Neurobiology of Essential Fatty Acids

437 Pages·1992·12.61 MB·English

by  H. van den Bosch

NEUROBIOLOGY OF
ESSENTIAL FATTY
ACIDS
ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY
Editorial Board:
NATHAN BACK, State University of New York at Buffalo
IRUN R. COHEN, The Weizmann Institute of Science
DAVID KRITCHEVSKY, Wistar Institute
ABEL LAJTHA, N.S. Kline Institute for Psychiatric Research
RODOLFO PAOLETTI, University of Milan
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NEUROBIOLOGY OF ESSENTIAL FATTY ACIDS
Edited by Nicolas G. Bazan, Mary G. Murphy, and Gino Toffano
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NEUROBIOLOGY OF
ESSENTIAL FATTY
ACIDS
Edited by
Nicolas G. Bazan
Louisiana State University Eye Center and
. Neuroscience Center
Louisiana State University School of Medicine
New Orleans, Louisiana
Mary G. Murphy
Dalhousie University
Halifax, Nova Scotia, Canada
and
Gino Toffano
FIDIA Research Laboratories
Abano Terme, Italy
SPRINGER SCIENCE+BUSINESS MEDIA, LLC
Library of Congress Catalog 1ng-1n-Pub11cat1on Data
Neurobiology of essential fatty adds / edited by Nicolas G. Bazan,
Mary G. Murphy, and G1no Toffano.
p. cm. — (Advances 1n experimental medicine and biology ; v.
318)
"Proceedings of a symposium on the neurobiology of essential fatty
acids, held July 10-12, 1991, in Palm Cove, Far North Queensland,
Australia"—T.p. verso.
Includes bibliographical references and Index.
ISBN 978-1-4613-6515-0 ISBN 978-1-4615-3426-6 (eBook)
DOI 10.1007/978-1-4615-3426-6
1. Essential fatty acids—Physiological effect—Congresses.
2. Neurochemistry—Congresses. 3. Second messengers (Biochemistry)-
-Congresses. 4. Cellular signal transduction—Congresses.
1. Bazan, Nicolas G. II. Murphy, Mary G. III. Toffano, G.
IV. Series.
[DNLM: 1. Fatty Acids, Essential—physiology—congresses.
2. Second Messenger Systems—congresses. W1 AD559 v.318 / QU 90
N494 1991]
QP752.E84N48 1992
612.8'042--dc20
DNLM/DLC
for Library of Congress 92-16989
CIP
Proceedings of a symposium on the Neurobiology of Essential Fatty Acids,
held July 10-12, 1991, in Palm Cove, Far North Queensland, Australia
ISBN 978-1-4613-6515-0
© 1992 Springer Science+Business Media New York
Originally published by Plenum Press, New York in 1992
Softcover reprint of the hardcover 1st edition 1992
All rights reserved
No part of this book may be reproduced, stored in a retrieval system, or transmitted
in any form or by any means, electronic, mechanical, photocopying, microfilming,
recording, or otherwise, without written permission from the Publisher
PREFACE
It is increasingly evident that polyunsaturated fatty acids (PUFA), which in the past
were often believed to be mere components of cellular membranes of neural tissue, are
actually major determinants of the functional properties of neural cells and are
intimately involved in brain disease processes. The two families of PUFA , which are
derived from the essential polyenes, linoleic (18:2<0>6) and a-linolenic (18:3<0>3) acids,
constitute a major proportion (-30%) of the total fatty acids esterified to brain
phospholipids. Each family is distributed in membranes in a highly specific manner with
respect to brain region, cell type, and position within each of the phosphoglycerides.
Unlike their behavior in other organs, the PUFA components of brain turn over slowly
and are relatively resistant to dietary modification. Their unique distribution and
stability suggest that they play an important role in determining the functional
properties of neural cells. However, until recently very little was known regarding the
precise nature of their involvement.
