ISSN:0892-6638    

DOI:10.1096/fasebj.3.13.2806778

出版商:Wiley    

年代:1989

数据来源: WILEY

摘要:

This paper selectively reviews cellular‐level studies of neurons and neural networks that function to generate rhythmic physiological and behavioral events. Studies of biological rhythms during the last 75 years have modified Sherrington's concept of nervous tissue as primarily reflexive to include the fact that some neuronal activity is also endogenously rhythmic. As a functional group, neurons that initiate and maintain physiological or behavioral rhythms are referred to as central pattern generators. Comparative studies reveal a disorienting variety of biological rhythms and underlying central pattern generator control mechanisms. This paper outlines the taxonomic diversity of biological rhythms, the strengths and limitations of various models for studying central pattern generators, and the ongoing search for general principles of rhythm generation. Studies of rhythmic phenomena displayed by intact, unanesthetized mammals have been greatly enriched by data and concepts derived from invertebrate central pattern generators. This multidisciplinary influence is illustrated by reviewing recent work that aims to localize and characterize the cellular bases of circadian rhythms, reproductive rhythms, and rhythmic changes in motor control related to the sleep cycle. The paper concludes by describing studies that aim to derive a cellular‐level account for oscillator interaction, sensory feedback, and the homeostatic modulation of biological rhythms.— Lydic, R. Central pattern‐generating neurons and the search for general principles.FASEB J.3: 2457‐2468; 1989.

ISSN:0892-6638    

DOI:10.1096/fasebj.3.13.2680703

出版商:Wiley    

年代:1989

数据来源: WILEY

摘要:

The rearranging immunoglobulins (Igs) are a family of recognition and defense proteins found in all vertebrate classes. These proteins consist of two types of polypeptide chains; each of these contains a variable (V) domain, a joining (J) segment, and a constant (C) region, which can itself consist of one to four domains. The distinction betweeen light and heavy chains is an ancient one phylogenetically that is reflected in the structures of V, J, and C regions. Despite the early emergence of these genetic elements, conservatism is apparent in the peptide structures encoded by V, J, and C exons. C regions of heavy chains did not evolve as single units; rather the individual domains show their own clustering patterns, which apparently are independent of heavy‐chain designation or species. C‐region domains of light chains and the T cell receptor β chain are similar to one another and to the most carboxyl‐terminal domain of heavy chains. Comparison of the light chains of sharks, bullfrogs, chickens, and mammals indicated that a phylogenetic distinction can be made betweenxand λ light chains. V and J segments of the rearranging T cell receptors α, γ, and δ are homologous to the corresponding segments of Igs, but their C regions form a group that is markedly distinct from those of conventional Igs and Tcr β.—Marchalonis, J. J.; Schluter, S. F. Evolution of variable and constant domains and joining segments of rearranging immunoglobulins.FASEB J.3: 2469‐2479; 1989.

ISSN:0892-6638    

DOI:10.1096/fasebj.3.13.2509274

出版商:Wiley    

年代:1989

数据来源: WILEY

摘要:

The membrane transport and cytosolic solubilization of hydrophobic ligands, including sterols, fatty acids, retinoids, and certain hydrophobic carcinogens, are facilitated by a group of similar low molecular weight proteins: plasma membrane transport protein, fatty acid binding proteins, sterol carrier protein, and retinoid binding proteins. The cellular content of these proteins, which establishes the capacity of a cell to utilize the various ligands, is determined by events regulating transcription and translation, e.g., the mRNA abundance of liver‐ and gut‐type FABPs is increased by dietary fat, and translation of hepatic FABP appears to be stimulated by insulin. Functions attributable to these lipid binding proteins remain unclear, but data are presented that indicate physiological roles in1) fatty acid transport, esterification, and oxidation,2) steroidogenesis, and3) retinoid uptake, retinaldehyde reduction, and retinol esterification. An exciting and novel prospect for cellular trafficking proteins is the role they may play in regulating gene expression. In this respect, cellular lipid binding proteins, e.g., retinoid binding proteins, may deliver their ligands to nucleartrans‐acting proteins, and thereby modulate genes coding for key proteins involved in lipid metabolism or differentiation. Even though the functions of these proteins still need to be unequivocally established, it is clear that they are important in the overall homeostasis of lipid metabolism.—Clarke, S. D.; Armstrong, M. K. Cellular lipid binding proteins: expression, function, and nutritional regulation.FASEB J.3: 2480‐2487; 1989.

