Litwack Anandamide

1. Auflage 2009
ISBN: 978-0-08-088789-0
Verlag: Elsevier Science & Techn.
Format: EPUB
Kopierschutz: 6 - ePub Watermark

E-Book, Englisch, 537 Seiten

First published in 1943, Vitamins and Hormones is the longest-running serial published by Academic Press. The Editorial Board now reflects expertise in the field of hormone action, vitamin action, X-ray crystal structure, physiology, and enzyme mechanisms. Under the capable and qualified editorial leadership of Dr. Gerald Litwack, Vitamins and Hormones continues to publish cutting-edge reviews of interest to endocrinologists, biochemists, nutritionists, pharmacologists, cell biologists, and molecular biologists. Others interested in the structure and function of biologically active molecules like hormones and vitamins will, as always, turn to this series for comprehensive reviews by leading contributors to this and related disciplines. This volume reviews recent advances in the formation of endogenous cannabinoids and their receptors, metabolism and relation to disease processes.
*Longest running series published by Academic Press *Contributions by leading international authorities

Autoren/Hrsg.

Litwack, Gerald

Inhaltsverzeichnis

1;Front Cover;1
2;Vitamins and Hormones;4
3;Copyright Page;5
4;Contents;8
5;Contributors;16
6;Preface;22
7;Chapter 1: Enzymatic Formation of Anandamide;24
7.1;I. The Transacylation-Phosphodiesterase Pathway for Anandamide Formation;25
7.2;II. NAT;27
7.2.1;A. Ca-NAT;27
7.2.2;B. iNAT;29
7.3;III. NAPE-PLD;32
7.3.1;A. Structure;32
7.3.2;B. Function;35
7.3.3;C. Tissue distribution;37
7.4;IV. Alternative Pathways Forming NAEs from NAPEs;38
7.5;V. Conclusions;41
7.6;References;42
8;Chapter 2: Organized Trafficking of Anandamide and Related Lipids;48
8.1;I. AEA and the Endocannabinoid System;49
8.1.1;A. Discovery of endocannabinoids;49
8.1.2;B. AEA synthesis;49
8.1.3;C. AEA signaling;50
8.1.4;D. AEA degradation;51
8.1.5;E. Lipid rafts and the fate of AEA metabolites;52
8.2;II. AEA Transport;54
8.2.1;A. Fatty acid transporters;55
8.2.2;B. Lipid transfer proteins;58
8.2.3;C. Characteristics of AEA transport;59
8.2.4;D. Proposed models for cellular AEA accumulation;60
8.2.5;E. Implications of pharmacologically altered AEA signaling;67
8.3;Acknowledgment;68
8.4;References;68
9;Chapter 3: Biosynthesis of Oleamide;78
9.1;I. Introduction;79
9.2;II. Fatty Acid Amide Messengers: Structural Considerations;79
9.3;III. Natural Occurrence of Oleamide;80
9.4;IV. Biologic Actions of Oleamide;81
9.5;V. Proposed Mechanisms for the Biosynthesis of Oleamide;82
9.6;VI. Oleamide Biosynthesis by Peptidylglycine Alpha-amidating Monooxygenase;83
9.7;VII. Discovery of Cytochrome c as an Oleamide Synthase;85
9.8;VIII. Cytochrome c also Catalyzes the Formation of Oleoylglycine and Other Long-Chain Fatty Acylamino Acids;87
9.9;IX. Proposal for an Oleamide Synthesome;89
9.10;X. Apoptosis: A Model for the Mechanism and Regulation of Oleamide Biosynthesis;90
9.11;XI. Considerations for the Investigation of Oleamide Biosynthesis;93
9.12;XII. Future Directions and Concluding Remarks;93
9.13;References;94
10;Chapter 4: Anandamide Receptor Signal Transduction;102
10.1;I. Introduction;103
10.2;II. Cannabinoid Receptor 1;104
10.2.1;A. Regulation of cyclic 106
10.2.2;B. Nuclear signaling pathways;106
10.2.3;C. CB1 Receptor-mediated regulation of ion channels;108
10.2.3.1;1. Calcium channels;108
10.2.3.2;2. Potassium channels;109
10.2.3.3;3. Neuronal plasticity;110
10.3;III. Cannabinoid Receptor 2;112
10.3.1;A. Signaling pathways;112
10.4;IV. Transient Receptor Potential Vanilloid 1;113
10.4.1;A. In the nervous system;114
10.4.2;B. In vasodilation and bronchoconstriction;115