A great deal of excitement has been generated by the increasing realization that
PUFA and phospholipids play integral roles in transmission of signals across neural
membranes. PUFA, and particularly arachidonic acid (AA), can act as second messen
gers per se, or as substrates for synthesis of eicosanoids (e.g., prostaglandins, 12-lipoxy
genase products) that fulfill this function. Release of PUFA from parent phospholipids,
such as phosphatidyIcholine and phosphatidylinositol, involves the concerted actions of
various lipases, including phospholipase A2 and C, and diacylglycerol lipase. Each of
these appears to be distinct with respect to its substrate requirements and sensitivity to
inhibitors.
A variety of cell-surface receptors are now known to use PUFA or their derivatives
as second messengers. In response to inhibitory transmitters such as FRMFa or dopa
mine, AA is released from Aplysia sensory neurons and 12-HPETE, and related
bioactive products are produced. This triggers increased opening ofK+ channels, hyper
polarization of sensory neurons, and a consequent reduction in activity in the post
synaptic motor cell. By comparison, stimulation of NMDA-type glutamate receptors
results in release of free AA (and perhaps other PUFA), which appears to be
associated directly with inhibition of glutamate uptake into neurons and astrocytes.
Depolarization of hippocampal mossy fibers also involves release of AA which is related
to stimulation of the glutamate receptors that play a central role in the development
of long-term potentiation. It is reasonable to assume that PUFA are intimately involved
in this phenomenon.
Independent of their roles as specific messengers for signal transduction, fatty acids
and phospholipids modulate cell functions through interactions with functional proteins.
Considerable excitement has been generated from observations that unsaturated fatty
acids act synergistically with diacylglycerol (DAG) to activate species of protein kinase
C (PKC), even at basal levels of Ca2+, and may thereby provide a mechanism for
y
sustained cross-talk between receptors. Other studies are using molecular biological ap
proaches to identify specific regions of lipid-PKC interactions.
It has been known for some time that acute pathological events, such as ischemia,
epileptic seizures, hypoglycemic coma, and trauma, trigger phospholipase activation and
accumulation of free PUFA (particularly arachidonic and docosahexaenoic acids) and
other potential second messengers (e.g., DAG, IP3 ' eicosanoids). Possible consequences
of these events include uncontrolled receptor and/or enzyme activation, loss of ionic
(e.g., Ca2+) homeostasis, and lipid peroxidation. Another product of phospholipid
remodeling, and a relative newcomer in lipid neuropathology, is the alkyl-acetyl
phospholipid, platelet-activating factor (PA F). P AF produced in response to ischemic
injury appears to exert its deleterious effects through actions at synaptic membranes,
with possible involvement of excitatory amino acids. However, it is now evident that
P AF also acts at intracellular receptors where it stimulates expression of immediate
early genes, including c{os and c-jun. These rapid but brief genomic responses can be
linked with long-term transcriptional changes and, in this manner, can provide a
mechanism for the neuronal plasticity that is required for repair processes. Such a
mechanism may also be involved in the phenomenon of long-term potentiation.
This book summarizes the results of a Satellite Symposium, "The Neurobiology of
Essential Fatty Acids," that was held in Palm Cove, Far North Queensland, Australia,
in July, 1991. The conference was generously supported by the Fidia Research Founda
tion. The purpose of the symposium was to discuss exciting recent developments
concerning the dynamic involvement of fatty acids and phospholipids both in nervous
system function and in disease processes. The topics spanned a variety of research
interests including the molecular biology of enzyme and gene regulation, physiological
and pharmacological aspects of lipid metabolism, mechanisms of biological signal
transduction (and possible behavioral relationships), as well as the molecular mechan
isms of cerebral ischemia, convulsive disorders, and inborn errors of fatty-acid
catabolism. We were particularly pleased to have some newcomers in the group. It is
largely through this interdisciplinary approach that we are able to gain new perspectives
and to fully appreciate the many challenges that lie ahead. This is certainly one of the
most exciting scientific research fields of our time.
