Advances in Cellular Neurobiology, Volume 1 discusses the topographical anatomy and functional relation of the brain and spinal cord. This book is divided into three main sections-cell differentiation and interaction, aging and pathology, and methodologies. The topics discussed include specializations of non-neuronal cell membranes in the vertebrate nervous system; effects of neurohormones on glial cells; cerebellar granule cells in normal and neurological mutants of mice; and age-related changes in neuronal and glial enzyme activities. The glial fibrillary acidic (GFA) protein in normal neural cells and in pathological conditions; in vitro behavior of isolated oligodendrocytes; and biochemical mapping of specific neuronal pathways are also deliberated in this text. This publication is intended for neurologists, but is also beneficial to students researching on the central nervous system.
Front Cover 1
Advances in Cellular Neurobiology 4
Copyright Page 5
Table of Contents 6
LIST OF CONTRIBUTORS 10
PREFACE 12
SECTION 1: CELL DIFFERENTIATION AND INTERACTION 16
CHAPTER 1. SPECIALIZATIONS OF NONNEURONAL CELL MEMBRANES IN THE VERTEBRATE NERVOUS SYSTEM 18
I. Introduction 18
II. Gap Junctions 19
III. Tight Junctions 25
IV. Assemblies 31
References 41
CHAPTER 2. EFFECTS OF NEUROHORMONES ON GLIAL CELLS 46
I. Introduction 47
II. Models for Glial Cells 48
III. Receptors for Putative Neurohormones 49
IV. Events Secondary to Receptor Activation 58
V. Conclusions 65
References 70
CHAPTER 3. RETROGRADE AXONAL TRANSPORT 84
I. Introduction 84
II. Mechanism of Retrograde Axonal Transport 86
III. Retrograde Transport of Materials Endogenous to the Neuron 98
IV. Retrograde Transport of Materials Exogenous to the Neuron 105
V. Functions of Retrograde Transport of Exogenous Materials 110
VI. Conclusion 119
References 120
CHAPTER 4. BIOCHEMICAL CHARACTERISTICS OF INDIVIDUAL NEURONS 134
I. Introduction 134
II. Single-Cell Samples 136
III. Cell Structure 141
IV. Biochemical Components 145
V. Conclusion 177
References 178
SECTION 2. AGING AND PATHOLOGY 192
CHAPTER 5. CEREBELLAR GRANULE CELLS IN NORMAL AND NEUROLOGICAL MUTANTS OF MICE 194
I. Introduction 195
II. Possible Effect of Purkinje Cells on Proliferation of Granule Cells 198
III. Effect of Glial Cells on Granule Cell Migration 206
IV. Survival of Granule Cells in Mutant Mice (Staggerer and Weaver) 209
V. Parallel Fiber–Purkinje Cell Synapses 212
VI. Granule Cell Transmitter 213
VII. Comments on the Use of Neurological Mutants as Model Systems 217
References 218
CHAPTER 6. CELL GENERATION AND AGING OF NONTRANSFORMED GLIAL CELLS FROM ADULT HUMANS 224
I. Cell Generation and Aging 224
II. Origin of Adult Human Glia-Like Cell Lines 225
III. Theories about Cellular Aging 230
IV. Basic Characteristics of Adult Human Glia-Like Cells in Vitro 234
V. Relation between Cell Generation and Aging in Human Glia-Like Cells 235
VI. Miniclone Analysis of Glia-Like Cells 236
VII. Conclusions 238
References 239
CHAPTER 7. AGE-RELATED CHANGES IN NEURONAL AND GLIAL ENZYME ACTIVITIES 244
I. General Introduction 245
II. Neuron-Specific Enzymes 245
III. Glia-Specific Enzymes 272