10.5;V. Evidence for Additional Receptors;115
10.5.1;A. Direct activation of ion channels;115
10.5.1.1;1. Voltage-gated Ca2+ channels;115
10.5.1.2;2. Voltage-gated sodium channels;116
10.5.1.3;3. Voltage-gated potassium channels;117
10.5.1.4;4. Task-1;117
10.5.2;B. 5-HT3A receptors;117
10.5.3;C. Nicotinic acetylcholine receptors;118
10.5.4;D. Glycine receptors;118
10.5.5;E. NMDA receptors;119
10.5.6;F. Peroxisome proliferator-activated receptors;119
10.5.7;G. Other GPCRs;120
10.6;VI. Concluding Remarks;121
10.7;References;122
11;Chapter 5: Is GPR55 an Anandamide Receptor?;134
11.1;I. Delta9-Tetrahydrocannabinol, CB1, and CB2 Receptors;135
11.2;II. Functional Evidence for Novel Cannabinoid Receptors;136
11.3;III. Genomics of G Protein-Coupled Cannabinoid Receptors;139
11.4;IV. The Orphan Receptor GPR55;140
11.4.1;A. Patent reports;141
11.4.2;B. Pharmacology of GPR55;142
11.5;V. Endogenous Ligands for GPR55;144
11.5.1;A. Lysophosphatidylinositol;144
11.5.2;B. LPI as a signaling molecule;145
11.5.3;C. LPI and cannabinoids at GPR55: Biased agonism;145
11.6;VI. GPR55 Cellular Signaling Pathways;146
11.6.1;A. Galpha12 and Galpha13;146
11.6.2;B. Signaling downstream of Galpha12 and Galpha13;146
11.6.3;C. GPR55 and Ca2+ signals;147
11.7;VII. Interactions Between GPR55 and CB1 Receptors;149
11.8;VIII. Conclusion: GPR55 as an Anandamide Receptor;151
11.8.1;A. Multiple signaling modalities for GPR55;151
11.8.2;B. Receptor dimerization in GPCRs;153
11.8.3;C. Allosteric effects and biased agonism;154
11.8.4;D. Pharmacology in recombinant and natural systems;154
11.8.5;E. Anandamide and GPR55;155
11.9;References;156
12;Chapter 6: The Endocannabinoid System During Development: Emphasis on Perinatal Events and Delayed Effects;162
12.1;I. Introduction;163
12.2;II. Early Gestation;164
12.2.1;A. The preimplantation embryo and implantation-Critical role for the ECS system;164
12.2.2;B. CB1 receptors and preterm birth: Corticosterone and prenatal stress;167
12.3;III. Neural Development;169
12.4;IV. Postnatal Development;170
12.5;V. Effects of Developmental Manipulation of the ECS System on the Offspring;173
12.6;VI. Conclusions;175
12.7;Acknowledgments;176
12.8;References;176
13;Chapter 7: Cannabinoid Receptor CB1 Antagonists: State of the Art and Challenges;182
13.1;I. Introduction;183
13.2;II. Endocannabinoid System: Control of Energy Balance;184
13.3;III. Cannabinoid CB1 Receptors and CB1 Antagonists;185
13.4;IV. CB1 Antagonists in the Treatment of Obesity and Related Comorbidities;192
13.4.1;A. Clinical trials;192
13.4.2;B. Studies in vitro and in animal models;195
13.4.3;C. Safety and adverse effects;197
13.5;V. Other Emerging Effects of CB1 Antagonists;199
13.6;VI. Therapeutic Prospects;202
13.7;VII. Conclusions;203
13.8;Acknowledgments;204
13.9;References;204
14;Chapter 8: Novel Endogenous N-Acyl Glycines: Identification and Characterization;214
14.1;I. Historical View of Lipid Signaling Discoveries;215
14.2;II. The Identification of Endogenous Signaling Lipids with Cannabimimetic Activity;215
14.3;III. Identification of Additional N-Acyl Amides;216
14.4;IV. N-Arachidonoyl Glycine Biological Activity;217
14.5;V. N-Arachidonoyl Glycine Biosynthesis;217
14.6;VI. N-Palmitoyl Glycine Biological Activity;218
14.7;VII. N-Palmitoyl Glycine Biosynthesis;220
14.8;VIII. PalGly Metabolism;220
14.9;IX. Identification and Characterization of Additional Members of the N-Acyl Glycines;221
14.10;X. Biological Activity of Novel N-Acyl Glycines;223
14.11;XI. Conclusions;224
14.12;References;226
15;Chapter 9: The Endocannabinoid Anandamide: From Immunomodulation to Neuroprotection. Implications for Multiple Sclerosis;230
15.1;I. Introduction;231
15.2;II. AEA as a Neuroimmune Signal;235
