DOCSLIB.ORG

Regulation of Catecholamine Release from the Adrenal Medulla Under the Physiological Stress Response

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Regulation of Catecholamine Release from the Adrenal Medulla Under the Physiological Stress Response REGULATION OF CATECHOLAMINE RELEASE FROM THE ADRENAL MEDULLA UNDER THE PHYSIOLOGICAL STRESS RESPONSE BY BARBARA A. KURI Submitted in partial fulfillment of the requirements For the degree of Doctor of Philosophy Dissertation Adviser: Dr. Corey Smith Department of Physiology and Biophysics CASE WESTERN RESERVE UNIVERSITY January 2010 CASE WESTERN RESERVE UNIVERSITY SCHOOL OF GRADUATE STUDIES We hereby approve the thesis/dissertation of ______________________________________________________ candidate for the ________________________________degree *. (signed)_______________________________________________ (chair of the committee) ________________________________________________ ________________________________________________ ________________________________________________ ________________________________________________ ________________________________________________ (date) _______________________ *We also certify that written approval has been obtained for any proprietary material contained therein. TABLE OF CONTENTS Table of Contents ii List of Figures iv Acknowledgements vi List of Abbreviations vii Abstract ix Chapter 1: Adrenal Medulla Contribution to Release of Catecholamine Under Stress 1.1 The Adrenal Gland 2 1.2 Stress 7 1.3 Regulation of Catecholamine Release 11 1.4 Cellular Mechanisms Regulating Exocytosis in Chromaffin 18 Cells 1.5 Methods Used to Study Catecholamine Release in Adrenal 22 Chromaffin Cells 1.6 Summary Statement of Thesis Project 32 Chapter 2: Increased Secretory Capacity of Mouse Adrenal Chromaffin Cells by Chronic Intermittent Hypoxia: A Role for Protein Kinase C 2.1 Introduction 36 2.2 Materials and Methods 38 2.3 Results 42 2.4 Discussion 53 ii Chapter 3: PACAP Regulates Immediate Catecholamine Release from Adrenal Chromaffin Cells in an Activity Dependent Manner through a Protein Kinase C Dependent Pathway 3.1 Introduction 57 3.2 Materials and Methods 61 3.3 Results 67 3.4 Discussion 91 Chapter 4: Discussion and Future Directions 4.1 PKC 95 4.2 Sodium Calcium Exchange 102 4.3 T-type Calcium Channels 112 2+ 4.4 IP3 Release of Ca from Internal Stores 112 4.5 Epac 113 4.6 Overall Conclusion 114 4.7 Future Directions 116 Work Cited 123 iii LIST OF FIGURES Figure 1.1 The biosynthesis of catecholamine 6 Figure 1.2 PACAP is an activator of adenylate cyclase and a potent 16 secretagogue Figure 1.3 Capacitance recordings provide a high resolution measure of 26 quantal catecholamine release Figure 1.4 Carbon fiber amperometry quantitatively measures 29 catecholamine release Figure 2.1 Intermittent hypoxia leads to an increased RRP 44 Figure 2.2 Continuous hypoxia does not lead to an increased RRP 46 Figure 2.3 Superoxide dismutase mimetic blocks the CIH-dependent 48 increase in RRP Figure 2.4 The CIH-d4-mediated increase in the RRP is due to an 51 increased PKC phosphorylation Figure 3.1 PACAP stimulation of adrenal chromaffin cells results in an 70 immediate and robust release of catecholamine Figure 3.2 PACAP evokes catecholamine release under elevated 73 sympathetic input Figure 3.3 PACAP-dependent secretion is dependent on extracellular 77 Ca2+ and blocked by PLC and PKC inhibition Figure 3.4 PACAP-dependent Ca2+ signals are dependent on 78 extracellular Ca2+ and blocked by PLC and PKC inhibition Figure 3.5 Ni2+ -sensitive Ca2+ currents in adrenal tissue slices 82 iv Figure 3.6 PACAP-dependent catecholamine secretion is blocked by 85 benzamil, voltage clamp and extracellular Ni2+ Figure 3.7 PACAP-dependent Ca2+ signals are blocked by benzamil, 86 voltage clamp and extracellular Ni2+ Figure 3.8 Epac stimulation elicits nickel-sensitive catecholamine 88 secretion Figure 3.9 Summary diagram for the proposed