Bagetta / Corasaniti / Sakurada Advances in Neuropharmacology

1. Auflage 2009
ISBN: 978-0-08-095386-1
Verlag: Elsevier Science & Techn.
Format: EPUB
Kopierschutz: 6 - ePub Watermark

E-Book, Englisch, 504 Seiten

Reihe: ISSN

This volume provides a broad overview of important new advances in the field of Neuropharmacology. In 20 chapters, a selection of international contributors discuss topics including endocannabinoid function, pain, stress, astrocytes etc, and new possibilities for treatments of neurological diseases with neuropharmacological approaches.
- Cutting-edge articles in neuropharmacology
- Discusses new possibilities for treatments of neurological disorders
- Very international authorship providing a global view of the state of research

Autoren/Hrsg.

Bagetta, Giacinto

Corasaniti, M. Tiziana

Sakurada, T.

Sakurada, S.

Inhaltsverzeichnis

1;Front Cover;1
2;Advances in Neuropharmacology;4
3;Copyright;5
4;Contents;6
5;Contributors;16
6;Preface;26
7;Chapter 1: Involvement of the Prefrontal Cortex in Problem Solving;28
7.1;I. Introduction;29
7.2;II. Problem-Solving Behavior, Using a Path-Planning Task;31
7.3;III. Goal Representation and Planning in the Prefrontal Cortex;32
7.4;IV. Synchrony as a State Transition and Goal Transformation;33
7.5;V. Involvement of the Prefrontal Cortex in Planning and Execution;34
7.6;VI. Monitoring Action;35
7.7;VII. Summary and Conclusions;37
7.8;References;37
8;Chapter 2: Gluk1 Receptor Antagonists and Hippocampal Mossy Fiber Function;40
8.1;I. Introduction;41
8.2;II. Pharmacological Tools to Investigate the Roles of KARs;42
8.3;III. Conclusions;51
8.4;References;51
9;Chapter 3: Monoamine Transporter as a Target Molecule for Psychostimulants;56
9.1;I. Introduction;56
9.2;II. MAP-Induced Behavioral Sensitization;57
9.3;III. MAP-Induced Hyperthermia and Neuronal Toxicity;58
9.4;Acknowledgments;59
9.5;References;59
10;Chapter 4: Targeted Lipidomics as a Tool to Investigate Endocannabinoid Function;62
10.1;I. Introduction;63
10.2;II. Endocannabinoids;63
10.3;III. Targeted Lipidomics of the Anandamide Pathway;67
10.4;IV. Targeted Lipidomics of the 2-AG Pathway;72
10.5;V. Conclusions;77
10.6;References;77
11;Chapter 5: The Endocannabinoid System as a Target for Novel Anxiolytic and Antidepressant Drugs;84
11.1;I. The Endogenous Cannabinoid System;85
11.2;II. Endocannabinoid Role in Emotional Reactivity and Mood Tone;87
11.3;III. Effects of Exogenously Administered Cannabinoid Agonists and Antagonists;88
11.4;IV. Enhancement of the Endogenous Cannabinoid Tone;89
11.5;V. Faah-Knockout Phenotype;92
11.6;VI. Conclusions;92
11.7;References;93
12;Chapter 6: Gabaa Receptor Function and Gene Expression During Pregnancy and Postpartum;100
12.1;I. Introduction;101
12.2;II. Concentrations of 3a,5a-THP in Rat Brain and Plasma During Pregnancy and After Delivery;102
12.3;III. Changes in Synaptic GABAA-R Gene Expression During Pregnancy and After Delivery;103
12.4;IV. Changes in Extrasynaptic delta-Containing GABAA-R Gene Expression During Pregnancy and After Delivery;107
12.5;V. Changes in GABAA-R Function in the Rat Hippocampus During Pregnancy and After Delivery;109
12.6;VI. Role of Neuroactive Steroids in GABAA-R Plasticity During Pregnancy: Effects of Chronic Blockade of 5a-Reductase by Finaste;112
12.7;VII. Conclusions;115
12.8;References;118
13;Chapter 7: Early Postnatal Stress And Neural Circuit Underlying Emotional Regulation;122
13.1;I. Introduction;123
13.2;II. Behavioral Response and Neural Circuits in Early Postnatal Stressed Rats;124
13.3;III. Conclusions;131
13.4;References;132
14;Chapter 8: Roles of the Histaminergic Neurotransmission on Methamphetamine-Induced Locomotor Sensitization and Reward: A Study ;136
14.1;I. Introduction;137
14.2;II. Methods and Materials;138
14.3;III. Results and Discussion;139