IV. Enzymes Associated with Specific Cellular Processes 280
References 286
CHAPTER 8. GLIAL FIBRILLARY ACIDIC (GFA) PROTEIN IN NORMAL NEURAL CELLS AND IN PATHOLOGICAL CONDITIONS 300
I. Introduction 301
II. Biochemical Properties of GFA Protein 301
III. Preparation of Antisera 306
IV. Immunohistochemical Localization of GFA Protein in Adult CNS 307
V. Gliogenesis 310
VI. Astroglial Response to Injury 313
VII. Astroglial Marker in Vitro 314
VIII. Diagnosis of Brain Tumors 317
References 319
SECTION 3. METHODOLOGIES 326
CHAPTER 9. IN VITRO BEHAVIOR OF ISOLATED OLIGODENDROCYTES 328
I. Introduction 329
II. Isolation of Oligodendrocytes 331
III. Oligodendrocyte Subpopulations 343
IV. Culture of Oligodendrocytes 345
V. Conclusions 356
References 357
CHAPTER 10. BIOCHEMICAL MAPPING OF SPECIFIC NEURONAL PATHWAYS 362
I. Introduction 362
II. Techniques for Biochemical Classification of Neurons 363
III. Identification of Interconnections between Neurons Using Different Transmitters 384
References 385
CHAPTER 11. SEPARATION OF NEURONAL AND GLIAL CELLS AND SUBCELLULAR CONSTITUENTS 388
I. Introduction 388
II. Methods of Cell Isolation 390
III. Subcellular CNS Fractions 403
IV. New Isolation Techniques 408
V. The Use of Cell Fractions 410
References 415
CHAPTER 12. SEPARATION OF NEURONS AND GLIAL CELLS BY AFFINITY METHODS 420
I. Introduction 420
II. Techniques of Separation by Affinity Systems 421
III. Ligands for Neural Cell Surfaces 435
IV. Concluding Remarks 447
References 448
Subject Index 458
Effects of Neurohormones on Glial Cells1
Dietrich Van Calker, Max-Planck-Institut für Biochemie, Martinsried, Federal Republic of Germany
Bernd Hamprecht, Physiologisch–Chemisches Institut, Universität Wüzburg, Würzburg, Federal Republic of Germany
Publisher Summary
This chapter focusses on the effects of neurohormones on glial cells. The receptors for several putative neurohormones are expressed by transformed glial cells and by immature glial cells from rodent brain. The two most enigmatic fields of neuroscience, namely, the glial function and the problem of learning and memory, have been combined in the speculation that interactions between neurons and glial cells may be the basis of the higher adaptive functions of the brain. The glial cells and neurons not only exchange trophic or mitotic factors but also integrate their information-processing capacity by the exchange of hormonal signals. Both anatomical and physiological evidence suggests that, in addition to their role as neurotransmitters, biogenic amines might also act as neuromodulators or neurohormones, a mode of operation intermediate between the private addressing of classical synaptic messengers and the broadcasting of neuroendocrine secretion. The problem of obtaining mature glial cells of sufficient purity and integrity from adult brain is still unsolved. Most studies are performed using cultured glial cells, either permanent cell lines derived from tumors or primary cultures from perinatal rodent brain enriched in glia-like cells. The chapter briefly discusses the question of the reliability of these cells as models for neuroglia.