PACAP signaling 90 pathway Figure 4.1 Phosphorylated Protein Kinase Cδ is found in mouse 99 adrenal medullary tissue Figure 4.2 PACAP knockout mice fail to elicit a secretory response 120 under burst-mode stress stimulation Figure 4.3 PACAP knockout mice express the PACR-1 receptor 121 Figure 4.4 PACAP knockout mice respond to exogenous PACAP 122 v Acknowledgements I would like to thank, first and foremost, my advisor Dr. Corey Smith for his support both professionally and personally. I would like to thank my committee members; Dr Cathleen Carlin, Dr. Carole Liedtke, Dr. Andrea Romani, Dr. Steve Jones, and Dr. Thomas Dick for their guidance and support. Additionally, I would like to thank my lab-mates Dr. Shyue-An Chan, Dr. Bryan Doreian, and Jackie Hill for their support, technical assistance, personal support and friendship. Finally, I would like to thank my family and friends for their unending support. vi List of Abbreviations A Adrenaline Ach Acetylcholine ACTH Adrenocorticotropic Hormone ANOVA Analysis of Variance Cm Capacitance CA Catecholamine CaM Kinase Calmodulin Dependent Protein Kinase cAMP Cyclic Adenosine Monophosphoate CH Continuous Hypoxia CIH Chronic Intermittent Hypoxia DAG Diacylglycerol DBH Dopamine P-hydroxylase Epac Exchange Proteins Activated Directly by cAMP FURA-2 AM Fura-2-acetoxymethyl ester GIRK G-protein Coupled Inward Rectifying K+ Channel GPCR G-protein Coupled Receptor HVA High Voltage Activated Ca2+ Channels IHC Immunihistochemistry IP3 Inositol1,4,5 trisphosphate LVA Low Voltage Activated Ca2+ Channels MnTMPyP manganese (III) tetrakis (1-methyl-4-pyridyl) porphyrin pentachloride NA Noradrenaline vii nAChR Nicotinic Acetylcholine Receptor NCX Sodium Calcium Exchanger PACAP Pituitary Adenylate Cyclase Activating Peptide PACR-1 PACAP Receptor- 1 PFA Paraformaldehyde PKA Protein Kinase A PKC Protein Kinase C PLC Phospholipase C PMA phorbol 12-myristate 13-acetate PNMT Phenylethanolamine N-methyltransferase ROS Reactive Oxygen Species RRP Readily Releasable Pool TBARS Thiobarbituric Acid Reactive Substances TRP Transient Receptor Potential Cation Channels TSH Thyroid Stimulating hormone TTX Tetrodotoxin VIP Vasointestinal peptide XIP Endogenous Exchanger Inhibitory Region viii Regulation of Catecholamine Release from the Adrenal Medulla Under the Physiological Stress Response Abstract by BARBARA A. KURI Release of catecholamine from the adrenal glands is a highly regulated process. The chromaffin cells of the adrenal medulla are the parenchymal cells of the adrenal gland and are capable of releasing catecholamine (adrenaline and noradrenaline) and neuroactive peptides into the circulation. Under autonomic nervous control, the innervating splanchnic nerve directs the release of catecholamine. In this study, we show how chronic intermittent hypoxia (CIH), a common form of metabolic stress, affects the release of catecholamine from the adrenal chromaffin cells, in situ. Using electrophysiological capacitance recording techniques we show that exposure to CIH results in an increase of the amount of catecholamine available for release, upon a given stimulus, through the recruitment of catecholamine containing granules to the readily releasable pool. We show that this is possible through the generation of reactive oxygen species (ROS) and subsequent activation of protein kinase C (PKC). To further address the regulation of catecholamine release under sympathetic stimulation we developed a bipolar stimulation protocol that mimics stimulation frequencies ix at rest and under burst mode stress firing. Using an in situ adrenal gland slice preparation we show that there is an activity dependent regulation of catecholamine release involving pituitary adenylate cyclase activating peptide (PACAP) which is released from the splanchnic nerve under conditions mimicking the burst mode stress firing. We show that PACAP acts through a novel mechanistic pathway that is independent