15.2.1;A. AEA as modulator of immune function;235
15.2.2;B. AEA as modulator of cytokine network in glial cells;237
15.2.3;C. Regulatory role of anandamide on the production of cytokines the IL-12 family;238
15.3;III. Anandamide and Multiple Sclerosis;242
15.3.1;A. Inhibitors of AEA uptake and metabolism;242
15.3.2;B. Anandamide upregulation under neuroinflammatory condition;243
15.3.3;C. AEA as a neuroprotective agent;245
15.4;IV. Concluding Remarks;246
15.5;Acknowledgment;247
15.6;References;247
16;Chapter 10: Modulation of the Endocannabinoid-Degrading Enzyme Fatty Acid Amide Hydrolase by Follicle-Stimulating;254
16.1;I. Follicle-Stimulating Hormone: Signal Transduction and Molecular Targets;255
16.2;II. Sertoli Cells: Activities and Biological Relevance;260
16.3;III. Overview of the Endocannabinoid System;262
16.4;IV. The ECS in Sertoli Cells;264
16.5;V. Regulation of FAAH by FSH in Sertoli Cells;266
16.6;VI. FAAH Is an Integrator of Fertility Signals;267
16.7;VII. Conclusions;277
16.8;Acknowledgments;278
16.9;References;278
17;Chapter 11: Glucocorticoid-Regulated Crosstalk Between Arachidonic Acid and Endocannabinoid Biochemical Pathways Coordin;286
17.1;I. Introduction;287
17.2;II. The Arachidonic Acid Cascade;289
17.3;III. Glucocorticoid-Mediated Inhibition of cPLA2-Dependent AA Release from Membrane Phospholipids;292
17.4;IV. Biosynthesis of the AA-Containing Endocannabinoids AEA and 2-AG;294
17.5;V. Nongenomic Glucocorticoid-Induced Activation of Endocannabinoid Biosynthesis;297
17.6;VI. Endocannabinoids Metabolization;301
17.7;VII. Crosstalk Between GCs and COX2 in the Control of Neuroinflammation and Neuroprotection;305
17.8;VIII. Crosstalk Between GCs and COX2 in the Control of Synaptic Plasticity and Learning Processes;308
17.9;IX. Coordination of GC-Mediated Control of the Neuroimmune Response and Energy Homeostasis Control;311
17.10;Acknowledgments;318
17.11;References;318
18;Chapter 12: Modulation of the Cys-Loop Ligand-Gated Ion Channels by Fatty Acid and Cannabinoids;338
18.1;I. CB Receptor-Dependent and -Independent Effects of Endocannabinoids;339
18.2;II. Structure and Function of the Cys-Loop LGICs;340
18.3;III. Inhibition of 5-HT3 Receptors by Cannabinoids;341
18.4;IV. Modulation of Gly Receptor Function by Cannabinoids;347
18.5;V. Inhibition of nACh Receptors by Endocannabinoids;351
18.6;VI. Modulation of GABAA Receptor Function by Fatty Acids;352
18.7;VII. Concluding Discussion;353
18.8;References;354
19;Chapter 13: Endogenous Cannabinoids and Neutrophil Chemotaxis;360
19.1;I. Cellular Motility and Neutrophils;361
19.2;II. The Endogenous Cannabinoid System;362
19.3;III. Cannabinoids Modulate Cell Migration;365
19.4;IV. Endocannabinoid Effects on Basal Locomotion of Neutrophils;366
19.5;V. Endocannabinoid Effects on Induced Migration of Neutrophils;366
19.6;VI. Cannabinoid Receptor Expression in Neutrophils;367
19.7;VII. Inhibition of Induced Migration: Which Receptors are Involved?;368
19.7.1;A. CB1 cannabinoid receptors;369
19.7.2;B. CB2 cannabinoid receptors;370
19.7.3;C. Novel cannabinoid receptors;370
19.8;VIII. Inhibitory Signal Transduction Mechanisms: Receptor Crosstalk;373
19.9;IX. Inhibitory Signal Transduction Mechanisms: Disruption of the Actin Cytoskeleton;374
19.10;X. Conclusion;379
19.11;References;380
20;Chapter 14: CB1 Activity in Male Reproduction: Mammalian and Nonmammalian Animal Models;390
20.1;I. Introduction;391
20.2;II. Receptor Properties;391
20.3;III. Brain-Pituitary Axis;394
20.4;IV. Testis;397
20.5;V. Excurrent Duct System;402
20.6;VI. Concluding Remarks;405
20.7;References;405
21;Chapter 15: Anandamide and the Vanilloid Receptor (TRPV1);412
21.1;I. Cannabinoid and Vanilloid Receptors;413