We are grateful to the Fidia Research Foundation for providing the financial
support that made the symposium possible and to Ms. Oriana Casadei, the meeting's
manager. Many thanks also to Ms. Paula Gebhardt for her expert and patient editorial
assistance in the production of this book. And, of course, we are grateful to the
speakers and other participants who contributed their efforts to make this symposium
so valuable.
Nicolas G. Bazan
Mary G. Murphy
Gino Toffano
\II
CONTENTS
PHOSPHOLIPASES A2: PROPERTIES AND MODUlATION
THE INDUCfION OF CELLULAR GROUP II PHOSPHOLIPASE A2
BY CYTOKINES AND ITS PREVENTION
BY DEXAMETHASONE ............. . . . . . . . . . . . . . . . . . . . . . .. 1
H. van den Bosch, C. Schalkwijk, J. Pfeilschifter, and F. Marki
BRAIN PHOSPHOLIPA SES AND THEIR ROLE
IN SIGNAL TRANSDUCfION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 11
Akhlaq A. Farooqui, Yutaka Hirashima, and Lloyd A. Horrocks
CHARACTERISTICS AND POSSIBLE FUNCfIONS
OF MAST CELL PHOSPHOLIPA SES A2 . . . . . . . . . . . . . . . . . . . . . .. 27
Makoto Murakami, Ichiro Kudo, and Keizo Inoue
EXTRACELLULAR PHOSPHOLIPASE A2 . . . . . . . . . . . . . . . . . . . . . . . . .. 35
Edward A. Dennis, Raymond A. Deems, and Lin Yu
ISCHEMIC BRAIN DAMAGE:
FOCUS ON LIPIDS AND LIPID MEDIATORS . . . . . . . . . . . . . . . . .. 41
Bo K. Siesjo and Kenichiro Katsura
CELL SIGNALING AND ESSENTIAL FATlY ACIDS:
CROSS-TALK BE1WEEN RECEPTORS AND MESSENGERS
RECIPROCAL REGULATION OF FArry ACID RELEASE
IN THE BRAIN BY GABA AND GLUTAMATE. . . . . . . . . . . . . . . .. 57
Dale L. Birkle
NMDA RECEPTOR-MEDIATED ARACHIDONIC ACID RELEASE
IN NEURONS: ROLE IN SIGNAL TRANSDUCfION
AND PATHOLOGICAL ASPECfS ........................... 73
Jerzy W. Lazarewicz, E. Salinska, and J.T. Wroblewski
NON-EICOSANOID FUNCfIONS OF ESSENTIAL FArry ACIDS:
REGULATION OF ADENOSINE-RELATED FUNCfIONS
IN CULTURED NEUROBLASTOMA CELLS . . . . . . . . . . . . . . . . . .. 91
Mary G. Murphy and Zenobia Byczko
vii
CONTRIBUTIONS TO ARACHIDONIC ACID RELEASE IN MOUSE
CEREBRUM BY THE PHOSPHOINOSITIDE-
PHOSPHOLIPASE C AND PHOSPHOLIPASE A2 PATHWAyS ..... 103
Grace Y. Sun
MODULATION OF ARACHIDONIC ACID METABOLISM
IN CULTURED RAT ASTROGLIAL CELLS
BY LONG-CHAIN N-3 FATTY ACIDS ........................ 115
C. Galli, F. Marangoni, and A Petroni
MODULATION OF GLUTAMATE RELEASE
FROM HIPPOCAMPAL MOSSY FIBER NERVE ENDINGS
BY ARACHIDONIC ACID AND EICOSANOIDS ................ 121
RV. Dorman, T.F.R Hamm, D.S. Damron, and E.J. Freeman
METABOTROPIC GLUTAMATE RECEPTORS