of the conventional sympathetic cholinergic pathway. This characteristic of PACAP makes it an ideal neurotransmitter under high intensity, burst mode sympathetic firing, in that it does not desensitize like the cholinergic pathway. We show that PACAP acts through a G-protein coupled receptor to activate phospholipase C (PLC) which in turn activates PKC. Activation of PKC plays a role in increasing the activity of the sodium calcium exchanger (NCX) in the forward direction to depolarize the cell membrane to potentials that increase the open probability of a Ni2+ sensitive, low voltage activated Ca2+ channel. It is the influx of Ca2+ through this channel to generate the Ca2+ dependent release of catecholamine. x Chapter 1: Adrenal Medulla Contribution to Release of Catecholamine Under Stress 1.1 The Adrenal Gland The adrenal gland is the primary peripheral endocrine gland in the sympathetic stress response. The parenchymal cells of the adrenal medulla are the chromaffin cells [1]. Belonging to the paraneuron family, chromaffin cells of the adrenal medulla are of neural crest origin, capable of eliciting action potentials, and secrete catecholamines under appropriate stimulation [1-3]. Formed during the early stages of development, there are two separate precursors migrate suprarenally and eventually differentiate to make up the adrenal gland. The outer layer of the adrenal gland is derived from mesoderm tissue and becomes the adrenal cortex [4]. The adrenal cortical cells, are not excitable, are not of neural crest origin but, are secretory and responsible for the production and release of glucocorticoids: aldosterone, cortisol and androgens [4]. The cortex comprises approximately 90% of the total adrenal gland mass. The remaining 10% of the adrenal gland is comprised of the fore mentioned chromaffin cells. The adrenal medulla is derived of sympathetic ganglion cells from the neural crest during development. After
Load more

Recommended publications
  • Expression Pattern of Delta-Like 1 Homolog in Developing Sympathetic Neurons and Chromaffin Cells
    Published in "Gene Expression Patterns 30: 49–54, 2018" which should be cited to refer to this work. Expression pattern of delta-like 1 homolog in developing sympathetic neurons and chromaffin cells ∗ Tehani El Faitwria,b, Katrin Hubera,c, a Institute of Anatomy & Cell Biology, Albert-Ludwigs-University Freiburg, Albert-Str. 17, 79104, Freiburg, Germany b Department of Histology and Anatomy, Faculty of Medicine, Benghazi University, Benghazi, Libya c Department of Medicine, University of Fribourg, Route Albert-Gockel 1, 1700, Fribourg, Switzerland ABSTRACT Keywords: Delta-like 1 homolog (DLK1) is a member of the epidermal growth factor (EGF)-like family and an atypical notch Sympathetic neurons ligand that is widely expressed during early mammalian development with putative functions in the regulation Chromaffin cells of cell differentiation and proliferation. During later stages of development, DLK1 is downregulated and becomes DLK1 increasingly restricted to specific cell types, including several types of endocrine cells. DLK1 has been linked to Adrenal gland various tumors and associated with tumor stem cell features. Sympathoadrenal precursors are neural crest de- Organ of Zuckerkandl rived cells that give rise to either sympathetic neurons of the autonomic nervous system or the endocrine Development ffi Neural crest chroma n cells located in the adrenal medulla or extraadrenal positions. As these cells are the putative cellular Phox2B origin of neuroblastoma, one of the most common malignant tumors in early childhood, their molecular char- acterization is of high clinical importance. In this study we have examined the precise spatiotemporal expression of DLK1 in developing sympathoadrenal cells. We show that DLK1 mRNA is highly expressed in early sympa- thetic neuron progenitors and that its expression depends on the presence of Phox2B.
