterinary Histological Nomenclature (ICVHN) to the World Association of Veterinary Anatomists Published on the website of the World Association of Veterinary Anatomists www.wava-amav.org 2017 CONTENTS Introduction i Principles of term construction in N.H.V. iii Cytologia – Cytology 1 Textus epithelialis – Epithelial tissue 10 Textus connectivus – Connective tissue 13 Sanguis et Lympha – Blood and Lymph 17 Textus muscularis – Muscle tissue 19 Textus nervosus – Nerve tissue 20 Splanchnologia – Viscera 23 Systema digestorium – Digestive system 24 Systema respiratorium – Respiratory system 32 Systema urinarium – Urinary system 35 Organa genitalia masculina – Male genital system 38 Organa genitalia feminina – Female genital system 42 Systema endocrinum – Endocrine system 45 Systema cardiovasculare et lymphaticum [Angiologia] – Cardiovascular and lymphatic system 47 Systema nervosum – Nervous system 52 Receptores sensorii et Organa sensuum – Sensory receptors and Sense organs 58 Integumentum – Integument 64 INTRODUCTION The preparations leading to the publication of the present first edition of the Nomina Histologica Veterinaria has a long history spanning more than 50 years. Under the auspices of the World Association of Veterinary Anatomists (W.A.V.A.), the International Committee on Veterinary Anatomical Nomenclature (I.C.V.A.N.) appointed in Giessen, 1965, a Subcommittee on Histology and Embryology which started a working relation with the Subcommittee on Histology of the former International Anatomical Nomenclature Committee. In Mexico City, 1971, this Subcommittee presented a document entitled Nomina Histologica Veterinaria: A Working Draft as a basis for the continued work of the newly-appointed Subcommittee on Histological Nomenclature. This resulted in the editing of the Nomina Histologica Veterinaria: A Working Draft II (Toulouse, 1974), followed by preparations for publication of a Nomina Histologica Veterinaria. -
Squid Giant Axon (Glia/Neurons/Secretion)
Proc. Nat. Acad. Sci. USA Vol. 71, No. 4, pp. 1188-1192, April 1974 Transfer of Newly Synthesized Proteins from Schwann Cells to the Squid Giant Axon (glia/neurons/secretion) R. J. LASEK*, H. GAINERt, AND R. J. PRZYBYLSKI* Marine Biological Laboratory, Woods Hole, Massachusetts 02543 Communicated by Walle J. H. Nauta, November 28, 1973 ABSTRACT The squid giant axon is presented as a teins synthesized in the Schwann cells surrounding the axon model for the study of macromolecular interaction be- tween cells in the nervous system. When the isolated giant are subsequently transferred into the axoplasm. axon was incubated in sea water containing [3Hjleucine MATERIALS AND METHODS for 0.5-5 hr, newly synthesized proteins appeared in the sheath and axoplasm as demonstrated by: (i) radioautogra- Protein synthesis was studied in squid giant axons obtained phy, (ii) separation of the -sheath and axoplasm by extru- from live squid which were kept in a sea tank and used within sion, and (iii) perfusion of electrically excitable axons. hr of obtained The absence of ribosomal RNA in the axoplasm [Lasek, 48 capture. The giant axons were by decapitat- R. J. et al. (1973) Nature 244, 162-165] coupled with other ing the squid and dissecting the axons under a stream of run- evidence indicates that the labeled proteins that are found ning sea water. The axons, 4-6 cm long, were tied with thread in the axoplasm originate in the Schwann cells surrounding at both ends, removed from the mantle, and cleaned of ad- the axon. Approximately 50%70 of the newly synthesized hering connective tissue in a petri dish filled with sea water Schwann cell proteins are transferred to the giant axon. -
11 Introduction to the Nervous System and Nervous Tissue
11 Introduction to the Nervous System and Nervous Tissue ou can’t turn on the television or radio, much less go online, without seeing some- 11.1 Overview of the Nervous thing to remind you of the nervous system. From advertisements for medications System 381 Yto treat depression and other psychiatric conditions to stories about celebrities and 11.2 Nervous Tissue 384 their battles with illegal drugs, information about the nervous system is everywhere in 11.3 Electrophysiology our popular culture. And there is good reason for this—the nervous system controls our of Neurons 393 perception and experience of the world. In addition, it directs voluntary movement, and 11.4 Neuronal Synapses 406 is the seat of our consciousness, personality, and learning and memory. Along with the 11.5 Neurotransmitters 413 endocrine system, the nervous system regulates many aspects of homeostasis, including 11.6 Functional Groups respiratory rate, blood pressure, body temperature, the sleep/wake cycle, and blood pH. of Neurons 417 In this chapter we introduce the multitasking nervous system and its basic functions and divisions. We then examine the structure and physiology of the main tissue of the nervous system: nervous tissue. As you read, notice that many of the same principles you discovered in the muscle tissue chapter (see Chapter 10) apply here as well. MODULE 11.1 Overview of the Nervous System Learning Outcomes 1. Describe the major functions of the nervous system. 2. Describe the structures and basic functions of each organ of the central and peripheral nervous systems. 3. Explain the major differences between the two functional divisions of the peripheral nervous system. -
Neuronal Signaling Neuroscience Fundamentals > the Nerve Cell > the Nerve Cell