AND NEURONAL TOXICITY ............................... 137
G. Aleppo, A Pisani, A Copani, V. Bruno, E. Aronica,
V. D'Agata, P.L. Canonico, and F. Nicoletti
METABOLITES OF ESSENTIAL FATTY ACIDS AND OTHER
MEMBRANE-DERIVED SECOND MESSENGERS IN CELL SIGNALING
A ROLE FOR THE ARACHIDONIC ACID CASCADE IN FAST
SYNAPTIC MODULATION: ION CHANNELS AND
TRANSMITTER UPTAKE SYSTEMS AS TARGET PROTEINS ..... 147
A Volterra, D. Trotti, P. Cassutti, C. Tromba, R Galimberti,
P. Lecchi, and G. Racagni
APLYSIA CALIFORNlCA CONTAINS A NOVEL 12-LIPOXYGENASE
WHICH GENERATES BIOLOGICALLY ACTIVE PRODUCTS
FROM ARACHIDONIC ACID ............................... 159
Steven J. Feinmark, Douglas J. Steel, Anoopkumar Thekkuveettil,
Mayumi Abe, Xiang-Duan Li, and James H. Schwartz
ESSENTIAL FATTY ACID DEFICIENCY IN CULTURED SK-N-SH
HUMAN NEUROBLASTOMA CELLS ........................ 171
E.B. Stubbs, Jr., RO. Carlson, C. Lee, S.K. Fisher, AK. Hajra,
and B.W. Agranoff
PHOSPHOLIPID METABOLISM AND SECOND MESSENGER
SYSTEM AFTER BRAIN ISCHEMIA ......................... 183
Koji Abe, Tsutomu Araki, Jun-ichi Kawagoe, Masashi Aoki,
and Kyuya Kogure
DIETARY SUPPLY OF ESSENTIAL FATTY ACIDS,
SYNAPTOGENESIS, AND PHOTORECEPTOR MEMBRANE BIOGENESIS
IMPACT OF DIETARY FATTY ACID BALANCE ON MEMBRANE
STRUCTURE AND FUNCTION OF NEURAL TISSUES .......... 197
M.T. Clandinin, M. Suh, and K. Hargreaves
viii
STRUCTURAL AND FUNCTIONAL IMPORTANCE OF DIETARY
POLYUNSATURATED FATTY ACIDS
IN THE NERVOUS SYSTEM ............................... 211
Jean-Marie Bourre, Michelle Bonneil, Jean Chaudiere, Michel Clement,
Odile Dumont, Georges Durand, Huguette Lafont, Gilles Nalbone,
Gerard Pascal, and Michele Piciotti
LONG AND VERY LONG POLYUNSATURATED FATTY ACIDS
OF RETINA AND SPERMATOZOA: THE WHOLE
COMPLEMENT OF POLYENOIC FATTY ACID SERIES ......... 231
Marta 1. Aveldafto
PHOSPHOLIPID METABOLISM IN RAT INTESTINAL MUCOSA
AFTER ORAL ADMINISTRATION
OF L YSOPHOSPHOLIPIDS ................................. 243
Alessandro Bruni, Paolo Orlando, Lucia Mietto, and Giampietro Viola
CARBACHOL-STIMULATED RELEASE OF ARACHIDONIC ACID
AND EICOSANOIDS FROM BRAIN CORTEX
SYNAPTONEUROSOME LIPIDS OF ADULT
AND AGED RATS ........................................ 251
Joanna Strosznajder and Marek Samochocki
CARBACHOL-INDUCED STIMULATION OF
INOSITOL PHOSPHATES, ARACHIDONIC ACID AND
PROSTAGLANDIN F2a IN RABBIT RETINA ................... 259
Neville N. Osborne
INDUCED AND SPONTANEOUS SEIZURES IN MAN
PRODUCE INCREASES IN REGIONAL BRAIN LIPID