    [Show full text]
  • Novel Autocrine Feedback Control of Catecholamine Release a Discrete Chromogranin a Fragment Is a Noncompetitive Nicotinic Cholinergic Antagonist Sushil K
    Novel Autocrine Feedback Control of Catecholamine Release A Discrete Chromogranin A Fragment is a Noncompetitive Nicotinic Cholinergic Antagonist Sushil K. Mahata,* Daniel T. O’Connor,* Manjula Mahata,* Seung Hyun Yoo,‡ Laurent Taupenot,* Hongjiang Wu,* Bruce M. Gill,* and Robert J. Parmer* *Department of Medicine and Center for Molecular Genetics, University of California, San Diego, California 92093 and Department of Veterans Affairs Medical Center, San Diego, California 92161, and ‡National Institute of Deafness and Communicative Disorders, National Institutes of Health, Bethesda, Maryland 20892 Abstract completely established, recent evidence implicates chromogra- nin A as a precursor of several small biologically active secre- Catecholamine secretory vesicle core proteins (chromog- tion-inhibitory peptides that may play an autocrine regulatory ranins) contain an activity that inhibits catecholamine re- role in neuroendocrine secretion from a variety of cell types (3, lease, but the identity of the responsible peptide has been 7–10). The primary structure of chromogranin A reveals 8–10 elusive. Size-fractionated chromogranins antagonized nico- conserved pairs of basic amino acids that represent potential tinic cholinergic-stimulated catecholamine secretion; the in- proteolytic cleavage sites for the generation of such peptides hibitor was enriched in processed chromogranin fragments, (11–17), and chromogranin A is a substrate for the prohor- and was liberated from purified chromogranin A. Of 15 syn- mone convertases (18–20). of chromogranin A, one To date, several chromogranin A–derived peptides have %80 ف thetic peptides spanning (bovine chromogranin A344–364 [RSMRLSFRARGYGFRG- been identified that affect the secretory function of the parent PGLQL], or catestatin) was a potent, dose-dependent (IC50 cells.
    [Show full text]
  • Extra-Adrenal Chromaffin Cells of the Zuckerkandl´S Paraganglion: Morphological and Electrophysiological Study
    275 Extra-adrenal chromaffin cells of the Zuckerkandl´s paraganglion: morphological and electrophysiological study. Beatriz Galán-Rodríguez, M. Pilar Ramírez-Ponce, Fadwa El Banoua, Juan A. Flores, Juan Bellido and Emilio Fernández-Espejo. Departamento de Fisiología Médica y Biofísica. Universidad de Sevilla. Spain. Correspondence: Dra. Beatriz Galán Rodríguez or Dr. Emilio Fernández-Espejo, Departamento de Fisiología Médica y Biofísica, Facultad de Medicina, Universidad de Sevilla, 41009. Sevilla. Spain. Phone: 34-954-556584; Fax: 34-954-551769; Email: [email protected] ; [email protected] Cell Biology of the Chromaffin Cell R. Borges & L. Gandía Eds. Instituto Teófilo Hernando, Spain, 2004 Cell Biology of the Chromaffin Cell 276 Parkinson´s disease is one of the most important neurodegenerative disorders that affects to one out of a hundred of the world population elder than 65. It has been observed in our laboratory, for the first time, that intrabrain transplantation of chromaffin cell aggregates from the Zuckerkandl´s organ, an extraadrenal paraganglion located adjacent to the lower abdominal aorta, induced gradual improvement of functional deficits in animal models of Parkinson´s disease1. This functional regeneration was likely caused by long-survival of grafted cells and chronic trophic action of dopaminotrophic factors, glial cell line-derived 2,3 4,5 factor (GDNF) and transforming growth factor beta1 (TGF-b1) , which are expressed and delivered by long-surviving grafted chromaffin cells. The objective of this study is to discern the morphological and cytological characteristics of extra-adrenal cells of the Zuckerkandl’s organ. On the other hand, long survival of extra-adrenal chromaffin cells could be related to resistance to hypoxia, since it is certainly know that hypoxia is a primary factor involved in cell death after intrabrain grafting.