21.1.1;A. Endogenous cannabinoid/vanilloid receptor ligands;414
21.1.2;B. General overlap between the cannabinoid system and the vanilloid receptor;415
21.2;II. Biochemistry of Anandamide;415
21.2.1;A. Anandamide synthesis;415
21.2.2;B. Anandamide transport;417
21.2.3;Anandamide metabolism;418
21.2.3.1;Anandamide breakdown by fatty acid amide hydrolase (FAAH);418
21.2.3.2;Anandamide metabolism by cyclooxigenase-2 (COX-2);418
21.3;III. Anandamide as Vanilloid Receptor (TRPV1) Ligand;419
21.3.1;A. Affinity, potency, and efficacy of anandamide on TRPV1;420
21.3.2;B. Regulation of TRPV1 responsiveness to anandamide;421
21.3.3;C. Anandamide activation of cannabinoid receptors affects TRPV1 responsiveness;422
21.3.4;D. TRPV1 activation regulates anandamide synthesis;424
21.3.5;E. Anandamide metabolism affects TRPV1 responses;425
21.3.6;F. Convergent physiological actions of anandamide and TRPV1 agonists do not necessarily represent direct effects on TRPV1 in both;426
21.3.7;Coactivation of the cannabinoid receptors and TRPV1 often complicates the distinction between these pathways;426
21.4;IV. Other Anandamide Receptors;427
21.5;V. Physiological Actions of Anandamide on TRPV1;427
21.5.1;A. Central nervous system (CNS);427
21.5.2;B. Analgesia;429
21.5.3;C. Peripheral nervous system;430
21.5.4;D. Vascular effects;431
21.5.5;E. Temperature regulation;432
21.5.6;F. Body weight/fat regulation;433
21.6;VI. Future Directions;433
21.7;References;434
22;Chapter 16: Endocannabinoid System and Fear Conditioning;444
22.1;I. Introduction;444
22.2;II. Fear Conditioning;446
22.3;III. Influence of Endocannabinoids on Fear Conditioning;449
22.4;IV. Brain Regions in which Endocannabinoids may Modulate Fear Conditioning;452
22.5;V. Conclusion;456
22.6;References;456
23;Chapter 17: Regulation of Gene Transcription and Keratinocyte Differentiation by Anandamide;464
23.1;I. Introduction;465
23.2;II. Epidermis;468
23.2.1;A. Stages of epidermal differentiation;469
23.3;III. Transcriptional Control of Skin Differentiation;476
23.4;IV. Endocannabinoid System in Epidermis;478
23.5;V. Modulation of the Endocannabinoid System in Differentiating Keratinocytes;479
23.6;VI. Repression of Gene Transcription by Anandamide;480
23.7;VII. Conclusions;482
23.8;Acknowledgments;483
23.9;References;484
24;Chapter 18: Changes in the Endocannabinoid System May Give Insight into new and Effective Treatments for Cancer;492
24.1;I. Introduction;493
24.2;II. Changes in the Endocannabinoid System in Cancer;494
24.3;III. Antiproliferative Effects of Anandamide;496
24.3.1;A. Receptor mediated effects;496
24.3.2;B. Receptor-independent effects;498
24.4;IV. Effects of AEA on Migration, Invasion, and Angiogenesis;499
24.5;V. Targeting Degradation Enzymes of Cannabinoids as an Anticancer Therapy;502
24.6;VI. Tumor Promoting Effects of Anandamide;503
24.7;VII. Conclusions;503
24.8;Acknowledgments;504
24.9;References;504
25;Chapter 19: Use of Cannabinoids as a Novel Therapeutic Modality Against Autoimmune Hepatitis;510
25.1;I. Introduction;511
25.2;II. The Endogenous Cannabinoid System;512
25.3;III. The Biosynthesis of Endocannabinoids;513
25.4;IV. Endocannabinoid System is Autoprotective;513
25.4.1;A. The endocannabinoid system and pathophysiology of liver diseases;513
25.4.2;B. Anti-inflammatory effects of endocannabinoids;515
25.5;V. Autoimmune Hepatitis;515
25.6;VI. Treatment Drawbacks;517
25.7;VII. Cannabinoid/Endocannabinoid System in Hepatitis;517
25.7.1;A. Controversies on the beneficial and deleterious roles of cannabinoid receptors in the regulation of liver disease;521
25.8;VIII. Conclusions and Future Directions;522
25.9;Acknowledgments;523
25.10;References;523
26;Index;528