Neuronal Signaling Neuroscience Fundamentals > The Nerve Cell > The Nerve Cell NEURONAL SIGNALING SUMMARY ACTION POTENTIALS See: Action Potentials Key Features • All-or-nothing events • Self-propagating • Conduction speed determined by axon diameter (thicker means faster) and amount of myelination (more myelin means faster transmission). CHEMICAL SYNAPSE Steps of Chemical Synapsis 1) The action potential travels down axon of presynaptic neuron. 2) Vesicle fuses with plasma membrane and releases neurotransmitter into the synaptic cleft. 3) Neurotransmitters bind to ligand-gated ion channels, opening them. 4) Ions entering through the open channels cause a depolarization of the membrane, opening voltage-gated ion channels. 5) Ions pass through these voltage-gated ion channels, causing further depolarization of the membrane. 6) This depolarization (action potential) travels along the membrane as more voltage-gated ion channels are opened. ELECTRICAL SYNAPSE • Cytoplasms of adjacent neurons are connected, allowing ions (and action potentials) to travel directly to the next cell. NEURONAL CODING OF STIMULUS STRENGTH Action Potential Frequency • Stimulus strength is based on frequency of action potentials. Action Potential Strength • Strong stimuli can produce another action potential during the relative refractory period. 1 / 7 ABSOLUTE REFRACTORY PERIOD No further action potentials • Voltage-gated sodium channels are open or inactivated so another stimulus, no matter its strength, CANNOT elicit another action potential. RELATIVE REFRACTORY -
Myelination and Axonal Electrical Activity Modulate the Distribution and Motility of Mitochondria at CNS Nodes of Ranvier
The Journal of Neuroscience, May 18, 2011 • 31(20):7249–7258 • 7249 Cellular/Molecular Myelination and Axonal Electrical Activity Modulate the Distribution and Motility of Mitochondria at CNS Nodes of Ranvier Nobuhiko Ohno,1 Grahame J. Kidd,1 Don Mahad,1 Sumiko Kiryu-Seo,1 Amir Avishai,2 Hitoshi Komuro,1 and Bruce D. Trapp1 1Department of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio 44195, and 2Department of Materials Science and Engineering, Case Western Reserve University, Cleveland, Ohio, 44106 Energy production presents a formidable challenge to axons as their mitochondria are synthesized and degraded in neuronal cell bodies. To meet the energy demands of nerve conduction, small mitochondria are transported to and enriched at mitochondrial stationary sites located throughout the axon. In this study, we investigated whether size and motility of mitochondria in small myelinated CNS axons are differentially regulated at nodes, and whether mitochondrial distribution and motility are modulated by axonal electrical activity. The size/volume of mitochondrial stationary sites was significantly larger in juxtaparanodal/internodal axoplasm than in nodal/paranodal axoplasm. With three-dimensional electron microscopy, we observed that axonal mitochondrial stationary sites were composed of multiple mitochondria of varying length, except at nodes where mitochondria were uniformly short and frequently absent altogether. Mitochondrial transport speed was significantly reduced in nodal axoplasm compared with internodal axoplasm. Increased axonal electrical activity decreased mitochondrial transport and increased the size of mitochondrial stationary sites in nodal/paranodal axoplasm. Decreased axonal electrical activity had the opposite effect. In cerebellar axons of the myelin-deficient rat, which contain voltage-gated Na ϩ channel clusters but lack paranodal specializations, axonal mitochondrial motility and stationary site size were similar at Na ϩ channel clusters and other axonal regions. -
Synapse Transmission
Synapse Transmission There are two types of synapses found in your body: electrical and chemical. Electrical synapses allow the direct passage of ions and signaling molecules from cell to cell. In contrast, chemical synapses do not pass the signal directly from the presynaptic cell to the postsynaptic cell. In a chemical synapse, an action potential in the presynaptic neuron leads to the release of a chemical messenger called aneurotransmitter. The neurotransmitter then diffuses across the synapse and binds to receptors on the postsynaptic cell. Binding of the neurotransmitter leads to the production of an electrical signal in the postsynaptic cell. Why does the body have two types of synapses? Each type of synapse has functional advantages and disadvantages. An electrical synapse passes the signal very quickly, which allows groups of cells to act in unison. A chemical synapse takes much longer to transmit the signal from one cell to the next; however, chemical synapses allow neurons to integrate information from multiple presynaptic neurons, determining whether or not the postsynaptic cell will continue to propagate the signal. Neurons respond differently based on information transmitted by multiple chemical synapses. Let’s take a closer look at the structure and function of each type of synapse. Electrical synapses transmit action potentials via the direct flow of electrical current at gap junctions. Gap junctions are formed when two adjacent cells have transmembrane pores that align. The membranes of the two cells are linked together and the aligned pores form a passage between the cells. Consequently, several types of molecules and ions are allowed to pass between the cells.