    [Show full text]
  • Cell Proliferation
    Proc. Nati. Acad. Sci. USA Vol. 91, pp. 1771-1775, March 1994 Neurobiology Insulin-like growth factors act synergistically with basic fibroblast growth factor and nerve growth factor to promote chromaffin cell proliferation MORTEN FRODIN* AND STEEN GAMMELTOFT*t Department of Clinical Chemistry, Bispebjerg Hospital, DK 2400 Copenhagen NV, Denmark Communicated by Viktor Mutt, November 29, 1993 (receivedfor review August 26, 1993) ABSTRACT We have investigated the effects of insulin- addition, NGF and bFGF stimulate transdifferentiation of like growth factors (IGFs), basic fibroblast growth factor cultured chromaffin cells into a sympathetic neuron-like (bFGF), and nerve growth factor (NGF) on DNA synthesis in phenotype and increase cell survival and catecholamine cultured chromaffin cells from fetal, neonatal, and adult rats synthesis (8, 9, 13-15). In adult rats, chromaffmi-cell replace- by using 5-bromo-2'-deoxyuridine (BrdUrd) pulse labeling for ment decreases after denervation of the adrenal medulla, 24 or 48 h and immunocytochemical staining of cell nuclei. suggesting that neurogenic stimuli can regulate chromaffmi- After 6 days in culture in the absence ofgrowth factors, nuclear cell proliferation (16). BrdUrd incorporation was detected in 30% offetal chromafFin Insulin-like growth factor I and II (IGF-I and IGF-II, cells, 1.5% of neonatal cells, and 0.1% of adult cells. Addition respectively) act as neurotrophic factors in various parts of of 10 nM IGF-I or IGF-ll increased the fraction of BrdUrd- the developing and adult nervous system (17). IGF-II mRNA labeled nuclei to 50% offetal, 20% ofneonatal, and 2% ofadult and immunoreactivity have been demonstrated in adult hu- chromaffn cells.
    [Show full text]
  • The Generation of Monoclonal Antibodies That Bind Preferentially to Adrenal Chromaffin Cells and the Cells of Embryonic Sympathetic Ganglia
    The Journal of Neuroscience, November 1991, 7 7(11): 34933506 The Generation of Monoclonal Antibodies that Bind Preferentially to Adrenal Chromaffin Cells and the Cells of Embryonic Sympathetic Ganglia Josette F. Carnahaw and Paul l-i. Patterson Biology Division, California Institute of Technology, Pasadena, California 91125 Adrenal chromaffin ceils, sympathetic neurons, and small technical limitation in this effort is the lack of markers specific intensely fluorescent (SIF) cells are each derived from the for the various stagesof development within a particular lineage. neural crest, produce catecholamines, and share certain Without such markers, cells making key phenotypic decisions morphological features. These cell types are also partially cannot be identified. It has been especially difficult to find mo- interconvertible in cell culture (Doupe et al., 1985a,b; An- lecular labels for committed progenitor cells. Monoclonal an- derson and Axel, 1988). Thus, these cells are said to be tibodies can be used as highly specific markers, and the hybrid- members of the sympathoadrenal (SA) lineage and could oma method can be manipulated so asto enhancethe likelihood share a common progenitor. To investigate the origins of this of obtaining antibodies against rare antigens of interest (Mat- lineage further, we used the cyclophosphamide immuno- thew and Patterson, 1983; Barald and Wessels,1984; Agius and suppression method (Matthew and Patterson, 1983) to gen- Richman, 1986; Barclay and Smith, 1986; Golumbeski and Di- erate five monoclonal antibodies (SAl-5) that bind strongly mond, 1986; Hockfield, 1987; Mahana et al., 1987; Matthew to chromaffin cells, with little or no labeling of sympathetic and Sandrock, 1987; Norton and Benjamini, 1987; Huse et al., neurons or SIF cells in frozen sections from adult rats.
    [Show full text]
  • Stimulus-Secretion Coupling in Chromaffin Cells Isolated
    Proc. Natl. Acad. Sci. USA Vol. 74, No. 11, pp. 5036-5040, November 1977 Cell Biology Stimulus-secretion coupling in chromaffin cells isolated from bovine adrenal medulla (catecholamine secretion/acetylcholine receptors/K+ depolarization/calcium requirement/microtubule disruption) ALLAN S. SCHNEIDER*, RUTH HERZ*, AND KURT ROSENHECKt * Sloan-Kettering Institute for Cancer Research, Cornell University Graduate School of Medical Sciences, New York, New York 10021; and tDepartment of Membrane Research, Weizmann Institute of Science, Rehovot, Israel Communicated by Francis 0. Schmitt, August 19,1977 ABSTRACT Bovine adrenal chromaffin cells were isolated membrane fusion and exocytosis, (iii) the possible role of cyclic by removal of the cortex and sequential collagenase digestion nucleotides coupled with ion translocation in mediating hor- of the medulla. The catecholamine secretory function of these cells was characterized with respect to acetylcholine stimula- mone and neurotransmitter synthesis and secretion, and (iv) tion, cation requirements, and cytoskeletal elements. The the role of microfilaments, microtubules, and/or a calcium- dose-response curve for stimulated release had its half-maxi- modulated contractile protein system in bringing secretory mum value at 10-5 M acetylcholine, and maximum secretion granules together with the plasma membrane to facilitate ex- was on the average 7 times that of control basal secretion. The ocytosis. Further advances may be possible on these and related differential release of epinephrine versus norepinephrine after questions through the use of isolated chromaffin cells. stimulation with 0.1 mM acetylcholine occurred in proportion to their distribution in the cell suspension. The cholinergic re- In the present work we provide a functional characterization ceptors were found to be predominantly nicotinic.