I Introduction
The enormous effort being made to understand the functions of neuroglia may be judged from the increasing number of monographs, anthologies, and reviews dealing with the subject (Glees, 1955; Windle, 1958; Nakai, 1963; Galambos, 1964; De Robertis and Carrea, 1965; Kuffler and Nicholls, 1966, 1977; Bunge, 1968; Lasansky, 1971; Fleischhauer, 1972; Johnston and Roots, 1972; de Vellis and Kukes, 1973; Watson, 1974; Privat, 1975; Somjen, 1975; Fedoroff and Hertz, 1978; Schoffeniels et al., 1978; Varon and Somjen, 1979). Nevertheless, our knowledge of what might be the biochemical function of glial cells is still very limited. The two most enigmatic fields of neuroscience, glial function and the problem of learning and memory, have been combined in the speculation that interactions between neurons and glial cells may be the basis of the “higher” adaptive functions of the brain (Galambos, 1961, 1964; Svaetichin et al., 1965; Roitbak, 1970). A prerequisite for this idea is that glial cells and neurons not only exchange trophic or mitotic factors (for a review of this subject, see Varon and Bunge, 1978) but also integrate their information-processing capacity by the exchange of hormonal signals. The question as to whether glial cells possess receptors for such signals is the subject of this review. Such signaling compounds neither fit into the definition of a “hormone” (which is released into the circulation) nor represent a classic “neurotransmitter” (which is released by the presynaptic terminal and acts at the membranes facing the synaptic cleft, the pre- and postsynaptic membranes). Indeed, both anatomical and physiological evidence suggests that, in addition to their role as neurotransmitters, biogenic amines might also act as “neuromodulators” or “neurohormones,” “a mode of operation intermediate between the private addressing of classical synaptic messengers and the broadcasting of neuroendocrine secretion” (Dismukes, 1977; see also Henn, 1978). A similar role may be assessed to the newly discovered “peptidergic” systems in the brain (Scharrer, 1978). In this article the term “neurohormone” is used to designate compounds that have been shown to or are suspected of, transmitting information across the extracellular space, classic hormones and neurotransmitters as well as agents not yet classified. However, we shall not discuss factors, the only known functions of which are to supply growth-promoting, trophic, mitotic, or “differentiating” influences. These have been comprehensively reviewed by others (Westermark and Wasteson, 1975; Lim et al., 1978; Varon and Bunge, 1978).
II Models for Glial Cells
The problem of obtaining mature glial cells of sufficient purity and integrity from adult brain is still unsolved, although some progress has been made recently (see Henn, this volume). Most studies, therefore, were performed using cultured glial cells, either permanent cell lines derived from tumors or primary cultures from perinatal rodent brain enriched in glia-like cells. This section briefly discusses the question of the reliability of these cells as models for neuroglia.
A Clonal Glial Cell Lines
Since glial cell lines have recently been reviewed (Pfeiffer et al., 1978), only some brief remarks are given to provide background. By far the most widely studied glial cell line is the rat glioma line C6, which was cloned from a N-nitrosomethylurea-induced brain tumor (Benda et al., 1968, 1971) of Wistar–Furth strain rats (P. Benda, personal communication). Although often referred to as “astrocytoma” cells, C6 cells display markers of oligodendroglia such as 2′, 3′-cyclic-AMP phosphohydrolase (Zanetta et al., 1972; Volpe et al., 1975) and inducibility by hydrocortisone or glycerolphosphate dehydrogenase (GPDH) (Davidson and Benda, 1970; de Vellis et al., 1971, 1977; de Vellis and Brooker, 1973), as well as markers of astrocytes such as the glial fibrillary acidic (GFA) protein (Bissell et al., 1975). C6 cells also contain S-100 protein, another putative glial marker (Benda et al., 1968, 1971). For recent reviews on glial markers see Varon (1978), Varon and Somjen (1979), and Laerum et al. (1978). Of the numerous other glial lines that have been developed (Pfeiffer et al., 1978) only human astrocytoma cells were investigated in some detail as far as receptors for neurohormones were concerned. 138MG cells (Pontén and Macintyre, 1968) were derived from a grade III astrocytoma–glioblastoma. These cells contain S-100 and GFA proteins (Edström et al., 1973; Walum, 1975). 1181N1 cells (Perkins et al., 1971) and 1321N1 cells (a subclone of 1181N1, see Clark et al., 1974) are clonal cell lines derived from 118MG cells which originated from human glioblastoma multiforme (Pontén and Macintyre, 1968). EH-118MG cells were developed through the action of the Engelbreth–Holm strain of Rous sarcoma virus on 118MG cells (Pontén and Macintyre, 1968; Macintyre et al., 1969). It is possible that the combinations of markers or functions expressed in the various clonal glial strains reflect the potentialities of glial cells, but that they are not identical with those of any kind of glial cell in the nervous...
Erscheint lt. Verlag | 22.10.2013 |
---|---|
Sprache | englisch |
Themenwelt | Sachbuch/Ratgeber ► Natur / Technik ► Naturführer |
Naturwissenschaften ► Biologie ► Zoologie | |
Technik | |
ISBN-10 | 1-4832-6787-3 / 1483267873 |
ISBN-13 | 978-1-4832-6787-6 / 9781483267876 |
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