DETECTED BY IN VIVO PROTON MAGNETIC
RESONANCE SPECTROSCOPY ............................. 267
Bryan T. Woods and Tak-Ming Chiu
NETWORK OF SIGNAL TRANSDUCTION PATHWAYS
INVOLVING LIPIDS: PROTEIN KINASE C-DEPENDENT
AND -INDEPENDENT PATHWAyS .......................... 275
R Bell, D. Burns, T. Okazaki, and Y. Hannun
ESSENTIAL FATlY ACIDS, EXCITABLE MEMBRANE
PHOSPHOLIPIDS, AND PATHOPHYSIOLOGY
CONSERVATION OF DOCOSAHEXAENOIC ACID IN THE RETINA .... 285
RE. Anderson, P.J. O'Brien, RD. Wiegand, c.A. Kautz,
and A.M. Stinson
DOCOSAHEXAENOIC ACID UPTAKE AND METABOLISM IN
PHOTORECEPTORS: RETINAL CONSERVATION BY AN
EFFICIENT RETINAL PIGMENT EPITHELIAL
CELL-MEDIATED RECYCLING PROCESS .................... 295
Nicolas G. Bazan, William C. Gordon, and Elena B. Rodriguez de Turco
ix
ESSENTIAL FArrY ACIDS
AND NEURODEVELOPMENTAL DISORDER ................. 307
Michael A. Crawford
REGULATION OF ARACHIDONIC ACID METABOLISM
IN THE PERINATAL BRAIN DURING DEVELOPMENT
AND UNDER ISCHEMIC STRESS ........................... 315
Ephraim Yavin, Baruch Kunievsky, Nicolas G. Bazan,
and Shaul Harel
INTERACTIONS OF PHOSPHOLIPIDS AND FREE FArrY ACIDS
WITH ANTIDEPRESSANT RECOGNITION BINDING SITES
IN RAT BRAIN .......................................... 325
Marta Stockert, Luis M. Zieher, and Jorge H. Medina
VERY LONG-CHAIN FArrY ACIDS IN PEROXISOMAL DISEASE ...... 331
A. Poulos, K. Beckman, D.W. Johnson, B.C. Paton,
B.S. Robinson, P. Sharp, S. Usher, and H. Singh
LONG CHAIN OMEGA 3 POLY UNSATURATES
IN FORMULA-FED TERM INFANTS ......................... 341
R.A. Gibson, M. Makrides, K.J. Clark, M.A. Neumann,
and D.R. Lines
SEVERE CHANGES IN POLYUNSATURATED FATTY ACIDS
IN THE BRAIN, LIVER, KIDNEY, AND RETINA
IN PATIENTS WITH PEROXISOMAL DISORDERS ............. 347
Manuela Martinez
DEGRADATION OF PHOSPHOLIPIDS AND PROTEIN KINASE C
ACTNA TION FOR THE CONTROL
OF NEURONAL FUNCTIONS .............................. 361
Tetsutaro Shinomura, Hiroyuki Mishima, Shinji Matsushima,
Yoshinori Asaoka, Kimihisa Yoshida, Masahiro Oka,
and Yasutomi Nishizuka
ESSENTIAL FATlY ACIDS
AND EXCITABLE MEMBRANE PHOSPHOLIPIDS
DISPOSITION KINETICS OF PHOSPHOLIPID LIPOSOMES ............ 375
Pietro Palatini
BEHAVIORAL AND MORPHO-FUNCTIONAL CORRELATES
OF BRAIN AGING: A PRECLINICAL STUDY WITH
PHOSPHATIDYLSERINE .................................. 393
Maria Grazia Nunzi, Diego Guidolin, Lucia Petrelli,
Patrizia Polato, and Adriano Zanotti
RECEPTOR COUPLING TO PHOSPHOINOSITIDE SIGNALS .......... 399
P. Kurian, L.J. Chandler, R. Patel, and F.T. Crews