    [Show full text]
  • Advances in Paraganglioma– Pheochromocytoma Cell Lines and Xenografts
    27 12 Endocrine-Related J-P Bayley and P Devilee PPGL cell lines and xenografts 27:12 R433–R450 Cancer REVIEW Advances in paraganglioma– pheochromocytoma cell lines and xenografts Jean-Pierre Bayley 1 and Peter Devilee 1,2 1Department of Human Genetics, Leiden University Medical Center, Leiden, the Netherlands 2Department of Pathology, Leiden University Medical Center, Leiden, the Netherlands Correspondence should be addressed to J-P Bayley: [email protected] Abstract This review describes human and rodent-derived cell lines and xenografts developed over Key Words the last five decades that are suitable or potentially suitable models for paraganglioma– f paraganglioma pheochromocytoma research. We outline the strengths and weaknesses of various f pheochromocytoma models and emphasize the recurring theme that, despite the major challenges f succinate dehydrogenase involved, more effort is required in the search for valid human and animal cell models f models of paraganglioma–pheochromocytoma, particularly those relevant to cancers carrying f cell lines a mutation in one of the succinate dehydrogenase genes. Despite many setbacks, the f xenografts recent development of a potentially important new model, the RS0 cell line, gives reason f SV40 for optimism regarding the future of models in the paraganglioma–pheochromocytoma f MPC field. We also note that classic approaches to cell line derivation such as SV40-mediated f MTT immortalization and newer approaches such as organoid culture or iPSCs have been f imCC insufficiently explored. As many existing cell lines have been poorly characterized, we f hPheo1 provide recommendations for reporting of paraganglioma and pheochromocytoma f PC12 cell lines, including the strong recommendation that cell lines are made widely available via the ATCC or a similar cell repository.
    [Show full text]
  • Chromaffin Cell Development in Mash1 Mutant Mice 4731
    Development 129, 4729-4738 (2002) 4729 Printed in Great Britain © The Company of Biologists Limited 2002 DEV1866 Development of chromaffin cells depends on MASH1 function Katrin Huber1, Barbara Brühl1, François Guillemot2, Eric N. Olson3, Uwe Ernsberger1 and Klaus Unsicker1,* 1Neuroanatomy, Interdisciplinary Center for Neurosciences (IZN), University of Heidelberg, INF 307, D-69120 Heidelberg, Germany 2IGBMC,CNRS/INSERM/Université Louis Pasteur, BP 163, 67404 Illkirch Cédex, Cu de Strasbourg, France 3Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75239-9148, USA *Author for correspondence (e-mail: [email protected]) Accepted 8 July 2002 SUMMARY The sympathoadrenal (SA) cell lineage is a derivative of population seen in Mash1+/+ mice is maintained in Mash1–/– the neural crest (NC), which gives rise to sympathetic mice at birth. Similar to Phox2b, cells expressing Phox2a neurons and neuroendocrine chromaffin cells. Signals that and Hand2 (dHand) clearly outnumber TH-positive cells. are important for specification of these two types of cells Most cells in the adrenal medulla of Mash1–/– mice do not are largely unknown. MASH1 plays an important role for contain chromaffin granules, display a very immature, neuronal as well as catecholaminergic differentiation. neuroblast-like phenotype, and, unlike wild-type adrenal Mash1 knockout mice display severe deficits in sympathetic chromaffin cells, show prolonged expression of ganglia, yet their adrenal medulla has been reported to be neurofilament and Ret comparable with that observed in largely normal suggesting that MASH1 is essential for wild-type sympathetic ganglia. However, few chromaffin neuronal but not for neuroendocrine differentiation. We cells in Mash1–/– mice become PNMT positive and show now that MASH1 function is necessary for the downregulate neurofilament and Ret expression.