ISSN:0892-6638    

DOI:10.1096/fasebj.3.13.2680704

出版商:Wiley    

年代:1989

数据来源: WILEY

摘要:

Proteins bound for the cell surface, lysosomes, and secretory storage granules share a common pathway of intracellular transport. After their synthesis and translocation into the endoplasmic reticulum, these proteins traverse the secretory pathway by a series of vesicular transfers. Similarly, nutrient and signaling molecules enter cells by endocytosis, and move through the endocytic pathway by passage from one membrane‐bound compartment to another. Little is known about the mechanisms by which proteins are collected into transport vesicles, or how these vesicles form, identify their targets, and subsequently fuse with their target membranes. An important advance toward our understanding these processes has come from the establishment of cell‐free systems that reconstitute vesicular transfers in vitro. It is now possible to measure, in vitro, the transport of proteins from the endoplasmic reticulum to the Golgi, between Golgi cisternae, and the formation of transport vesicles en route from thetransGolgi network to the cell surface. Along the endocytic pathway, cell‐free systems are available to study clathrin‐coated vesicle formation, early endosome fusion, and the fusion of late endosomes with lysosomes. Moreover, the selective movement of receptors between late endosomes and thetransGolgi network has also been reconstituted. The molecular mechanisms of vesicular transport are now amenable to elucidation.—Goda, Y.; Pfeffer, S. R. Cell‐free systems to study vesicular transport along the secretory and endocytic pathways.FASEB J.3: 2488‐2495; 1989.

ISSN:0892-6638    

DOI:10.1096/fasebj.3.13.2680705

出版商:Wiley    

年代:1989

数据来源: WILEY

摘要:

This paper reviews some of the cellular events involved in the immune recognition of foreign proteins. The recognition of an antigen by T lymphocytes is essential for its effective elimination by the host. T lymphocytes of the CD4 or CD8 subset recognize antigen but only after the antigen is handled by antigen‐handling cells (antigen‐presenting cells). Antigen molecules are recognized after an internal processing event by antigen‐presenting cells that results in the generation of immunogenic peptides. Such peptides associate with histocompatibility molecules to form bimolecular complexes on the cell surface. The T cell receptors for antigen recognize the bimolecular complex and initiate the events that result in an inflammatory response. Antigen‐presenting cells also produce molecules — termed co‐stimulators — that stimulate the growth and differentiation of T lymphocytes.—Unanue, E. R.,andCerottini, J.‐C. Antigen presentation.FASEB J.3: 2496‐2502; 1989.

ISSN:0892-6638    

DOI:10.1096/fasebj.3.13.2572499

出版商:Wiley    

年代:1989

数据来源: WILEY

摘要:

Neuromuscular diseases are common in acquired immune deficiency syndrome (AIDS). Although the clinical incidence of peripheral neuropathy has not been systematically studied, various reports suggest that up to 40% of AIDS patients have clinical symptoms. Biopsy and autopsy studies have shown an inflammatory neuropathy with a variable component of demyelination and axonal loss. Evidence of direct involvement by the human immunodeficiency virus (HIV) is scant. Immunosuppression followed by cytomegalovirus (CMV) infection appears to be a direct cause of polyradiculoneuropathy and perhaps other forms of peripheral neuropathy in AIDS. The clinical incidence of myopathy in AIDS is less clear, and clinically less appreciated than the neuropathy. Scattered reports have identified an inflammatory myopathy that does not appear to be due to direct HIV infection, but could be mediated by another human retrovirus. HIV seropositive patients being treated with antiviral drugs develop a unique set of neuromuscular diseases that must be distinguished from the non‐drug‐related conditions.—Wiley, C. A. Neuromuscular diseases of AIDS.FASEB J.3: 2503‐2511; 1989.