14.4;IV. Conclusion;142
14.5;References;143
15;Chapter 9: Developmental Exposure To Cannabinoids Causes Subtle And Enduring Neurofunctional Alterations;144
15.1;I. Introduction;145
15.2;II. Ontogeny of the Endocannabinoid System;146
15.3;III. Morphological and Neurofunctional Outcomes Induced by Developmental Exposure to Cannabinoids;148
15.4;IV. Conclusions;154
15.5;References;155
16;Chapter 10: Neuronal Mechanisms for Pain-Induced Aversion: Behavioral Studies Using a Conditioned Place Aversion Test;162
16.1;I. Introduction;163
16.2;II. Anterior Cingulate Cortex;163
16.3;III. Amygdala;164
16.4;IV. Bed Nucleus of the Stria Terminalis;165
16.5;V. Other Brain Regions;167
16.6;VI. Conclusion;168
16.7;References;168
17;Chapter 11: Bv8/Prokineticins and their Receptors: A New Pronociceptive System;172
17.1;I. Introduction;173
17.2;II. Bv8-Related Mammalian Peptides;173
17.3;III. Bv8-Prokineticin Receptors;177
17.4;IV. Role of the Bv8-PK2/PKR System in the Neurobiology of Pain;178
17.5;V. Conclusion;181
17.6;References;182
18;Chapter 12: P2Y6-Evoked Microglial Phagocytosis;186
18.1;I. Introduction;186
18.2;II. Chemotaxis;187
18.3;III. Phagocytosis;188
18.4;IV. Conclusion;188
18.5;References;189
19;Chapter 13: PPAR and Pain;192
19.1;I. Introduction;193
19.2;II. Structure and Function of PPAR;194
19.3;III. PPAR and Inflammation;195
19.4;IV. Neuroinflammation and Pain;196
19.5;V. Role of PPAR in Pain;197
19.6;VI. Conclusion;200
19.7;References;201
20;Chapter 14: Involvement of Inflammatory Mediators in Neuropathic Pain Caused by Vincristine;206
20.1;I. Introduction;207
20.2;II. Characterization of Neuropathic Pain Caused by Vincristine;208
20.3;III. Effects of Vincristine on the PNS;208
20.4;IV. Effects of Vincristine on the CNS;210
20.5;V. Other Anticancer Agents that Elicit Neuropathic Pain;212
20.6;VI. Conclusion;212
20.7;References;214
21;Chapter 15: Nociceptive Behavior Induced by the Endogenous Opioid Peptides Dynorphins in Uninjured Mice: Evidence With Intrathecal N-Ethylmaleimide Inhibiting Dynorphin Degradation;218
21.1;I. Introduction;219
21.2;II. Interaction Between Dynorphins and the NMDA Receptor Ion-Channel Complex;220
21.3;III. Nociceptive Behavior Induced by i.t.-Administered Prodynorphin-Derived Peptides and Polycationic Compounds;221
21.4;IV. Degradation of Dynorphins by Cysteine Proteases;223
21.5;V. N-Ethylmaleimide-Induced Nociceptive Behavior Mediated Through Inhibition of Dynorphin Degradation;224
21.6;VI. Conclusion;227
21.7;References;228
22;Chapter 16: Mechanism Of Allodynia Evoked By Intrathecal Morphine-3-Glucuronide In Mice;234
22.1;I. Introduction;235
22.2;II. Mechanism of M3G-Induced Allodynia: Spinal Release of Substance P and Glutamate;236
22.3;III. Mechanism of M3G-Induced Allodynia: Spinal Activation of NO/cGMP/PKG Pathway;237
22.4;IV. Mechanism of M3G-Induced Allodynia: Spinal ERK Activation;238
22.5;V. Mechanism of M3G-Induced Allodynia; Spinal Astrocyte Activation239
22.6;References;241
23;Chapter 17: (-)-Linalool Attenuates Allodynia in Neuropathic Pain Induced by Spinal Nerve Ligation in C57/Bl6 Mice;248
23.1;I. Introduction;249
23.2;II. Materials and Methods;250
23.3;III. Results;253
23.4;IV. Discussion;258
23.5;References;260
24;Chapter 18: Intraplantar Injection Of Bergamot Essential Oil Into The Mouse Hindpaw: Effects On Capsaicin-Induced Nociceptive Behaviors;264
24.1;I. Introduction;265
24.2;II. General Characteristics of Bergamot Essential Oil;266
24.3;III. Antinociception Induced by the Essential Oil of Bergamot;267
24.4;IV. Linalool-Induced Antinociceptive Activity;270
24.5;References;272
25;Chapter 19: New Therapy for Neuropathic Pain;276
25.1;I. Neuropathic Pain;277
25.2;II. Drug Therapy of Neuropathic Pain-Effectiveness of Narcotic Analgesics;278
25.3;III. Alternative Neural Changes in Morphine-Resistant Neuropathic Pain States;279