    [Show full text]
  • HISTOLOGICAL TYPING of ENDOCRINE TUMOURS INTERNATIONAL HISTOLOGICAL CLASSIFICATION of TUMOURS No
    HISTOLOGICAL TYPING OF ENDOCRINE TUMOURS INTERNATIONAL HISTOLOGICAL CLASSIFICATION OF TUMOURS No. 23 HISTOLOGICAL TYPING OF ENDOCRINE TUMOURS E. D. WILLIAMS Head, WHO Collaboratmg Centre for the Histologica/ Classificatton of Endocrine Tumours. · Department of Pathology, The Welsh National School of Medicine, Cardiff. Wales, Umted Kingdom in collaboration with R. E. SIEBENMANN L. H. SOBIN lnstitute of Pathology, Pathologist, Stadtspital Triemli, World Hea/th Orgamzation, Zurich, Switzerland Geneva, Switzer/and and pathologists in 13 countries WORLD HEALTH ORGANIZATION GENEVA 1980 ISBN 92 4 176023 O © World Health Organization 1980 Pubhcations ofthe World Health Orgamzation enjoy copyright protection m accordance with the provisions of Protocol2 of the Universal Copyright Convention. For rights of reproduction or translation of WHO publicatwns, m part or in tofo, application should be made to the Office of Publications, World Health Orgamzatwn, Geneva, Sw1tzerland. The World Health Organi­ zation welcomes such applications. The designatwns employed and the presentatwn of the material in this publicatwn do not 1mply the expression of any opinion whatsoever on the part of the Duector-General of the World Health Organization concerning the legal status of any country, territory, city or area or of 1ts authorities, or concerning the delimitation of its front1ers or boundanes. The mention of specific compames or of certam manufacturers' products does not imply that they are endorsed or recommended by the W orld Health Organizatwn in preference to others of a similar nature that are not mentioned. Errors and omJsswns excepted, the names of proprietary products are distingmshed by imt1al capitalletters. Authors alone are responsible for v1ews expressed in th1s publication.
    [Show full text]
  • Uptake and Release of Ca2 by Chromaffin Vesicles
    S timulu s - S ecretion Coupling in Chromaffin Cells Volume I Editors Kurt Rosenheck, Ph.D. Associate Professor Department of Membrane Research The Weizmann Institute of Science Rehovot, Israel Peter I. Lelkes, Ph.D. Laboratory of Cell Biology and Genetics National Institutes of Health Bethesda, Maryland CRC Press, Inc. Boca Raton, Florida TABLE OF CONTENTS Volume 1 Chapter 1 Morphology and Innervation of the Adrenal Medulla 1 Stephen W. Carmichael Chapter 2 Chromaffin Granule Biogenesis and the Exocytosis/Endocytosis Cycle 31 John H. Phillips Chapter 3 The Structure and Dynamics of Chromaffin Granules 55 John H. Phillips Chapter 4 Neuropeptides of the Adrenal Medulla 87 Christopher D. Unsworth and O. Humberto Viveros Chapter 5 Uptake and Release of Ca2+ by Chromaffin Vesicles Ill Manfred Gratzl Chapter 6 Chromaffin Cell Calmodulin 125 J. M. Trifaro and R. L. Kenigsberg Chapter 7 Cytoskeletal Proteins and Chromaffin Cell Activity 155 Dominique Aunis, Dominique Perrin, and O. Keith Langley Index 177 Volume II Chapter 8 Cytosolic Proteins as Intracellular Mediators of Calcium Action During Exocytosis 1 Harvey B. Pollard, Alexander L. Burns, Andres Stutzin, Eduardo Rojas, Peter I. Lelkes, and Kyoji Morita Chapter 9 Liposome-Mediated Introduction of Macromolecules into Isolated Bovine Adrenal Chromaffin Cells 15 Peter I. Lelkes Chapter 10 The Chromaffin Cell Plasma Membrane 37 Kurt Rosenheck Chapter 11 Muscarinic Receptor Mechanisms in Adrenal Chromaffin Cells 51 Allan S. Schneider Chapter 12 Sodium and Calcium Channels in Cultured Bovine Adrenal Medulla Cells 71 Norman Kirshner Chapter 13 Recent Advances in Membrane Biophysics of the Adrenal Chromaffin Cell 87 Yoshiaki Kidokoro Chapter 14 Modulation by Calcium of the Kinetics of the Chromaffin Cell Secretory Response — 97 A.