ISSN:0892-6638    

DOI:10.1096/fasebj.3.13.2553521

出版商:Wiley    

年代:1989

数据来源: WILEY

摘要:

Rat pulmonary artery endothelial cells incubated with human serum that has been complement‐activated by addition of cobra venom factor reveal a pronounced conversion of xanthine dehydrogenase to xanthine oxidase. This process requires the availability of the fifth component of complement (C5) but not the presence of other components (C2 and C6‐C9). The phenomenon can be reproduced by addition to endothelial cells of purified human recombinant C5a but not C5a desArg or C3a. The enzyme conversion process is relatively rapid (occurring within 5‐10 min), requires the presence of intact endothelial cells, and does not require protein synthesis. Similar effects on endothelial cells have been obtained with human recombinant tumor necrosis factor a and the chemotactic peptide N‐formyl‐Met‐Leu‐Phe. In contrast, bradykinin, recombinant human interleukin 1β, and phorbol ester lack this biological activity. These findings suggest novel effects of inflammatory mediators on endothelial cells.— Friedl, H. P.; Till, G. O.; Ryan, U. S.; Ward, P. A. Mediator‐induced activation of xanthine oxidase in endothelial cells.FASEB J.3: 2512‐2518; 1989.

ISSN:0892-6638    

DOI:10.1096/fasebj.3.13.2806779

出版商:Wiley    

年代:1989

数据来源: WILEY

摘要:

The hypothesis that Na+‐dependent calcium extrusion is important in protecting against neuronal excitotoxicity was tested. In cocultures of embryonic rat hippocampal neurons and mouse neuroblastoma hybrid (NCB‐20) cells, calcium ionophore A23187 (1 μM) or high levels of extracellular K+killed hippocampal neurons selectively, leaving NCB‐20 cells unscathed. Hippocampal neurons showed large, sustained rises in intracellular calcium in response to A23187 or K+, whereas NCB‐20 cells showed only transient calcium responses. The abilities of NCB‐20 cells to reduce the calcium load and to survive exposure to A23187 or K+were dependent on extracellular Na+, suggesting that an active Na+/Ca2+exchange mechanism was important in protecting against cell death. Finally, removal of extracellular Na+reduced the threshold for glutamate neurotoxicity in hippocampal neurons, demonstrating the importance of Na+/Ca2+exchange in protecting against excitotoxicity. Taken together, these findings suggest that differences in cell calcium‐regulating systems may determine whether a neuron lives or degenerates in the face of an excitatory challenge.—Mattson, M. P.; Guthrie, P. B.; Kater, S. B. A role for Na+‐dependent Ca2+extrusion in protection against neuronal excitotoxicity.FASEB J.3: 2519‐2526; 1989.

ISSN:0892-6638    

DOI:10.1096/fasebj.3.13.2572500

出版商:Wiley    

年代:1989

数据来源: WILEY

摘要:

Glutathione metabolism and transport in the choroid plexus were probed by determining the effects of administration to rats of several compounds (buthionine sulfoximine, L‐2‐oxothiazolidine‐4‐carboxylate, L‐(α5,5S)‐α‐amino‐3‐chloro‐4,5‐dihydro‐5‐isoxazole acetic acid, γ‐glutamyl alanine, and glutathione monoethyl ester) on the levels of glutathione and cysteine in the cerebrospinal fluid. The findings indicate that glutathione is actively metabolized in the choroid plexus by pathways similar to those in kidney and other tissues. The level of glutathione in the cerebrospinal fluid can be decreased or increased by giving compounds that do not, under similar conditions, appreciably alter total brain levels of glutathione. Glutathione monoethyl ester is effectively transported into the cerebrospinal fluid.—Anderson, M. E.; Underwood, M.; Bridges, R. J.; Meister, A. Glutathione metabolism at the blood‐cerebrospinal fluid barrier.FASEB J.3: 2527‐2531; 1989.

ISSN:0892-6638    

DOI:10.1096/fasebj.3.13.2572501

出版商:Wiley    

年代:1989

数据来源: WILEY