25.4;IV. New Drug Therapy for Neuropathic Pain;280
25.5;V. Conclusion;283
25.6;References;283
26;Chapter 20: Regulated Exocytosis from Astrocytes:Physiological and Pathological Related Aspects;288
26.1;I. Introduction;289
26.2;II. Are Astrocytes Specialized Secretory Cells?;290
26.3;III. Calcium-Dependent Glutamate Release from Astrocytes is Deregulated in Pathological Conditions with an Inflammatory Component;307
26.4;References;310
27;Chapter 21: Glutamate Release From Astrocytic Gliosomes Under Physiological And Pathological Conditions;322
27.1;I. New Perspectives in Astrocyte Function;323
27.2;II. Gliosomes as a Model to Study Astrocyte Properties;324
27.3;III. Exocytotic Release of Glutamate from Gliosomes;328
27.4;IV. Glutamate Release Induced by Heterotransporter Activation;335
27.5;V. Glutamate Release from Gliosomes in a Mouse Model of Amyotrophic Lateral Sclerosis;338
27.6;VI. Concluding Remarks;340
27.7;References;341
28;Chapter 22: Neurotrophic and Neuroprotective Actions of an Enhancer of Ganglioside Biosynthesis;346
28.1;I. Introduction;347
28.2;II. Development of a Ceramide Analog PDMP;348
28.3;III. Effects of L- and D-PDMP on Neurite Extension;350
28.4;IV. Facilitation of Functional Synapse Formation and Ganglioside Synthesis by l-PDMP;351
28.5;V. Upregulation of p42 MAPK Activity;353
28.6;VI. Improvement of the Spatial Memory Deficit and the Apoptotic Neuronal Death in Ischemic Rats;353
28.7;VII. Effect of l-PDMP on Biosynthesis of Cortical Gangliosides after Repeated Cerebral Ischemia;356
28.8;VIII. Discussion;358
28.9;References;360
29;Chapter 23: Involvement of Endocannabinoid Signaling in the Neuroprotective Effects of Subtype 1 Metabotropic Glutamate Recepto;364
29.1;I. Introduction;365
29.2;II. Role of mGlu Receptors in CA1 Hippocampal Postischemic Neuronal Death;366
29.3;III. Interactions Between mGlu1 Receptors and Endocannabinoids in the CA1 Hippocampal Region;369
29.4;IV. Conclusions;372
29.5;References;374
30;Chapter 24: NF-kappaB Dimers in the Regulation of Neuronal Survival;378
30.1;I. Nuclear Factor-kappaB (NF-kB) in Brain;379
30.2;II. p50/RelA and c-Rel-Containing Dimers Elicit Opposite Regulation of Neuron Vulnerability ;381
30.3;References;385
31;Chapter 25: Oxidative Stress in Stroke Pathophysiology: Validation of Hydrogen Peroxide Metabolism as a Pharmacological Target to Afford Neuroprotection;390
31.1;I. Introduction;391
31.2;II. Experimental Procedures;392
31.3;III. Results;395
31.4;IV. Discussion;397
31.5;References;400
32;Chapter 26: Role of Akt and Erk Signaling in the Neurogenesisfollowing Brain Ischemia;402
32.1;I. Introduction;403
32.2;II. Stimulation of Endogenous Neural Progenitor Proliferation by Neurotrophic Factors in the Hippocampus;404
32.3;III. Transplantation of Neural Stem Cells and Gene Therapy in the Brain Ischemia;405
32.4;IV. Cell Signaling to Promote Neurogenesis in the Adult Brain;406
32.5;V. Vanadium Compounds are Attractive Therapeutics to Promote Neurogenesis in Neurodegenerative Disorders;406
32.6;VI. Conclusion;409
32.7;References;410
33;Chapter 27: Prevention of Glutamate Accumulation and Upregulation of Phospho-Akt may Account for Neuroprotection Afforded by Be;416
33.1;I. Introduction;417
33.2;II. Materials and Methods;418
33.3;III. Results;422
33.4;IV. Discussion;424
33.5;References;430
34;Chapter 28: Identification of Novel Pharmacological Targets to Minimize Excitotoxic Retinal Damage;434
34.1;I. Introduction;435
34.2;II. Neurochemical and Pharmacological Evidence to Support Excitotoxicity in the Mechanisms of RGC Death in Experimental Glaucom;436
34.3;III. Blockade of Excitotoxicity Sustains the PI3-K/Akt Prosurvival Pathway in Retinal Ischemia;441
34.4;IV. Conclusions;445
34.5;References;445
35;Index;452
36;Contents of Recent Volumes;464
37;Color Plates;493