    [Show full text]
  • Adrenergic Responses to Stress of Crassostrea Gigas 1249
    The Journal of Experimental Biology 204, 1247–1255 (2001) 1247 Printed in Great Britain © The Company of Biologists Limited 2001 JEB3148 EVIDENCE FOR A FORM OF ADRENERGIC RESPONSE TO STRESS IN THE MOLLUSC CRASSOSTREA GIGAS A. LACOSTE*, S. K. MALHAM, A. CUEFF, F. JALABERT, F. GÉLÉBART AND S. A. POULET Station Biologique de Roscoff, CNRS, INSU, Université Pierre et Marie Curie, Paris 6, BP 74, F-29682 ROSCOFF, France *e-mail: [email protected] Accepted 10 January; published on WWW 15 March 2001 Summary Catecholamines and pro-opiomelanocortin (POMC)- Moreover, the nicotinic antagonists hexamethonium and α- derived peptides, some of the central regulators of the bungarotoxin and the muscarinic antagonist atropine stress-response systems of vertebrates, are also present in caused no significant inhibition of catecholamine release in invertebrates. However, studies are needed to determine stressed oysters. Adrenocorticotropic hormone (ACTH) how these hormones participate in the organisation of induced a significant release of noradrenaline, but the neuroendocrine stress-response axes in invertebrates. Our release of dopamine in response to ACTH was not present work provides evidence for the presence of an significant. These results suggest that, unlike that of adrenergic stress-response system in the oyster Crassostrea vertebrates, the adrenergic stress-response system of gigas. Noradrenaline and dopamine are released into the oysters is not under the control of acetylcholine and that circulation in response to stress. Storage and release other factors, such as the neuropeptide ACTH, might of these hormones take place in neurosecretory cells control this system. presenting morphological and biochemical similarities with vertebrate chromaffin cells. Both in vivo and in vitro experiments showed that applications of the Key words: catecholamine, noradrenaline, dopamine, acetylcholine, neurotransmitters acetylcholine or carbachol caused no adrenocorticotropic hormone, chromaffin cell, stress, mollusc, significant release of noradrenaline or dopamine.
    [Show full text]
  • The Sympathoadrenal Cell Lineage: Specification, Diversification, and New Perspectives ⁎ Katrin Huber
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Developmental Biology 298 (2006) 335–343 www.elsevier.com/locate/ydbio Review The sympathoadrenal cell lineage: Specification, diversification, and new perspectives ⁎ Katrin Huber Department of Neuroanatomy and Interdisciplinary Center for Neurosciences, University of Heidelberg, INF 307, D-69120 Heidelberg, Germany Received for publication 7 January 2006; revised 8 July 2006; accepted 11 July 2006 Available online 14 July 2006 Abstract During the past years considerable progress has been made in understanding the generation of cell diversity in the neural crest (NC). Sympathoadrenal (SA) cells constitute a major lineage among NC derivatives; they give rise to sympathetic neurons, neuroendocrine chromaffin cells, and the intermediate small intensely fluorescent (SIF) cells. The classic perception of how this diversification is achieved implies that (i) there is a common progenitor cell for sympathetic neurons and chromaffin cells, (ii) NC cells are instructed to a SA cell fate by signals derived from the wall of the dorsal aorta, especially bone morphogenetic proteins (BMP), and (iii) the local environments of secondary sympathetic ganglia and adrenal gland, respectively, are crucial for inducing differentiation of SA cells into sympathetic neurons and adrenal chromaffin cells. However, recent studies have suggested that the adrenal cortex is dispensable for the acquisition of a chromaffin cell fate. This review summarizes the current understanding of the development of SA cells. It covers the specification of SA cells from multipotent NC crest cells, the role of transcription factors during their development, the classic model of their subsequent diversification as well as alternative views for explaining the generation of endocrine versus neuronal SA derivatives.
    [Show full text]