1;Behavioral Neurobiology of the Endocannabinoid System;31.1;Preface;51.2;Contents;61.3;Biochemistry, Pharmacology, Genetics & Chemistry;121.3.1;The Life Cycle of the Endocannabinoids: Formation and Inactivation;131.3.1.1;Cannabinoid Signalling in the CNS;151.3.1.2;What Are Endocannabinoids?;151.3.1.3;Ester Endocannabinoids;161.3.1.3.1;Synthesis of Ester Endocannabinoids;161.3.1.3.1.1;Regulation of Phospholipase C Activity;191.3.1.3.1.2;Regulation of DGL Activity;191.3.1.3.1.3;Alternative Pathways of DAG and 2AG Synthesis;201.3.1.3.2;Hydrolysis of Ester Endocannabinoids;221.3.1.4;Amide Endocannabinoids;241.3.1.4.1;Synthesis of NAPEs;241.3.1.4.2;Synthesis of Amide Endocannabinoids;251.3.1.4.2.1;Pharmacological and Biochemical Manipulation of NAPE-PLD Activity;261.3.1.4.2.2;Alternative Pathways of Amide ECB Generation;281.3.1.4.3;Hydrolysis of Amide Endocannabinoids;301.3.1.4.3.1;FAAH1 Activity;301.3.1.4.3.2;FAAH2 Activity;311.3.1.4.3.3;NAAA Activity;321.3.1.5;Other Routes of ECB Transformation;321.3.1.5.1;Oxidative Metabolism of ECBs;331.3.1.5.1.1;Cyclooxygenase Activity;331.3.1.5.1.2;Lipoxygenase Activity;341.3.1.5.1.3;Cytochrome P450s and Epoxygenase Activity;341.3.1.6;Stimulation of ECB Synthesis and Release;351.3.1.7;Conclusion;371.3.1.8;References;371.3.2;Endocannabinoid Receptor Pharmacology;461.3.2.1;GPCR Overview;471.3.2.2;Receptor Pharmacology;481.3.2.2.1;GPCR Signaling;481.3.2.2.2;Radioligand Binding;491.3.2.2.3;GTPgammaS Binding as a Measure of GPCR Function;501.3.2.3;CB1 Receptor Gene Structure;531.3.2.3.1;Chromosomal Structure, Potential Alternative Splicing;531.3.2.3.2;CNR1 Polymorphisms;531.3.2.4;CB2 Receptor Gene Structure;541.3.2.4.1;CB2 Receptor Chromosomal Localization and Potential Alternative Splicing;541.3.2.4.2;CNR2 Polymorphisms;551.3.2.5;Structural Characteristics of the CB1 Receptor;551.3.2.6;Structural Characteristics of the CB2 Receptor;571.3.2.7;CB1 and CB2 Receptor Localization;581.3.2.8;Cellular Signaling of CB1 and CB2 Receptors;581.3.2.8.1;Inhibition of Adenylyl Cyclase - Gi/o Coupling of CB1 and CB2 Receptors;581.3.2.8.2;Cannabinoid Receptor Activation of MAP Kinases;591.3.2.8.3;Crosstalk Between Cannabinoid and Other Receptors;591.3.2.8.4;Transactivation Between Cannabinoid Receptors and Tyrosine Kinase Receptors;591.3.2.8.5;Cannabinoid Receptor-Mediated Modulation of Ion Channels;601.3.2.9;Implications of Constitutive Receptor Activity, Protean Agonism, and Inverse Agonism;601.3.2.10;Cannabinoid Receptor Ligands;621.3.2.10.1;Non-Selective CB1/CB2 Receptor Agonists;621.3.2.10.2;CB1 Receptor Antagonists;641.3.2.10.3;CB2 Receptor Agonists;641.3.2.10.4;CB2 Receptor Antagonists;651.3.2.10.5;Allosteric Modulators of Cannabinoid Receptors;651.3.2.11;Non-CB1/Non-CB2 Receptors;661.3.2.11.1;GPR55;661.3.2.11.2;Interactions of Cannabinoids with Ion Channels;661.3.2.12;Conclusions;671.3.2.13;References;671.3.3;Endocannabinoid Receptors: CNS Localization of the CB1 Cannabinoid Receptor;731.3.3.1;Introduction;741.3.3.2;Methodological Considerations for Localization Studies on the Endocannabinoid System;761.3.3.2.1;Negative Controls for Positive Findings;761.3.3.2.2;Positive Controls for Negative Findings;771.3.3.2.3;Quantification of Positive Findings;781.3.3.3;Regional Distribution;781.3.3.4;Cellular Distribution;821.3.3.5;Subcellular Distribution;841.3.3.6;Distribution of Other Molecular Components Involved in 2-AG Signaling;871.3.3.7;Conclusions;881.3.3.8;References;901.3.4;Pharmacological Tools in Endocannabinoid Neurobiology;951.3.4.1;Cannabinoid Receptor Ligands;961.3.4.2;Natural Products and Non-Selective Ligands;971.3.4.2.1;Classical Cannabinoids;981.3.4.2.2;Non-Classical Cannabinoids;981.3.4.2.3;Aminoalkylindoles;991.3.4.2.4;Eicosanoids;991.3.4.3;CB1-Selective Ligands;1001.3.4.3.1;Agonists;1001.3.4.3.2;Antagonists and Inverse Agonists;1001.3.4.3.3;Allosteric Modulators;1021.3.4.4;CB2-Selective Ligands;1031.3.4.4.